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The Neuroscience of Tasting Sweet

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Jessica Varney's picture

I am notorious within my circle of friends for having a bit of a sweet tooth. I drink an a.m. soda, have dessert after both lunch and dinner, and can inhale a bag of candy in the blink of an eye. There is a range in human preference for sweets, from sugar addicts like myself to my black-coffee-drinking peers. While sugar is the most universally liked of the five basic tastes, the liking and enjoyment of sweet tastes is not uniform across people or populations (1). As human sugar consumption continues to rise, researchers have begun to examine the neurological mechanism of taste with a critical eye. By investigating the way sweet flavors are recognized and processed, scientists may be able to apply this knowledge to create a better artificial sweetener and help people manage side effects of sugar consumption.


Taste is a useful evolutionary tool. Many poisonous or rotten foods also have a foul taste that often prevents the consumer from ingesting it; pleasurable tastes encourage consumption, and many pleasurably tasting foods contain valuable nutrients. Sweet foods exemplify this, as they are consumed because they taste pleasant and contain sugars that provide energy that the body can readily break down (2). The detection of sweet food is evolutionarily favorable, and it follows that there is a genetic component of tasting sweetness.


The upper surface of the tongue is covered by approximately 10,000 taste buds. Individual taste buds contain between fifty and one hundred receptor cells that can detect the five primary tastes: sweet, sour, bitter, salty, and savory umami (2). Some taste buds are clustered on the tongue's surface in raised protrusions called papillae. Inside the papillae, taste receptor cells make two types of proteins that combine and are inserted into receptor cell's membrane to form taste receptors. The taste receptor cells contain neuropeptides that, when secreted, can modify and modulate the taste receptors in neighboring cells (1). When sugars come into contact with the tongue, they bind to a sweet taste receptor proteins that trigger a cascade of biochemical sweetness signals to the brain (3).


The genetic component of sweetness preference is thought to be the result of two genes, T1r2 and T1r3. The two genes code for the two proteins that combine to form the sweetness taste receptor. In addition, T1r3 is also activated by itself in the presence of high concentrations of pure sugar, but not by low concentrations or artificial sweeteners. It is believed that artificial sweeteners only activate the T1r2+T1r3 receptor, which may explain why artificial sweeteners, while chemically similar to natural sugars, aren't perceived as being as sweet as natural sugars. A genetic component to sweetness preference implies that human variation in sweetness preference may be explained by variability within the T1r2 and T1r3 genes instead of culture differences (3).


One of the factors in the variability of sweet detection is with the receptor proteins themselves. Bitterness and umami are perceived the same way as sweetness - a bitter taste receptor in the taste buds responds to the presence of bitter chemicals and transmits the bitterness sensation to the brain. If a bitter receptor was altered and became a sweetness receptor, the brain would perceive that chemical as being sweet (1).


Genes alone are not responsible for the variability of sweetness reception in humans. Leptin, a protein hormone known to play a role in the regulation of body mass, has an inhibitory effect on taste reception cells. The process by which leptin suppresses insulin secretion causes (the activation of ATP-sensitive K+ channels) alters membrane repolarization in taste receptors, reducing the amount of sweetness signals that are transmitted to the brain. This presumably makes sweet foods seem less attractive. During starvation, less leptin is produced, ultimately making sweet foods seem more attractive (4). Children are thought to be more receptive of sweetness than adults because they consume more soft drinks and foods with especially high concentrations of sweetness. During adolescence, the liking for concentrated sweetness fades, for reasons that may have to do with changes in caloric needs for growth. Differences in sweetness detection have also been noted by sex and geographical boundaries (1).


The discovery of the taste receptor proteins may change the way artificial sweeteners are developed. Mariana Max, a researcher at the Mount Sinai School of Medicine, is investigating how five hundred different sweet-tasting chemical compounds interact with and bind to the sweetness receptor proteins on the tongue. Max hopes that food chemists will someday be able to synthesize sweeter-tasting artificial sweeteners, though she does not say that it will be possible for scientists to create a compound that is just like sugar (5).


As sugar consumption continues to rise, it is necessary to begin to look at the consequences our sweet teeth may have. As children, we are told that too much candy and soda will cause cavities. As teenagers, we begin to worry that sugar causes acne, and as adults, we worry about our risk of developing diabetes. According to the National Academy of Sciences, diets high in sugar may lead to obesity, kidney stones, osteoporosis, heart disease, and dental caries (6). To remedy this, we can turn use artificial sweeteners to sweeten our foods, but as of now, the quality of artificial sweeteners is not as high and the risks of long term consumption are not well known. There is a concern that aspartame, marketed as Equal and NutraSweet, causes cancer, although at this time, the FDA has ruled that it is safe to ingest (7).


By examining the neuroscience behind the phenomenon of taste, it is possible to understand why humans are drawn to and even crave sweet-tasting foods. Sweetness implies that the food isn't spoiled or poisonous, and sugary foods deliver energy to the blood stream quickly. Variation in preference of sweet tasting foods may be accounted for by considering the genetic components of taste. While some prefer savory or salty foods, others prefer sweets. As for myself, writing this paper has made me really hungry....

Works Cited
[1] Reed, Danielle R., and Amanda H. McDaniel. "The Human Sweet Tooth." 11 May
2008. <http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2147592>
[2] "BBC Science & Nature: Nervous System - Taste" 11 May 2008.
<http://www.bbc.co.uk/science/humanbody/body/factfiles/taste/taste_animation.shtml>
[3] Zhao, Grace Q., Yifeng Zhang, Mark A. Hoon, Jayaram Chandrashekar, Isolde Erlenbach, Nicholas J.P. Ryba, and Charles S. Zuker. "Researchers Define Molecular Basis of Human 'Sweet Tooth' and Umami Taste." 11 May 2008. <http://hum-molgen.org/NewsGen/11-2003/000011.html>
[4] Lindemann, Bernd. "Receptors and Transduction in Taste." 11 May 2008. <http://www.nature.com/nature/journal/v413/n6852/full/413219a0.html>
[5] Carswell, Lindsay. "Searching For Sweet." 11 May 2008. <http://www.sciencentral.com/articles/view.php3?language=english&type=&article_id=218392549>
[6] "Sugar Consumption 'Off the Charts' Say Heallth Experts." 11 May 2008. <http://www.cspinet.org/new/sugar.htm>
[7] American Cancer Society. "ACS: Aspartame." 11 May 2008. <http://www.cancer.org/docroot/PED/content/PED_1_3X_Aspartame.asp?sitearea=PED>

Comments

Paul Grobstein's picture

sweetness and variability

I wonder if variation in a taste for sweetness is accompanied by/correlated with a variation in the benefits/risks of eating sweet things?