What causes fruit taste enhancement?

What causes fruit taste enhancement?

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I'm not sure if this is a biology or chemistry question, maybe both? Some fruits, such as quince and quondong, taste of nothing when raw but have an extremely strong flavour when cooked. Why?

I am a little confused that does the word "cooked" means ripe?If yes, then the question will be easy to answer. Fruit has a kind of ripener, ethlyene. Ethlyene will help fructose break down and make up more glucose. That is why you may taste a strong flavour when fruit is cooked.

Bitter taste identifies poisons in foods

IMAGE: Turnips contain glucosinolates, compounds that inhhibit iodine uptake by the thyroid. Individuals with the sensitive form of the hTAS2R38 taste receptor gene rate turnips as being more bitter than people. view more

Scientists at the Monell Chemical Senses Center report that bitter taste perception of vegetables is influenced by an interaction between variants of taste genes and the presence of naturally-occurring toxins in a given vegetable. The study appears in the September 19 issue of Current Biology.

Scientists have long assumed that bitter taste evolved as a defense mechanism to detect potentially harmful toxins in plants. The Current Biology paper provides the first direct evidence in support of this hypothesis by establishing that variants of the bitter taste receptor TAS2R38 can detect glucosinolates, a class of compounds with potentially harmful physiological actions, in natural foods.

"The findings show that our taste receptors are capable of detecting toxins in the natural setting of the fruit and vegetable plant matrix," said senior author Paul Breslin, a Monell sensory scientist.

Glucosinolates act as anti-thyroid compounds. The thyroid converts iodine into thyroid hormones, which are essential for protein synthesis and regulation of the body's metabolism. Glucosinolates inhibit iodine uptake by the thyroid, increasing risk for goiter and altering levels of thyroid hormones. The ability to detect and avoid naturally-occurring glucosinolates would confer a selective advantage to the over 1 billion people who presently have low iodine status and are at risk for thyroid insufficiency.

In the study, 35 healthy adults were genotyped for the hTAS2R38 bitter taste receptor gene the three genotypes were PAV/PAV (sensitive to the bitter-tasting chemical PTC,) AVI/AVI (insensitive), and PAV/AVI (intermediate).

Subjects then rated bitterness of various vegetables some contained glucosinolates while others did not. Examples of the 17 glucosinolate-containing vegetables include watercress, broccoli, bok choy, kale, kohlrabi, and turnip the 11 non-glucosinolate foods included radicchio, endive, eggplant and spinach. Subjects with the sensitive PAV/PAV form of the receptor rated the glucosinolate-containing vegetables as 60% more bitter than did subjects with the insensitive (AVI/AVI) form. The other vegetables were rated equally bitter by the two groups, demonstrating that variations in the hTAS2R38 gene affect bitter perception specifically of foods containing glucosinolate toxins.

Together, the findings provide a complete picture describing individual differences in responses to actual foods at multiple levels: evolutionary, genetic, receptor, and perceptual. "The sense of taste enables us to detect bitter toxins within foods, and genetically-based differences in our bitter taste receptors affect how we each perceive foods containing a particular set of toxins," summarizes Breslin.

Breslin notes, "The contents of the veggies are a double-edged sword, depending upon the physiological context of the individual eating them. Most people in industrialized cultures can and should enjoy these foods. In addition to providing essential nutrients and vitamins, many are reported to have anti-cancer properties."

Lead author Mari Sandell comments on additional nutritional and practical implications of the study, "Taste has a great impact on food acceptability and choice. A comprehensive understanding how food components contribute to taste is necessary to develop modern tools for both nutritional counseling and food development."

The Monell Chemical Senses Center is a nonprofit basic research institute based in Philadelphia, Pennsylvania. For 35 years, Monell has been the nation's leading research center focused on understanding the senses of smell, taste and chemical irritation: how they function and affect lives from before birth through old age. Using a multidisciplinary approach, scientists collaborate in the areas of: sensation and perception, neuroscience and molecular biology, environmental and occupational health, nutrition and appetite, health and well being, and chemical ecology and communication. For more information about Monell, please visit

CITATION: Mari A. Sandell and Paul A.S. Breslin. Variability in a taste-receptor gene determines whether we taste toxins in food. Current Biology, 2006, 16, R792-R794.

FUNDING: National Institute on Deafness and Other Communication Disorders, National Institutes of Health

FOR FURTHER INFORMATION CONTACT: Leslie Stein, Monell Chemical Senses Center, 215.898.4982, [email protected]

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

Fruit chloroplast development and fruit photosynthesis

It is generally assumed that leaves are the powerhouses of the plant as they provide photo-assimilates, while fruits and roots are basically heterotrophic as they rely on transport from leaves to grow and develop to their final size and composition. If this is the case, what is the need for fruits of tomato to be green before ripening? Do fruit chloroplasts have any role? Do they have any effect on final fruit quality? To begin with, what do we know about chloroplast formation and fruit photosynthesis?

Our understanding of fruit chloroplast formation and of the role of fruit photosynthesis at the different stages of fruit organ development is somewhat incomplete when compared with that of the leaf. Similarly to those in the leaf, it is known that fruit chloroplast formation, chlorophyll synthesis, and assembly of the photosynthetic apparatus require exposure to light and the activation of a series of developmental cues. Chloroplast proteins involved in light-harvesting complexes, electron transfer, and CO2 fixation are all expressed in the fruit cells and they are regulated by transcription factors, in a manner similar to that in leaves ( Hetherington et al., 1998 Carrara et al., 2001). Recent proteomic analyses corroborate this at the protein level for all the components of photosynthesis, the Calvin cycle, and photorespiration reactions ( Barsan et al., 2010, 2012). There is, however, some fruit-specific regulation of nuclear-encoded photosynthetic genes ( Sugita and Gruissem, 1987 Piechulla and Gruissem, 1987 Piechulla et al., 1987 Wanner and Gruissem, 1991 Manzara et al., 1993), the purpose of which is not clear, but is probably to optimize function in the context of the fruit.

Are these fruit chloroplasts capable of photosynthesis? Are fruit chloroplast net contributors or is the bulk of fruit development and carbon accumulation simply reliant on photoassimilates imported from leaves? What is the contribution of fruit chloroplasts and fruit photosynthesis to fruit metabolism before ripening? What role do chloroplast and fruit photosynthesis play in chloroplast to chromoplast conversion and in fruit quality at the red ripe stage?

The role of fruit photosynthesis in fruit metabolism and development has been extensively discussed ( Piechulla et al., 1987 Wanner and Gruissem, 1991 Schaffer and Petreikov, 1997 Carrari et al., 2006 Steinhauser et al., 2010), but, even now, information about its importance is controversial. One of the issues is whether the fruits are or are not net fixed-carbon producers. There are reports indicating that tomato fruits are unlikely to be net assimilators of CO2 despite the high level of expression of photosynthetic genes in this organ ( Blanke and Lenz, 1989 Carrara et al., 2001). Exceedingly high expression of genes associated with photosynthesis occurs in specific fruit tissues with difficult access to light, such as the locules ( Lemaire-Chamley et al., 2005), which, although capable of photosynthesis ( Laval-Martin et al., 1977), are also likely to display higher rates of respiration. Moreover, the triose-phosphate and glucose-phosphate transporters are both active in tomato chloroplasts, indicating that they could, in principle, both import and export phosphoesters.

A number of studies in tomato support that the vast majority of photo-assimilates in the fruit are supplied by the leaves rather than produced de novo in the fruit ( Hackel et al., 2006 Schauer et al., 2006 Zanor et al., 2009 Do et al., 2010). Consistent with this major import contribution to fruit, the correct development and sugar composition of fruit largely depend on the size of the photosynthate pool available in leaves and also on the sink strength of the fruit ( Baldet et al., 2006 Burstin et al., 2007). Genetic analyses of fruit growth and composition have also confirmed the importance of both the size of the pool available ( Schauer et al., 2006) and the sink strength ( Fridman et al., 2000, 2004). These results and others coming from a series of studies involving quantitative trait locus (QTL) analysis, network analysis, and molecular biology analysis revealed for instance that the major QTLs for fruit size and fruit sugars have to do with genes affecting cell division/number of cells ( Frary et al., 2000) and auxin signalling ( Cong et al., 2008) in the initial stages of fruit development, as well as with the ability to convert imported sucrose into glucose and fructose by an invertase later in fruit development ( Fridman et al., 2004), all consistent with the importance of developing a strong sink organ and with no indications for a major contribution of fruit photosynthesis. Further support for the importance of leaf versus fruit photosynthesis comes from a number of studies where elevation of tomato leaf photosynthesis results in a proportional increase in fruit yield ( Araujo et al., 2011 Nunes-Nesi et al., 2011).

The carbohydrate pool size in leaves and its partitioning between leaves and fruit are affected by a variety of environmental conditions including those cultural practices which are known to determine fruit growth and quality ( Heuvelink, 1997 Gautier et al., 2001 Bertin et al., 2003). Furthermore, an increase in soluble sugars in ripe tomato fruit that have been exposed to salinity, as a cultural practice to obtain better quality tomatoes, appears to be a consequence of up-regulation of sucrose transport from leaves and increased activity of ADP-glucose pyrophosporylase in fruits during early development. This increase in sugar mobilization results in accumulation of starch in the immature fruits, and this affects later fruit quality as a source for sugars in red fruit ( Yin et al., 2010). Fruit size and fruit quality-related metabolite levels are often inversely correlated, further supporting that competition for imported resources is a critical determinant.

Seemingly to close the issue for good, Lytovchenko et al. (2011) indicated that fruit photosynthesis is not required for correct fruit development, or for the photosynthate accumulation in the fruit, including those metabolites impacting taste. In that study, transgenic Money Maker tomato plants, exhibiting decreased expression of the chlorophyll biosynthesis gene glutamate 1-semialdehyde aminotransferase (GSA) under the control of the pre-ripening fruit-specific TFM5 promoter showed a reduced photosynthetic rate, as determined by both CO2 exchange and by the levels of intermediates of the Calvin–Benson cycle. Fruits of those plants were affected neither in size nor in any of the main primary or intermediary metabolites, thus suggesting that transport from leaves can compensate for loss of fruit photosynthesis. Only a delay in seed development was observed in those fruits, suggesting that fruit photosynthesis may be important for timely seed development. These results support the contention that the contribution of fruit photosynthesis to fruit formation and fruit energy metabolism is dispensable, although it may be relevant under specific environmental conditions.

Despite all the above, it remains the case that as much as 20% of the total carbon of the fruit has been estimated to result from photosynthetic activity in the fruit itself ( Hetherington et al., 1998). All three stages in which fruit development is traditionally described—cell division, cell enlargement, and ripening—contribute to final sugar accumulation in the fruit. In particular, the second stage is accompanied by the degradation of starch into soluble sugars ( Davies and Cocking, 1965 Schaffer and Petreikov, 1997), with early studies already indicating that the level of soluble solids in ripe tomato fruit is related to the level of the starch in immature and mature green fruit ( Davies and Cocking, 1965). The contribution of fruit photosynthesis to fruit growth and net sugar accumulation has been supported by early fruit shading experiments which analysed the rate of fruit growth and concluded that the fruit contributes by its own fixed carbon between 10% and 15% of the total ( Tanaka et al., 1974). There have been criticisms about these experiments as the bagging procedure may impact light receptors which are required for normal fruit development ( Giliberto et al., 2005 Azari et al., 2010). Additional support for the contribution and importance of fruit photosynthesis comes from experiments showing a 15–20% negative effect on fruit development by depleting photosynthesis in the fruit following the antisense inhibition of the fruit chloroplastic fructose-1,6-bisphosphatase (FBPase Obiadalla-Ali et al., 2004). The importance of fruit photosynthesis in early fruit development is also suggested by the results of combined metabolomic and transcriptomic analyses ( Wang et al., 2009).

In addition to photosynthesis, fruit are able to fix carbon (refixation), via malate, with the CO2 supply for this derived from mitochondrial respiration of imported carbon ( Blanke and Lenz, 1989) rather than from intercellular/stomatal/diffusible CO2, whose accessibility could be in part compromised in bulky organs such as the tomato fruit with a thick cuticle and near absence of stomata. The possibility also exists that CO2 generated by the oxidative pentose pathway could be re-assimilated by Rubisco in green fruits, as shown in green seeds ( Schwender et al., 2004), thus providing further efficiency to the system.

Taking all these reports together, fruit photosynthesis contributes to fruit development and carbon economy. This contribution can be dispensable under normal growth but may become important under certain, limiting environmental conditions. The use of different genetic backgrounds and different environmental growth conditions (light) in the studies may also have contributed to the sometimes contradictory results. Interestingly, we now know that the genetic background is a determinant of the degree of contribution of fruit photosynthesis to fruit growth and fruit carbon economy.

Indeed, this conundrum about the importance of fruit chloroplasts and fruit photosynthesis has received an unexpected twist with the identification of the genetic nature of the ‘uniform ripening’ u mutation ( Powell et al., 2012). Tomato U gene mutants exhibit defective fruits in that chloroplast number and thylakoid grana are dramatically reduced as compared with the wild type, and yet fruit develops to normal size and ripens at the same time as the wild type, although the accumulation of sugars in red fruit is repressed by 10–15%. Consistent with this, the so-called uniform ripening tomato mutants show a pale green fruit phenotype at the mature green stage, which contrasts with the darker green-shouldered phenotype of the wild-type fruit ( Yeager, 1935 Bohn and Scott, 1945 Kemp and Nonnecke, 1960). The introgression of the wild-type U locus into fruits of (u/u) converts tomato pale immature fruit into dark-green-shouldered fruits with higher starch accumulation. The U gene has been recently identified by positional cloning, and the u mutants were revealed to carry an additional A in a small A-repeat region in exon I of the Golden 2-like GLK2 gene that introduces a premature termination codon in the encoded protein. Since GLK2 is the predominant GLK form expressed in the fruit, and since GLKs are members of the GARP family of transcription factors that regulate the expression of chloroplast genes ( Waters et al., 2008, 2009 Waters and Langdale 2009), u mutants qualify as fruit chloroplast mutants, the rest of the plant's needs being satisfied by the GLK1 gene, with redundant GLK roles in vegetative tissues.

Adding wild-type alleles of GLK, either by crossing or by genetic transformation under different promoter sequences, produces fruit with more chloroplasts that have more grana/thylakoids, and higher accumulation of chlorophyll and starch at the mature green stage ( Powell et al., 2012). Fruits with activated GLKs express higher levels of transcripts for photosystem II (PSII) and PSI components, as well as of other genes involved in sugar (GLK2) or other aspects of metabolism (GLK1) ( Powell et al., 2012 AG, unpublished results). Furthermore, GLK-overexpressing lines accumulate more sugars and lycopene in the red ripe stage, opening up a way to increase fruit quality by acting at the GLK level.

Most of the cultivated tomato varieties that fill the aisles of large supermarkets, including the variety used for the GSA experiment ( Lytovchenko et al., 2011), carry the u mutation and therefore have defective fruit chloroplasts with the associated effects of lower sugars and lycopene levels (see below) that they could potentially have.

No matter what the contribution of fruit chloroplasts is to net photosynthesis in green fruits, tomato fruits clearly undergo a physiological transition associated with the differentiation of chromoplasts from photosynthetically active chloroplasts occurring during fruit ripening ( Buker et al., 1998 Kahlau and Bock, 2008). This transition appears to be coupled with a decline in both nuclear- and plastid-encoded gene expression ( Piechulla et al., 1987 Wanner and Gruissem, 1991 Carrari et al., 2006 Kahlau and Bock, 2008) and in enzymatic activities ( Schaffer and Petreikov, 1997 Steinhauser et al., 2010) that are associated with carbon assimilation and chloroplast components. Furthermore, most nuclear gene expression for chloroplast proteins, and all plastid-encoded photosynthesis gene expression, is developmentally regulated, already decreasing during the late stages of green fruit development prior to ripening ( Kahlau and Bock, 2008) in anticipation of the partially phototrophic to completely heterotrophic shift occurring in the fruit at ripening. Only in some mutants is this process partially blocked, as is the case in the stay-green mutants ( Barry et al., 2008). It is noteworthy that most of the proteins of the Calvin–Benson cycle, including Rubisco, and of the oxidative pentose pathway were identified in the proteome of the tomato chromoplast ( Barsan et al., 2010). If all these pathways were active, the CO2 generated by the oxidative pentose pathway could be re-assimilated by Rubisco ( Schwender et al., 2004) to satisfy the specific metabolic needs of the ripe fruit.

Therefore, as fruits ripen, their chloroplasts are remodelled into chromoplasts that no longer contain chlorophyll but synthesize and accumulate lycopene, β-carotene, and other metabolites important for ripe fruit sensory and nutritional attributes ( Hetherington et al., 1998 Egea et al., 2010 Klee and Giovannoni, 2011). How then can fruit chloroplasts and photosynthesis in green fruit affect the metabolite constitution of ripen fruit? Early studies have related the content of soluble solids in ripe tomato fruit to the starch level in the immature and mature green fruit stages ( Dinar and Stevens, 1981 Schaffer and Petreikov, 1997), but this is probably only part of the story.

Can Pineapple Really Change the Taste of Your Semen?

Admit it &mdash you've definitely Googled this before.

Most curious guys have wondered at one point or another what their semen tastes like. But if you've ever given into your curiosity and actually tasted it for yourself (which is totally fine! We don't judge!), you know that it's not. how shall we put this. the most awesome taste in the world. Some have even compared it to laundry detergent or battery acid.

But are there ways you can actually make your semen taste better? The answer is yes &mdash and specifically, pineapple juice has long been rumored to do the trick.

But does eating pineapple or drinking pineapple juice actually improve the taste of your semen? Or is this just another sex urban legend? Keep reading to find out if pineapple juice can make oral sex more pleasant for your partner &mdash and which foods actively make your semen taste worse.

So what, exactly, is in your semen in the first place?

Contrary to popular belief, semen isn't just made up of sperm. 80% of it is water, according to Nelson Bennett, MD, urologist at Northwestern Memorial.

"It also contains proteins and amino acids. It has fructose and glucose (both are sugars), zinc, calcium, vitamin C, and a few other nutrients," Bennett says.

In fact, sperm themselves make up less than one percent of your semen. Fascinating!

How does your diet affect your semen?

Putting the issue of taste aside for a second, what you eat greatly affects the quality of your swimmers. A 2012 Oxford study compared two groups of men following different diets. One group followed a diet consisting largely of red and processed meat, refined grains, pizza, snacks, high-energy drinks and sweets, while the second group ate more fish, chicken, fruit, vegetables, legumes, and whole grains.

The group that followed the healthier diet reported "progressive sperm motility" compared to those that followed the less healthy diet, meaning their sperm moved faster and were thus more fertile.

How does your diet affect the taste of your semen?

"Anything that we ingest, whether it be food, drink, tobacco, etc., has the propensity to affect the taste and smell of our bodily fluids and secretions," says Bennett. That includes sweat, saliva, and yes, semen.

It all comes down to the pH levels: sperm is alkaline, meaning it typically has a pH higher than 7. (Think back to your high school chemistry class.) There's good reason for this: because the vagina is naturally acidic, the pH of your sperm helps protect it in that environment, thus ensuring reproductive success.

Because sperm is alkaline, that means that semen is naturally bitter-tasting. Additionally, the quantity of fluid that you consume may play a role in how it tastes.

"Higher fluid intake also increases the amount of seminal fluid that a man produces," says Dr. Bennett. The more hydrated you are, the more volume you can expect, and an improved taste.

OK, but does pineapple improve the taste of semen?

Well, yes and no. "The rumor is partially true," says Bennett. While there have not been any scientific studies on the matter, any sugary liquid or food may skew the fructose and glucose content or the pH of the semen just enough to be perceptible."

Because pineapple is pretty acidic, eating a lot of it or drinking a lot of pineapple juice can help cut down on the bitter taste of semen. That's true for other acidic fruits like lemons and cranberries as well. "Cranberries help balance the pH levels in semen, making for a better taste," says Dr. Bennett.

What other foods improve the taste of your semen?

As a general rule, fruit is your friend, since it will enhance fructose and glucose already present in your semen.

"Naturally sugary fruits like kiwi fruits, blueberries and stone fruit (plums, peaches, dates, nectarines) also improve your taste," says Dr. Bennett.

Other spices and herbs can improve the taste of your semen as well. "Cinnamon, wheatgrass, peppermint, spearmint and parsley all sweeten the taste of your semen," says Bennett.

One vegetable in particular may help as well: "celery is high in vitamin C, which will help flush out the salty flavor," says Bennett.

What foods should you avoid?

Though we don't exactly know why this is, "coffee (caffeine), tobacco, alcohol, and marijuana can make the semen bitter tasting, and the by-products of these substances are excreted in bodily secretions like sweat, urine and semen," says Bennett.

Additionally, red meat, dairy, chocolate, asparagus, broccoli, spinach can make the semen taste salty, strong and sharp. "Those of us who eat asparagus have experienced unsavory smelling urine a few hours later," says Bennett. The same applies to your semen.

How long will it take to tell a difference?

If you want to try to improve the taste of your semen through your diet, be aware that the effects aren't instantaneous.

"Changes in semen taste as a result of ingesting certain foods and liquids takes several days to weeks to manifest," says Dr. Bennett. "The prostatic fluid that makes up a large portion of semen volume is made several days before ejaculation, so drinking a quart of pineapple juice today will not sweeten the semen tonight." (It's also not that great for your overall health to ingest that much sugar at once, so try to space it out a bit.)

Overall, while there are ways to hack your semen to make it taste slightly better, the effects aren't going to be that significant. Still, if your partner makes a face every time they go down on you, first of all, rude, and second of all, it may be worth making these small dietary tweaks to see if they make a difference.

What causes a picky eater?

The foods you eat during pregnancy may influence the foods that your baby will like for years to come. Giving the babies prenatal or early postnatal exposure (via breastfeeding) to carrot juice enhanced their enjoyment of that flavor, one study found.

Some scientists say that the foods you eat during pregnancy could shape your baby&rsquos eating habits &mdash and his odds of obesity and diabetes &mdash throughout the rest of his life.

So what flavors should you expose your baby to during pregnancy? Aim to eat a balanced and varied diet, and choose fresh fruits and vegetables over processed snacks.

This not only helps keep you healthy during pregnancy, but it also sets the stage for your baby to love diverse tastes. Don&rsquot shy away from eating flavorful foods that you enjoy and want your baby to learn to like, including distinct ones like garlic, mint and curry.

From the What to Expect editorial team and Heidi Murkoff, author of What to Expect When You're Expecting. What to Expect has strict reporting guidelines and uses only credible primary sources. Health information on this site is regularly monitored based on peer-reviewed medical journals and highly respected health organizations and institutions. Learn how we keep our content accurate and up-to-date by reading our medical review and editorial policy.

The ethene signal

So why do bananas appear to speed up the ripening process of other fruits too?

"Bananas make other fruit ripen because they release a gas called ethene (formerly ethylene)," added Dr Bebber.

"This gas causes ripening, or softening of fruit by the breakdown of cell walls, conversion of starches to sugars and the disappearance of acids.

"Some fruits, like oranges, don't respond to ethene, but there are many processes in plants that respond to ethene as a signal."

So what is the key to stopping this process?

Research carried out by M&S found that by spraying bananas as soon as they are peeled with a mixture of citric acid and amino acid, it manages to keep them firm and yellow, but without affecting the taste.

It is a similar principle to using lemon juice to keep fruit fresh, as the enzyme doesn't respond well to acidic conditions.

Rose Wilkinson, fruit technologist at M&S, said: "We've spent years trying to overcome this so that we can include it in our prepared fruit salads and were delighted when we discovered a clever trick using fruit acid - just like you would at home with lemon juice."

The company also tested different varieties of banana to find the one which aged the slowest, discovering Cavendish bananas were the best of the bunch.

Now, you can find chopped banana in their fruit pots - all thanks to science.

Why Your Brain Craves Junk Food (and What You Can Do About It)

Most of us know that junk food is unhealthy. We know that poor nutrition is related to heart problems, high blood pressure, and a host of other health ailments. You might even know that studies show that eating junk food has been linked to increases in depression . But if it's so bad for us, why do we keep doing it?

There is an answer. And the science behind it will surprise you.

Why We Crave Junk Food

Steven Witherly is a food scientist who has spent the last 20 years studying what makes certain foods more addictive (and tasty) than others. Much of the science that follows is from his excellent report, Why Humans Like Junk Food . According to Witherly, when you eat tasty food, there are two factors that make the experience pleasurable.

First, there is the sensation of eating the food. This includes what it tastes like (salty, sweet, umami, etc.), what it smells like, and how it feels in your mouth. This last quality— known as "orosensation"—can be particularly important. Food companies will spend millions of dollars to discover the most satisfying level of crunch in a potato chip. Their scientists will test for the perfect amount of fizzle in a soda. These factors all combine to create the sensation that your brain associates with a particular food or drink.

The second factor is the actual macronutrient makeup of the food—the blend of proteins, fats, and carbohydrates that it contains. In the case of junk food, food manufacturers are looking for a perfect combination of salt, sugar, and fat that excites your brain and gets you coming back for more.

How Science Creates Cravings

There are a range of factors that scientists and food manufacturers use to make food more addictive.

Dynamic Contrast

Dynamic contrast refers to a combination of different sensations in the same food. In the words of Witherly, foods with dynamic contrast have "an edible shell that goes crunch followed by something soft or creamy and full of taste-active compounds. This rule applies to a variety of our favorite food structures—the caramelized top of a creme brulee, a slice of pizza, or an Oreo cookie— the brain finds crunching through something like this very novel and thrilling."

Hack Your Brain to Use Cravings To Your Advantage

Think about a munching on a bag of your favorite potato chips. Let that image sit in your brain for

Salivary Response

Salivation is part of the experience of eating food and the more that a food causes you to salivate, the more it will swim throughout your mouth and cover your taste buds. For example, emulsified foods like butter, chocolate, salad dressing, ice cream, and mayonnaise promote a salivary response that helps to lather your taste buds with goodness. This is one reason why many people enjoy foods that have sauces or glazes on them. The result is that foods that promote salivation do a happy little tap dance on your brain and taste better than ones that don't.

Rapid Food Meltdown and Vanishing Caloric Density

Foods that rapidly vanish or "melt in your mouth" signal to your brain that you're not eating as much as you actually are. In other words, these foods literally tell your brain that you're not full, even though you're eating a lot of calories. The result: you tend to overeat.

In his best-selling book Salt Sugar Fat , author Michael Moss describes a conversation with Witherly that explains vanishing caloric density perfectly:

I brought him two shopping bags filled with a variety of chips to taste. He zeroed right in on the Cheetos. "This," Witherly said, "is one of the most marvelously constructed foods on the planet, in terms of pure pleasure." He ticked off a dozen attributes of the Cheetos that make the brain say more. But the one he focused on most was the puff's uncanny ability to melt in the mouth. "It's called vanishing caloric density," Witherly said. "If something melts down quickly, your brain thinks that there's no calories in it . . . you can just keep eating it forever."

Sensory Specific Response

Your brain likes variety. When it comes to food, if you experience the same taste over and over again, then you start to get less pleasure from it. In other words, the sensitivity of that specific sensor will decrease over time. This can happen in just minutes.

Junk foods, however, are designed to avoid this sensory specific response. They provide enough taste to be interesting (your brain doesn't get tired of eating them), but it's not so stimulating that your sensory response is dulled. This is why you can swallow an entire bag of potato chips and still be ready to eat another. To your brain, the crunch and sensation of eating Doritos is novel and interesting every time.

Calorie Density

Junk foods are designed to convince your brain that it is getting nutrition, but to not fill you up. Receptors in your mouth and stomach tell your brain about the mixture of proteins, fats, carbohydrates in a particular food, and how filling that food is for your body. Junk food provides just enough calories that your brain says, "Yes, this will give you some energy" but not so many calories that you think "That's enough, I'm full." The result is that you crave the food to begin with, but it takes quite some time to feel full from it.

A Calorie Is Not Just a Calorie, Study Shows

There is plenty of argument over whether all calories are equal, thanks to a singular experiment…

Memories of Past Eating Experiences

This is where the psychobiology of junk food really works against you. When you eat something tasty (say, a bag of potato chips), your brain registers that feeling. The next time you see that food, smell that food, or even read about that food, your brain starts to trigger the memories and responses that came when you ate it. These memories can actually cause physical responses like salivation and create the "mouth-watering" craving that you get when thinking about your favorite foods.

All of this brings us to the most important question of all: Food companies are spending millions of dollars to design foods with addictive sensations. What can you and I do about it? Is there any way to counteract the money, the science, and the advertising behind the junk food industry?

How to Kick the Junk Food Habit

The good news is that the research shows that the less junk food you eat, the less you crave it. My own experiences have mirrored this. As I've slowly begun to eat healthier, I've noticed myself wanting pizza and candy and ice cream less and less. Some people refer to this transition period as "gene reprogramming." Whatever you want to call it, the lesson is the same: if you can find ways to gradually eat healthier, you'll start to experience the cravings of junk food less and less. I've never claimed to have all the answers (or any, really), but here are three strategies that might help.

Find the Underlying Desire for Junk Food to Beat Bad Eating Habits

When you want to lose weight, you have to cut out some of your favorite unhealthy treats. Although

I knew that the issue existed, but I didn't think anything hot had been done on it, and I was right - Linda Bartoshuk

In the case of Bartoshuk and company's recent work, however, it isn't the complex overtones of flavour they are talking about. This is more fundamental. It's the sweetness itself.

Bartoshuk says that the idea that volatile compounds emanating from fruit could be linked to sweetness was being discussed in the 1970s. But the effects of individual volatiles were very small, and the amounts of each chemical in the fruit were small as well. “I knew that the issue existed, but I didn't think anything hot had been done on it, and I was right,” Bartoshuk says. A few years ago, however, while she and colleagues were working on a study attempting to dissect exactly which molecules are responsible for what you experience while eating a tomato, she found something surprising.

(Credit: Science Photo Library)

The team had analysed the make-up of 152 heirloom varieties of tomato, recording the levels of glucose, fructose, fruit acids, and 28 volatiles. At the same time, over the course of three years, they organised 13 panels of taste-testers to sample more than 66 of these varieties, rating each according to how much they liked it, its sweetness, its sourness, and other taste characteristics.

Bartoshuk still remembers the moment when she was sitting in her office with this mountain of data one afternoon and ran a test, out of curiosity, to see which compounds contributed most to sweetness. She was expecting the answer to be sugar, and it certainly was key, but “I about fell out of my chair,” she says. Also significantly contributing were seven volatiles.

Sweet mystery

Moreover, the volatiles seemed to account for why panellists had reported some tomato varieties to taste sweeter than others that had far more sugar. The team tested a variety called Yellow Jelly Bean, for instance, and another called Matina. The Yellow Jelly Bean has 4.5g of glucose and fructose in 100 millilitres of fruit and rated about a 13 on a scale used for perceived sweetness. The Matina has just under 4g but rated a whopping 25. The major biochemical difference between the two was that the Matina had at least twice as much of each of the seven volatiles as the Yellow Jelly Bean did. When the team isolated those volatiles from a tomato and added them to sugar water, its perceived sweetness jumped.

They've also investigated blueberries and strawberries, among other fruits. Strawberries have much less sugar than blueberries but are consistently rated much sweeter. Bartoshuk and colleagues suggest that this is because strawberries have so many more volatiles – something like 30 – than blueberries, which have “maybe three”, Bartoshuk estimates. They found that adding strawberry volatiles to sugar water boosted perceived sweetness even more than the tomato volatiles did, and adding volatiles from both together doubled it.

4 thoughts on &ldquo What Causes People to Have Different Spicy Food Tolerances? &rdquo

I really loved this one, especially because I am a girl who loves spicy food so much. Have you put into thought that maybe as a third factor that as toddlers and growing up your sister was fed more spicy foods, developing an immunity which you don’t have, allowing her to eat these spicier plates.

I found your blog to be really interesting and eye catching when it comes to me paying attention to how my taste buds react to certain foods. With all the questions that you answered throughout your blog, I am curious if texture and temperature can have an effect in tolerance. For example, could you react different to eating a hot and spicy soup compared to spicy buffalo chicken wings? I feel like this can make sense especially when comparing the reaction to really hot food and really cold foods.

I have never been one for spicy food, I’m not sure if that’s because I never gained a tolerance to it or maybe my personality isn’t “spicy” enough. I have found quite a lengthy and detailed analysis drawing parallels betweens spider toxins and the mechanisms in plants (capsaicin) that deter predators. This can explain why peppers and other plants are so hot and why some people might not enjoy them: they’re not meant to be eaten. That link is here: However, I do understand that people enjoy the thrill of trying spicy things because according to the following article, we are the only mammals that do..

I found your blog to be one of the most interesting I have read so far because this was truly a question I have always wondered. Why do some people like spicy food while others cannot handle it? I always assumed that it had to do with a person’d background and the food they were brought up on. While I find Indian food to be spicy, my Indian friends do not. (If I eat anything with the least bit of spiciness I automatically start tearing up.) I used to explain this because of my culture’s (Egyptian) food being predominately sweet I love sweets. After researching I found that there are ways to build tolerance. Start with small amounts of spiciness and as soon as you adapt to that higher the level of spiciness. This will increase your tolerance for spicy foods.

The Origin of Fruit Ripening

Bananas hanging on a tree or sitting in the produce section of the grocery store start out green, plenty hard and none too tasty. Over time, of course, they become softer and sweeter. The cause of fruit ripening is a natural form of a chemical synthesized to make PVC (polyvinyl chloride) piping and plastic bags&mdashnamely, a gaseous plant hormone called ethylene.

For thousands of years, people have used various techniques to boost ethylene production even if they did not quite know it. Ancient Egyptian harvesters slashed open the figs they collected to stimulate ripening, and Chinese farmers would leave pears in closed rooms with incense burning. Later research showed that wounding and high temperatures trigger plants to produce ethylene.

In 1901 Russian scientist Dimitry Neljubow showed that ethylene could affect plant growth after he identified it as the active ingredient in vapors leaking from a gas main. The vapors were causing surrounding plants to grow abnormally. Three decades later, researchers found that plants not only responded to ethylene, but they could produce their own, and production of the gas increased when the scientists cut (injured) the fruit with a knife.

Researchers later discovered that plants produce ethylene in many tissues in response to cues beyond the stress from heat and injury. It is made during certain developmental conditions to signal seeds to germinate, prompt leaves to change colors, and trigger flower petals to die. Because the gas diffuses easily it can travel within the plant from cell to cell as well as to neighboring plants, serving as a warning signal that danger is near and that it is time to activate the appropriate defense responses.

Special receptors in plant cells bind to the ethylene. The first known plant genes involved in this process, ETR1 and CTR1, were identified in 1993 they keep the fruit ripening genes from activating until ethylene is made. Once that happens, ETR1 and CTR1 turn off, which allows a cascade that ultimately turns on other genes that make various enzymes: pectinases to break down cell walls and soften the fruit amylases to convert carbohydrates into simple sugars and hydrolases to degrade the chlorophyll content of the fruit resulting in color change. Such changes invite animals to consume the fruit and disperse the mature undigested seeds via their defecation.

The evolution of the ethylene pathway, from the production of the gas to end responses like cell death, still puzzle scientists. Land plants are the only organisms known to contain the entire response system. Cyanobacteria can sense ethylene, but whether they can produce the compound is unknown. These microorganisms have an ETR1-like gene, but no CTR1 gene, so their ethylene response system would have to be different from that of land plants. Green algae, generally thought to lie between cyanobacteria and land plants in the evolutionary tree, do not perceive ethylene, so how ethylene responses jumped from cyanobacteria directly into land plants also interests researchers.

For economic reasons, scientists continue to explore the biomolecular details of the ethylene production&ndashresponse cycle, in hopes of developing better methods of preventing fresh-picked fruit from ripening during transport over long distances. The trick is to ensure that the fruit does not become ethylene-insensitive so that it never ripens. After all, who wants to eat green bananas that taste like fiberboard?