Sweets

12 Sweets and Desserts

Depending on the area, community, and religion, various types of sweets are made in India. Most of the sweets are made of refined sugar. However, jaggery (brown sugar) and palm sugar are also used. Sweets are an integral part of the Indian cuisine, and in some communities, they are a necessary item on the breakfast, lunch, and dinner menu. The sweets may be either cooked in milk, water, etc. or fried in dalda, ghee, or oil. Based on the primary ingredients, the sweets can be broadly classified as milk based, wheat based, rice based, fruit based, besan based, vegetable based, coconut based, and nut based. Ice creams, cakes and puddings, which are traditionally western food items are also popular. In most communities, consumption of sweets is high and the servings increase during the religious and happy occasions, and community events, such as festivals and celebrations. As most sweets contain high proportions of the refined sugar, oil, and fats, they contribute to atherogenesis, obesity, diabetes, and metabolic syndrome and also aggravate the medical conditions.

With regard to the correlation between consumption of sweets and cardiovascular diseases, there are contradicting reports. Some clinical studies have found that higher intake of sugar was associated with increased CVD (Parks and Hellerstein, 2000), while other studies have not found any relation between intake of sweets or desserts and the risk of CVD (Jacobs et al., 1998). Several studies have shown an inverse association between dietary sucrose and HDL cholesterol (Ernst et al., 1980). A diet high in sucrose is shown to be associated with an elevation of plasma triglyceride concentrations (Parks and Hellerstein, 2000). On the basis of overall data obtained from various studies it is recommended that high sugar intake should be avoided (refined sugars < 10% of total calories required), and that more quantity of complex carbohydrates should be included in the diet; foods with essential nutrients should not be replaced with foods high in refined sugars (Vasudevan et al., 2011).

3.5.3 A wholesome taste

The notion of sweetness evokes powerful emotional associations that go way beyond simple food tasting. It is an overwhelmingly positive feeling that prompts people to talk about sweet girls, the sweet spot on a racket, or home sweet home. Sweet is a flavor that comes with goodness written all over it. How could anybody not like lots of it? But the reality is that not everybody likes it very sweet all the time. Common genetic variants partially determine who does and who does not. By the way, this affinity to sweets is a very human feature that is not shared by our feline companions. They just would not know what we are talking about when we are calling them sweet, because they do not have functioning sweet taste receptors [122]. And while we are at it, the artificial sweetener aspartame also works only for us and our closest primate cousins [123], not for any of our pets.

The molecules that make foods taste sweet are mainly sugars, a few amino acids, and peptides (including the artificial sweetener aspartame, N-(L-α-aspartyl)-L-phenylalanine, 1-methyl ester, and an assortment of other natural and synthetic compounds). The exact three-dimensional structure of the food molecules makes all the difference. For example, isomaltose, which consists of two glucose molecules connected by an α-(1→6) linkage, has a pleasantly sweet taste. But if you bend the isomaltose molecule a bit and connect the two glucose moieties through β-(1→6) linkage (Figure 3.14), you get gentiobiose, which has a distinctly bitter taste detected by TAS2R16 (OMIM 604867) [124]. Gentiobiose is one of the products that form when glucose is caramelized by heating, thus tempering the sweetness of the sugar mass with its distinctive bitter note.

FIGURE 3.14. Isomaltose and gentiobiose both consist of two glucose molecules, but one tastes sweet and the other one bitter.

Two human sweet taste receptors, TAS1R2 (OMIM 606226) and TAS1R3 (OMIM 605865), functioning as heterodimers in taste buds, are the predominant molecules for sensing sweet substances in food [125]. The G protein alpha-gustducin (GNAT3; OMIM 139395) mediates the response signal downstream. Common variants occur in the receptor genes as well in GNAT3.

A common variant, -1572C>T (rs307355), in the promoter region of the TAS1R3 gene appears to reduce sucrose sensitivity [126]. A blinded taste test found that people with the homozygous C/C genotype were twice as good at detecting sucrose in water than those with other genotypes. The T allele occurs almost exclusively in people of African origin. Fushan et al. [126] suggested that the high-sensitivity allele T helped early populations migrating out of Africa to overcome the difficulty that cold-climate plants had much lower sugar content than the plants in their original African environment.

The TAS1R2 polymorphism, Ile191Val (rs35874116), has also been found to affect habitual sugar consumption [127]. Overweight and obese Canadians with the 191Val allele consume less sugar than otherwise matched individuals without this variant.

GNAT3 polymorphisms explain 13% of the variation in sucrose perception [128].

Sweet (Sweetness)

The taste of sweet, or sweetness, is primarily a pleasurable sensation (except in excess), and is largely derived from foods and beverages that contain some type of sugar.

The sensory appeal of sweetness is innate commonly universal. The foods and beverages that activate the sweet taste are typically simple carbohydrates or sugars in the forms of glucose, fructose and sucrose to be metabolized for energy, and complex carbohydrates in the form of starches for energy or storage.

The sweet taste is also often produced by the presence of D-amino acids, coumarins, dihydrochalcones, glycosides and modified sugars, peptides, proteins, selected salts, substituted aromatic substances, ureas and other nitrogenous compounds. The sweet taste that results may be the product of an exchange of hydrogen ions.

The sensation of sweetness is frequently connected to aldehydes and ketones with a carbonyl group. It is identified by a range of G protein-coupled receptors that are joined to the G protein gustducin on the taste buds. Two different variants of sweet receptors or more must be activated for the brain to identify the sweet taste.

Mostly all of the sensations of the sweet taste are the result of the bonding to two different receptors: T1R2+3 (heterodimer) and T1R3 (homodimer). The taste thresholds for the sweet taste are scored in relation to sucrose, which equates to “1” [8].

Classic combinations of sweet and sour (such as Asian sweet and sour sauce); sweet and fat (such as some rich and sweet bakery items); and sweet and bitter (such as some bittersweet chocolate varieties) are common examples of how the blends of sweetness and other basic tastes can be employed by chefs, home cooks and food manufacturers for flavor enjoyment.

Common sweet tastes may be found in the following foods and substances: bananas, berries, breadstuffs, butter, cake and pastries, caramel, cinnamon, cream, dates, honey, maple syrup, milk chocolate, nutmeg, peas, parsnips, ripe apples, scallops, vanilla extract and the many guises of sugar.

Sweet notes may be achieved in cooking and baking by adding pureed sweet root vegetables such as beets, carrots, celeriac (celery root), parsnips and/or sweet potatoes; sweet fruits such as bananas, dates, pears or prunes; agave, honey or maple syrup; sweet butter and other dairy products; or sweet wine to recipes. Like most cooking and baking techniques, prudence matters: while a little bit of sugar may help the “medicine go down,” too much sweetness in a recipe or meal may be distasteful. More ideas follow later in this chapter and in Chapter 10, Menus and Recipes That Appeal to Aging Palates.

5 Sweets and Snacks

Sweet preference is common in children already in infancy and decreases during adolescence (Ventura and Worobey, 2013). In dietary practice, most children and adolescents exceed the current recommendations of the WHO not to consume more than 10% of energy from free sugar (Alexy et al., 2003). In the sample menus presented here, added sugar accounts for 6% of energy, well below the WHO limit, although it would be higher if considering free sugar. The total food group of sweets and snacks, called “tolerated food” in the Optimized Mixed Diet, may contribute up to 10% of total energy intake if the consumption of the recommended food groups is balanced.

4.2 Rewards

4.2.1 Sweet taste

Sweetness signals the availability of immediate energy. While sugars are not as dense a caloric source as are fats, they are useful to the brain and muscles only minutes after consumption, and so play a crucial role in survival. Consequently, sweetness has a powerful hedonic appeal, and the word itself has become synonymous with pleasure.

Sugars and most other sweet molecules bind with specific—though as yet unidentified—proteins on taste receptor cells. Once activated, these receptors stimulate G-proteins to amplify the signal. This activates the enzyme adenylate cyclase (AC) which converts ATP to cAMP. It is cAMP that serves as the second messenger, causing protein kinase A (PKA) to close the potassium (K) channels of the cell's membrane. The positively-charge K ions that would otherwise exit through the membrane are instead sequestered within it, depolarizing the cell and causing calcium ion channels to open. This is the event that releases neurotransmitter from the taste receptor onto the peripheral nerve terminals, initiating the signal that is carried to the central nervous system.

13.2 The historical development of sweetness consumption

Nature decided sweet addiction of humans by favouring sweetness during natural selection. This was needed for the positive appraisal of food quality. Sweet is a synonym of benefit or favourable interaction. Sweet is a synonym for a person of a pleasant appearance, nice behaviour or just a success. On the contrary, a number of dangerous xenobiotics are marked negatively with bitterness which gives a warning to humans. This makes ‘adaptive sense, since sweetness is an indicator of calories in nature, and bitterness correlates with toxicity’ (Rozin, 1989). The adaptive significance of taste chemoreception makes sense only with the provision that sweetness as such is a rare quality in nature. ‘These genetic predispositions evolved over thousands of years of human history, when foods – especially foods high in energy density – were relatively scarce’ (Birch, 1999). Therefore, although we know a number of sweet tasting substances, sweetness is relatively exceptional.

Serendipity clearly backed humans in their original search for sweetness. Natural fruits and honey have been sought after since prehistoric times. It was recognised from Stone Age paintings that honey was obtained as early as 20,000 years ago and Egyptians domesticated bees to raise it. Honey sweetness was surrogated by sugar cane which has been known as early as 1000 bc in India, where it originally came from Oceania (Van der Wel et al., 1987). A first authentic reference to honey and sugar is a birchbark scroll that dates back to the 4th century (Inglett, 1976). Europeans were trading with sugar from the 7th century, and in the 18th century Margraff discovered sucrose in red beets, which allow for the development of modern sucrose production in Europe to replace sugar cane delivery which had been blocked during a British blockade of Napoleonic France (Inglett, 1976). On the other hand, the uniqueness of sweetness decided its luxury. Sugar taxation clearly put the final seal on that fact. However, sugar prices (1400–1960) given in new English pence, steadily decreased from year to year from 875 in 1400; 210 (1600); 70 (1800); 17.5 (1900) to 3.7 in 1960, respectively (Ruprecht, 2001). High availability of sucrose and a significant increase in its consumption is a relatively novel effect that starts from 1850 to 1950, differing from country to country. Sugar availability ‘has contributed to destroying the old agricultural meal order which centered around the meal that was prepared by and consumed within the family. Sugar was associated with fast food, in the double sense of production and consumption’ (Ruprecht, 2001). The availability or even an excess of sugar has deprived sweetness of its adaptive function; however; sweet desire and addiction has survived. This explains the origin of the search and development of artificial non-caloric sweeteners.

Sweet (Sweetness)

The sweet taste is considered as one of the more elemental of tastes. It is generally judged as a pleasurable sensation.

Sweetness is detected by the presence of sugars that are the foundation of many foods and beverages. Chemical compounds such as aldehydes, ketones and sugar alcohols also may also impart a sweet taste, as may some complex carbohydrates that are found in fruits, vegetables and grains that break down into simple sugars in the human body.

Fruits contain the simple sugar fructose, and dairy products contain the double-sugar lactose. It is common for people to develop an intolerance to lactose as they age. This is because a deficiency in lactase, an enzyme that is essential for the breakdown of lactose into the simple sugars of glucose and galactose, may develop.

As a result, aging people (and particularly those of African-American, Asian or those of Middle Eastern heritage) may avoid dairy products. However, lactose-reduced and lactose-free dairy products are widely available so that these groups of people may still ingest and benefit from the vital nutrients that accompany dairy products.

Different gene variations were discovered in the 1990s that showed laboratory animals preferred sweet foods to various extents. A sweet receptor protein complex is said to be responsible. Taste cells for sweet, bitter and umami appear to share a similar intracellular signally pathway.

Not only are there sweet receptors in the oral cavity, sweet taste receptors are also located in the enteroendocrine cells of the gut and pancreas that may play important roles in nutrient sensing and sugar absorption. These cells are needed for energy and to maintain the normal metabolism in the balance of glucose and insulin levels. Some research has supported the hypothesis that the number of taste buds may play a role in how the body handles sugar throughout the aging process. Further investigation is needed [17].

Since the taste of sweetness tends to indicate that a quick source of energy may follow, humans are genetically programmed to seek out sweet sources of foods and beverages. But individual variations tend to determine who craves what type of sweetness, when and how much.

Newborns have demonstrated preference for the sweet taste. This may be due to the fact that both amniotic fluid and breast milk are sweet and very satisfying. The satisfying aspects of sweetness have also been used to muffle pain: medications are often encapsulated or accompanied by sugary applications.

Because the sweet taste (and specifically sugar) has such functionality in food and beverage development, food preparation and cooking execution, sugar provides a versatile tool for paring with or suppressing other basic tastes, and in nourishing aging palates.

12.3.6 Sweetness

In contrast to bitter and sour tastes, humans and other mammals are born with an innate liking for sweetness (Cowart, 1981). Exposure to sweetness is pleasant, calming, and soothing and has an analgesic effect among children, such that sweet stimuli are often used to distract from the pain of vaccination in young babies (see Harrison et al. (2010), for a review). The dictionary definition of “sweet” is something pleasant, satisfying, agreeable, and delightful.

The psychohedonic optimal sweetness is significantly higher in infants than in adults, and slowly declines from early infancy throughout childhood and into early adolescence (Liem and Mennella, 2002; De Graaf and Zandstra, 1999). This figure aligns with the observation that the contribution of mono-and disaccharides to energy intake is about 33% in toddlers and declines to about 20% in adulthood, and these figures have been stable in the Netherlands since the 1980s (Van Rossum et al., 2020). Recent data on the predominant taste of calories consumed in the Dutch diet show that sweet-sour and sweet-fatty tasting foods comprise approximately 25%–30% of the energy intake (van Langeveld et al., 2018). However, much of the societal narrative around sweetness centers on the “sweet tooth,” and the excessive energy consumed from sugary soft drinks and foods considered as discretionary calories that promote energy consumption and eventually lead to obesity (Anderson, 1995). The rationale of this reasoning is that sweetness is pleasant and that people with obesity tend to consume a greater proportion of their energy from sweet foods than people in the normal weight range. However, this reasoning is not supported by available data. As is clear from Table 12.2, sweetness intensity is poorly correlated with the energy content of food, and this has been observed across the global diet from the USA, to Europe and Asia. A further proposition is that people with obesity must have a higher liking for sweetness compared to those in the normal weight range, but again this hypothesis is not backed by data. Multiple studies since the early 1980s fail to demonstrate a clear relationship between weight status and the psychohedonic function for sweetness (Cox et al., 2016). Experimental and observational data have failed to show a difference in sweetness preference by weight status in children (Bobowski and Mennella, 2017) or adults (Cox et al., 1998). Consumption of sweet foods also does not stratify by weight status (Teo et al., 2021; van Langeveld et al., 2018).

In the modern food environment there is pressure to reduce sugar from foods and beverage to reduce their energy content. However, what remains less clear is whether sugar content or the associated sweetness perception is the driver of consumption. Few trials to date have explored whether exposure is driving preferences and intake for sweet foods, and today it remains unclear whether high exposure to sweetness leads to increased liking for high “sweetness” level or conversely a low sweetness exposure leads to lower preference for “sweetness.” A recent systematic review showed no consistent data in this direction, and observed that whereas short-term effects of sweetness exposure lead to a decline in sweetness liking, there are limited available data to conclude on the longer-term implications of sweetness exposure (Appleton et al., 2018). One RCT to date has controlled for dietary exposure to sweetness and only found transitory changes in rated sweetness intensity, though no sustained changes in sweet liking (Wise et al., 2015). Further research is needed to better understand whether sweetness preferences are hard-conditioned from early life, or are malleable in response to tastant exposure within our food environment.

Earlier in the chapter we highlighted that umami preferences adapt in response to deviations in protein status, and sweetness perception also plays an important role in our metabolic response to sugar (mono- and disaccharide) consumption. Consumption of simple carbohydrates stimulates early cephalic release of enzymes and hormones, such that over time, sweetness becomes predictive of sugar and carbohydrate ingestion, and stimulates insulin release (Härtel et al., 1993; Teff et al., 1995). However, others have failed to show a clear and reproducible relationship between sweet stimulation and subsequent cephalic phase responses; therefore, the role of sweetness stimulation on carbohydrate-insulin metabolism remains an important debate among researchers in the sensory nutrition field. Relationships between sweet taste and the subsequent delivery of energy are learned, so any disruption in the link between the sensory cue (sweet taste) and subsequent nutrient deliver (carbohydrates/energy) content could potentially disrupt these learned associations and impact later food intake behavior. It has been suggested by some researchers that decoupling of sweetness from energy delivery may enhance appetite stimulating excessive energy intakes, or disruption of the normal glycemic response to carbohydrate ingestion (Swithers and Davidson, 2008; Swithers et al., 2010; Pepino, 2015). However early findings in animal studies have not been replicated in humans, and several recent metaanalyses of studies have shown use of nonnutritive sweeteners in place of sugar support reductions in energy intake, body weight, and BMI (Toews et al., 2019; Rogers et al., 2016). The balance of evidence supports the role of low and no-calorie sweeteners in reducing sugar content while still maintaining the sensory appeal.