In fact, even in response to primary taste qualities, the pattern of individual brain activity is consistent when one person is measured on several occasions, but people vary from each other, with each person's pattern being nearly unique [ 98 ]. Inside the taste receptor cell, two proteins combine to create a sweet receptor [ 99 , ].
In humans, if T1R3 pairs with the first member of this family, T1R1, the receptor is sensitive to compounds such as monosodium glutamate that are described as savory or umami , a Japanese word that translates as "delicious. Inbred mouse strains differ in their intake of saccharin and other sweeteners, and the results of experiments in breeding suggested that an allele of a single gene was partially responsible for these differences [ ].
Then, through positional cloning approaches, this gene was identified and found to be Tas1r3 [ 99 , - ]. Alleles of the mouse Tas1r3 gene are related to differences in the consumption of sweeteners [ ]. Recordings of the peripheral taste nerves suggest that mice with the low-preference Tas1r3 alleles exhibit lower nerve firing in response to saccharin or other sweeteners [ 52 , ].
Removal of the Tas1r3 gene in mice results in a diminished response to most sweeteners [ ], and when both genes, Tas1r2 and Tas1r3 , are removed or "knocked out," the response to sweeteners disappears [ ]. The results of mouse gene knockout studies disagree about the degree to which mice lacking these receptors learn to drink sweeteners if given periods of exposure to sweetened water. However, in mice unaccustomed to sweetened water, those with removal of one or both sweet receptors do not consume these solutions in preference to water. Likewise, domestic cats and tigers do not prefer sweet solutions compared with water.
This lack of interest in sugar is probably because they cannot taste sweetness because the DNA sequence of one of the relevant receptor genes TAS1R2 has decayed over time [ ].
“It Takes the Bitter and the Sweet”
If DNA sequence variants have a large effect on the intake of sweeteners in mice and cats, then it is possible that this may also be true in humans. Because the peripheral neural responses of humans to sugars predict their verbal reports about sweet intensity [ ], peripheral differences in taste sensitivity may be a component of human behavior toward sweetness. Cell-based assay systems have been developed to study the function of sweet receptors, and in experiments where the DNA sequence of the genes were modified, the results suggest that small changes in the specific amino acid sequence of in the human T1R2 and T1R3 protein can lead to differences in intracellular signaling in response to sweeteners [ , ].
These experiments, taken in conjunction with individual differences in the psychophysical responses to sweeteners [ - ], suggest that alleles of these receptors might influence sweet perception. A full range of human variation in sweet perception probably exists [ 12 , , ], and genetic variation in taste receptor genes may account for some or many of these person-to-person differences. How genetic differences in sweet perception or liking that might exist in humans might translate into food intake and food preference is unclear.
A review of the literature concluded that, although there was evidence that the degree of liking or preference for individual food items, including sweet items such as candy or sugared coffee, was genetically determined, the pattern of macronutrient consumption, such as whether the person ate more carbohydrate than fat, was more heritable [ ]. Since the publication of that review, two studies have reported that families demonstrated significant genetic linkage for sugar intake to several chromosomal locations [ , ], one of which is near a sweet receptor gene 1p Overall, there is modest evidence that genetic differences among people might account for a portion of individual differences in the consumption of sweet foods and drinks.
There are explanations for person-to-person differences in taste function other than genetic differences. For instance, hormones modify taste receptor cell activity and differ in concentration among people. Leptin is one example: although its receptors are located primarily in the hypothalamus, several peripheral sites of action have been discovered. One such site is on the taste receptor cell itself, and studies in mice have demonstrated a role for leptin in suppressing the physiological and behavioral responses to sweets [ ].
Mice were administered exogenous leptin, which, through its action on the sweet taste receptor, suppressed the neuronal activation to sweet stimuli in normal mice, which subsequently reduced their consumption of sweet solutions. As demonstrated in other studies that employ mice as model organisms, the extrapolation of mouse data to humans must be approached with caution.
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Although one study found no relationship between plasma leptin concentration and sweet preference in obese women [ 85 ], the manipulation of plasma leptin concentrations in humans and their consequences for the perception and preferences for sweets may be a logical next step in unraveling how the body uses the perception of taste to regulate energy consumption.
Hormones and neurotransmitters that participate in higher-order cortical brain systems that organize the conscious perception of sweet or that regulate the rewarding properties of sweet may further serve to control our reaction to sweet chemicals for a review, see Levine et al. Family studies of addiction have demonstrated that alcoholics and their family members prefer sweeter solutions than do nonalcoholic family members, suggesting that alcohol and sweeteners may share similar reward pathways in the brain [ 11 ].
The hypothesis that the rewarding properties of opioid-receptor-stimulating drugs and sweet taste are controlled by a common neural substrate is upheld further by the ability of naloxone, an opioid antagonist, to reduce both the positive properties of opiates and the preference for the taste of sweet [ , ]. Scientists are currently investigating alleles of genes that code for opioid receptors to determine if these alleles may be associated with the sensitivity to the rewarding properties of sugar and also to the suppressive abilities of naloxone. The perception of sweet has had an extensive role in our evolution, but no more so than the taste of bitter.
Vegetables contain many toxic compounds and are often bitter as a consequence, although humans have been working to breed out the bitter components and enhance the sweet components of our foods since selective plant breeding and human agriculture began. Plants cannot run from predators and so have developed chemical defenses that work by causing illness when eaten: by reducing enzyme activity, irritating the mouth and gut, provoking an allergic response, or altering hormone metabolism [ ]. Early humans learned to heat plants to the point that many bitter compounds were less bitter and less toxic, and to add sweeteners to bitter foods.
Both practices have expanded the human food supply. Sweetness is used to mask the bitterness of medicines, and one French aphorism summarizes despair as "an apothecary without sugar. Children with a genetic sensitivity to some bitters report that they like more highly concentrated sweetness compared with children who are less genetically sensitive to bitter [ 57 ].
Therefore, individual differences in bitter sensitivity may influence sweet intake, especially in children.
The Human Sweet Tooth
The term "sweet tooth" has been coined to describe the preferences of a person who "likes" sweets, but it is less clear whether simply liking sweets can predict the tendency to consume more sweets. Our actual behavior toward choosing to consume sweet foods is harder to decipher and may stem both from our liking and desire for their taste and from the environment and culture in which we live. Furthermore, our behaviors toward sweets have consequences for our health, and these consequences provide feedback that could serve to either reinforce or alter our future behaviors toward their consumption.
As described earlier in this chapter, there are a variety of different responses to the taste of sweet, and these surely play a role in our motivation to eat sweets. However, another reason that sugar may be consumed is for benefits other than taste e. Because there are several types of naturally occurring sugars and enzymatic steps associated with the specifics of their digestion, people vary in their ability to digest sugars. A difficulty in digesting sugar may, consciously or unconsciously, change behavior toward sugar.
Some people may even begin to find the taste of sweet unpalatable, because they begin to associate this taste with the negative digestive consequences caused by eating sweet foods [ ]. This behavioral effect is called a conditioned taste aversion [ ]. These behavioral changes may, in turn, have consequences on health. For example, people with hereditary fructose intolerance learn to avoid fructose; as a consequence, they often do not have dental caries or other secondary problems related to sugar consumption.
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Behaviors toward sweets may also be formed by our psychological need for the rewarding properties of sugars. Sweets may alleviate depression and premenstrual symptoms and provide relief from the cravings for other drugs, because sweet taste releases opiates into the blood [ ]. The pacification provided by sugar and sweets has been demonstrated to increase the liking of sweets [ ] and may also translate into a behavioral tendency to consume more sweets.
emharchaetizah.ga Studies that have examined the intake of sweets in women with psychiatric problems have reported that their consumption is increased compared with those without reported psychiatric problems [ 42 ]. Overall, sugar is consumed because of its pleasant taste, ease of digestion, and positive effect on mood, and these three reasons are not mutually exclusive; each probably makes a contribution to overall behavior.
People's behaviors toward sweets are also biased by circumstance and by their beliefs about the food or drink they taste. If people are told they are drinking a particular brand of soft drink, they will have a different pattern of brain activation compared with the activation seen when they drink the same drink but are not told the brand name, or if they are told the beverage is a different brand name [ ]. Although the chemical stimulation from the beverage is the same, previous experience and the person's beliefs about a particular brand alter the response of the brain as the beverage is tasted.
A humorous example of the power of learning and experience comes from a study of newly married women from Oaxaca, Mexico, who reported a change in their sweet preference after marriage that brought them closer to the preference of their mother-in-law [ ]. Thus, learning from our families and culture whether sweets are either acceptable or unacceptable may influence our behavior toward liking and consuming them and may have consequences for our health.
Our willingness to consume sweet nutrients is also probably influenced by supposed or known dietary effects that we have encountered personally, been advised of by health professionals, or read in popular literature.
The highly caloric nature of most nutrients that contain sugars has led many individuals to avoid or restrain their intake of such substances. In addition, adverse effects on dental health and the threat of other undesired health-related conditions may quell the desire to eat sweets. Thus, despite the almost universal liking for the "taste" of sweets, many find the idea of consuming them in excess to be "bittersweet. One such perceived negative effect on health is the fear that excess sugar consumption leads to obesity. However, studies on the effects of sweet intake on body weight have yielded conflicting evidence, some demonstrating a negative correlation between sweet intake and body weight and some reporting the opposite, a positive correlation between sweet intake and body weight for a review, see Hill and Prentice, [ ].
Studies that have measured food intake outside of the laboratory have mostly reported that lean subjects consume more of their total calories from sugar than overweight or obese subjects. This is not surprising given that some heavier people may be restraining their intake of foods that they consider more "fattening.
Research on the biochemistry of energy expenditure reveals the specific metabolic consequences of eating different food types, including sugars. In contrast to fats, sugars are biologically "expensive" to store and are therefore burned as calories before fats [ ]. Thus, if we contrast a diet high in sugars to a diet high in fat, a sugar-rich diet would seem to indicate a higher rate of metabolism and produce a leaner person.
However, our daily food intake is more complex, and many foods we consume that are high in sugar are also high in fat. In fact, according to one study, high sugar content improves the palatability of foods high in fat, which may cause one to consume more fatty food [ 54 ].
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In addition, the rewarding pleasurable qualities of sweet foods may lead some to consume sweet foods in excess of dietary requirements, to self-soothe. Furthermore, the state of the food i. In studies where subjects are asked to add sugar as a liquid supplement to their diets, they do not appear to compensate for the additional calories by decreasing their intake of other food sources [ ]; however, when sugar is introduced into the diet as a solid, there is a subsequent decrease in the amount of additional calories that are consumed [ ].
It appears that our choice to eat sweet foods either as a replacement or as an addition to other nutrients may be a more correct predictor of whether sweet foods will have an effect on body weight than are mere measurements of total sweet intake.
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Thus, both the attitudes we have toward eating sweets and our actual eating behaviors are important in our regulation of body weight. Another well-known consequence of consuming excess sugars is the negative impact on dental health [ ]. When sugar is consumed, particularly sucrose, naturally occurring bacteria inside the mouth interact with the sugar and produce acids that demineralize enamel on teeth. This demineralization process creates dental caries lesions on teeth , which produce pain and, if left untreated, will erode and destroy teeth.
The amount and severity of dental caries are positively correlated with sugar intake, and particularly with extrinsic sugars e. For example, foods such as bakery confections, including cookies, candies, and cakes, are much more cariogenic than are foods containing intrinsic sugars, such as milk and fruits.
Some have concluded that sugar is no longer a large threat to dental health because of the addition of fluoride a remineralizing agent to drinking water and to toothpastes. However, studies have revealed that, even in those receiving treatments of fluoride, a strong positive correlation remains between high sugar consumption and the prevalence of caries. Nevertheless, the combination of fluoride and lowered sugar intake does appear to have a synergistic effect on the reduction of dental caries.