5/1/2003 - It is the position of The American Dietetic Association that consumers can safely enjoy a range of nutritive and non-nutritive sweeteners when consumed in moderation and within the context of a diet consistent with the Dietary Guidelines for Americans.
J Am Diet Assoc. 1998;98:580-587.
Human beings are born liking the sensation of sweetness. A number of food ingredients stimulate this sensation by interacting with taste buds in the mouth and throat. The sweetening power of these ingredients varies with the properties of the food system, such as physical state, temperature, and the presence of other flavors. Furthermore, perception of sweet taste can be influenced by genetics, health status, and aging (1).
Nutritive sweeteners provide a sweet taste and a source of energy; nonnutritive sweeteners are sweet without providing energy. The claim that nutritive sweeteners have caused an increase in chronic disease (eg, obesity, cardiovascular disease, diabetes, dental caries, behavioral disorders) is not substantiated (2) but many consumers want the taste of sweetness without added energy.
The food industry has responded to this demand by producing a number of energy-reduced or nonnutritive sweeteners.
It is the position of The American Dietetic Association that consumers can safely enjoy a range of nutritive and non-nutritive sweeteners when consumed in moderation and within the context of a diet consistent with the Dietary Guidelines for Americans.
Types Of Sweeteners
Although sweeteners can be grouped a number of different ways, the grouping "nutritive" and "nonnutritive" acknowledges a difference in the amount of energy provided by sweeteners. Nutritive sweeteners include sugar sweeteners (eg, refined sugars, high fructose corn syrup, crystalline fructose, glucose, dextrose, corn sweeteners, honey, lactose, maltose, various syrups, invert sugars, concentrated fruit juice) and reduced-energy polyols or sugar alcohols (eg, sorbitol, mannitol, xylitol, isomalt, and hydrogenated starch hydrolysates).
Nonnutritive sweeteners (eg, saccharin, aspartame, acesulfame-K, and sucralose) offer no energy, and, as they sweeten with little volume, can also be referred to as high-intensity sweeteners. Both polyols and nonnutritive sweeteners can replace sugar sweeteners and are therefore termed macronutrient substitutes, sugar substitutes, sugar replacers, or alternative sweeteners.
Some sweeteners are considered Generally Recognized As Safe (GRAS) ingredients and others are considered food additives. These terms were defined by the 1958 Food Additives Amendment to the Food, Drug, and Cosmetic Act.
The 1958 amendment also states that the US Food and Drug Administration (FDA) must approve the safety of all additives (3). The safety limit of food additives or conditions of use are expressed as the acceptable daily intake (ADI), that is, the estimated amount per kilogram body weight that a person can safely consume every day over a lifetime without risk.
ADI is a conservative level--it usually reflects an amount 100 times less than the maximum level at which no observed adverse effect occurs in animal (very occasionally human being) studies. The ADI concept is used by FDA and the Joint Expert Committee of Food Additions (JECFA) of the United Nations Food and Agricultural Organization and World Health Organization.
The table provides a summary of the amount of energy provided, the regulatory status, and descriptions of the approved nutritive and nonnutritive sweeteners.
||Granulated: coarse, regular, fine; Powdered: confectioner's; Brown: turbinado, demerara; Liquid: molasses
||Sweetens; enhances flavor; tenderizes, allows browning, and enhances appearance in baking; adds characteristic flavor with unrefined sugar
||High fructose corn syrups: 42%, 55%, 90% fructose; Crystalline fructose: 99% fructose
||Sweetens; functions like sucrose in baking. Some persons experience a laxative response from a load of fructose (greater than or equal to 20 g). May produce lower glycemic response than sucrose
||GRAS (label must warn about a laxative effect)
||Same as chemical name
||50% to 70% as sweet as sucrose. Some persons may experience a laxative effect from a load of sorbitol (greater than or equal to 50 g)
||Permitted for use onan interim basis (label must warn about a laxative effect)
||Same as chemical name
||50% to 70% as sweet as sucrose. Some persons may experience a laxative effect from a load of mannitol (greater than or equal to 20 g)
||Same as chemical name
||As sweet as sucrose
||GRAS (affirmations accepted for filing)
||Same as chemical name
||70% as sweet as sucrose
||GRAS (affirmations accepted for filing)
||Same as chemical name
||30% to 40% as sweet as sucrose; used as a bulking agent
||GRAS (affirmations accepted for filing)
||Same as chemical name
||45% to 65% as sweet as sucrose; used as a bulking agent
||GRAS (affirmations accepted for filing)
||Same as chemical name
||90% as sweet as sucrose
|Hydrogenated starch hydrolysates
||GRAS (affirmations accepted for filing)
||HSH; maltitol syrup
||25% to 50% as sweet on sucrose (depending on the monosaccharide composition)
||Permitted for use on interim basis (label must contain cancer warning and amount of saccharin in the product)
||Sweet and Low
||200 to 700 times sweeter than sucrose. Noncariogenic and produces no glycemic response. Synergizes the sweetening power of nutritive and nonnutritive sweeteners. Sweetening power is not reduced with heating.
||Approved as ageneral-purpose sweetener
||160 to 220 times sweeter than sucrose. Noncariogenic and produces limited glycemic response. New forms can increase its sweetening power in cooking and baking.
||Approved for use as a tabletop sweetener and as an additive in a variety of desserts, confections, and alcoholic beverages
||200 times sweeter than sucrose. Noncariogenic and produces no glycemic response. Sweetening power is not reduced with heating. Can synergize the sweetening power of other nutritive and nonnutritive sweeteners
||Approved for use as a tabletop sweetener, and as an additive in a variety of desserts, confections, and nonalcoholic beverages
||600 times sweeter than sucrose. Noncariogenic and produces no glycemic response. Sweetening power is not reduced with heating
a Provides limited energy to products because of its sweetening power.
b GRAS=Generally Recognized As Safe by the US Food and Drug Administration.
c Hoechst Food Ingredients, Edison, NJ.
d McNeil Specialty Products Company, New Brunswick, NJ.
The 1987-1988 Nationwide Food Consumption Survey provides estimates of nutritive sweetener consumption in the United States (4,5). Total intake of sugars (those added and naturally occurring in foods) was 94 to 95 g/day for the total population or 21% to 22% of total energy intake. Of this total, sugars added to food were estimated at 53 g/day (4).
The major sources of total sugar for children younger than age 10 years were milk/milk products, fruit drinks, and carbonated soft drinks (5). In adults aged 25 to 50 years, the top 3 food categories contributing to total sugar intake were: other (candy and gum, coffee/tea/alcohol, miscellaneous foods, carbonated soft drinks, and fruit drinks); milk/milk products; and bread, cereal, rice, and pasta (includes cookies, cakes, and pastries).
Consumers can monitor their intake of total sugars through the labels on foods and beverages. The Nutrition Labeling and Education Act of 1990 (6) defines labeling of sugars (ie, any monosaccharide or disaccharide) and sugar alcohols. The Act also includes guidelines for labeling a product as "sugar-free" (less than 0.5 g sugar), "reduced sugar" or "less sugar" (a reduction of sugar by 25%), and "no added sugar" (no sugars added during processing).
Sucrose and fructose, which are GRAS substances, are the primary sugar sweeteners that occur naturally in the food supply or are added as sugars, in corn sweeteners, or in syrups. These sweeteners add functional properties to foods through their effects on sensory (eg, flavor of molasses), physical (eg, crystallization, viscosity), microbial (eg, preservation, fermentation), and chemical (eg, carmelization, antioxidation) characteristics (7).
They all provide a similar amount of energy except in the cases of rare genetic abnormalities of carbohydrate metabolism (eg, galactosemia, inherited fructose intolerance). The metabolism of human beings does not distinguish between energy provided from natural and refined sugars.
Although some unrefined nutritive sweeteners provide minerals (eg, molasses contains calcium, iron, magnesium, and potassium), the amount per tablespoon is relatively small compared to the Dietary Reference Intakes (8). Thus, consumers should base their selection of sugar sweeteners on sensory or functional properties, not on misconceptions of differences in nutrient value.
Sucrose is a disaccharide composed of glucose and fructose and provides 4 kcal/g (approximately 16 kcal/tsp). Total sucrose intake ranges from 14 to 60 g/day or from 7% to 11% of energy intake (4). Commercially, sucrose comes from processing sugar cane or sugar beets. Refinement removes the yellow-brown pigments of unrefined sugar to produce the white crystal form of table sugar. Molasses is the least refined form of sucrose.
The monosaccharide fructose provides 4 kcal/g. Fructose is a component of sucrose, is present in fruit (also known as fruit sugar or levulose), and is added to foods and beverages as high fructose corn syrup (HFCS) or in the crystalline form. Fructose is manufactured through the isomerization of dextrose in corn starch.
Fructose has replaced sucrose in many foods and beverages because of its sweetening power and functional properties that enhance flavor, color, and product stability (9). Fructose also synergizes the sweetness potential of sucrose and other nonnutritive sweeteners (9).
Food consumption surveys show an increase in fructose consumption: the ratio of fructose intake as a proportion of total sugars has increased by nearly 30% from the 1977-1978 and 1987-1988 Nationwide Food Consumption Surveys (4,9).
High intakes of fructose have implications for gastrointestinal health, blood glucose control, and lipid metabolism. Fructose is primarily absorbed from the gut by facilitated diffusion (10). Persons vary in their abilities to absorb fructose--some experience symptoms of malabsorption with a 20- to 50-g load (11). (A 12-oz sweetened soda or fruit drink has between 14 and 22 g fructose; 1 c apple juice has 14 g fructose.)
Some of the malabsorption of fructose-containing products may be the result of other nutritive sweeteners that are poorly absorbed (eg, sugar alcohols in apple juice). Fructose is better absorbed when consumed in sucrose (10), than in products where the amount of free fructose exceeds the amount of glucose (eg, in honey, prunes, apples and juice, HFCS, or crystalline fructose) (11).
Because of the method of absorption, fructose intake may lead to a slower rise in blood glucose than sucrose-based sweeteners. This fact, along with rapid clearance of fructose from blood serum, may improve glycemic control (12). High intakes of fructose could, theoretically, increase production of lipid precursors and increase the risk of hypertriglyceridemia.
However, this effect is not consistently seen, even in those who are at high risk of elevated plasma triglycerides (13).
The US Food Guide Pyramid (14) encourages consumers to have the smallest proportion of their energy derived from fats, oils, and sugars. The Dietary Guidelines for Americans (15) urge consumers to choose a diet moderate in these sources of energy because excessive intake may provide the body with unnecessary energy and few nutrients. However, persons can include sugars in their diets and still consume a healthful diet.
A recent review of intake surveys from both the United States and the European Union showed no consistent or nutritionally meaningful variation in micronutrient intake across the range of sugar intakes (5). The association between sugar intake and nutrient adequacy of the diet has a U shape, suggesting that extreme intakes of sugar (too high or too low) are not optimal.
Persons show adequate nutrient intake across a wide range of sugar intakes (16). Those consuming low amounts of total sugar (less than 26.4 g/1,000 kcal) (17) tended to consume more energy from fat.
Polyols (Sugar Alcohols)
Polyols can also be categorized as sugar replacers (18) because they can replace sugar sweeteners, usually on a one-to-one basis; offer less energy; and offer potential health benefits (eg, reduced glycemic response and reduced dental caries risk). The polyols sorbitol, mannitol, and xylitol are found in plant products such as fruits and berries. Commercially, these sweeteners are synthesized and not extracted from natural sources.
All polyols are absorbed slowly and incompletely from the intestine by passive diffusion. Therefore, an excessive load (eg, greater than 50 g sorbitol per day,greater than 20 g mannitol per day) may cause diarrhea. If polyols were completely absorbed, direct metabolism could provide the usual 4 kcal/g.
However, incomplete absorption causes indirect metabolism of polyols via fermentive degradation by the intestinal flora. The energy return from indirect metabolism is less than the direct route; thus, polyols are referred to as reduced-energy or low-energy sweeteners. FDA allows these nutritive sweeteners to be labeled as having fewer kilocalories per gram than other nutritive sweeteners. (See the Table for kilocalories per gram for eachpolyol.)
The safety and use of polyols has been extensively reviewed (19,20). Because of the incomplete absorption, polyols produce a low glycemic response. Products with sorbitol and mannitol may have the following statement on the label because high intakes increase the risk of malabsorption: "excess consumption may have a laxative effect."
Sorbitol is on the GRAS list for use in candies, chewing gum, jams/jellies, baked goods, and frozen confections. Mannitol is permitted for use on an interim basis pending further study of health effects. The interim status is provided to food additives that have a history of use but their safety has been brought into question by new information, even if it is not conclusive (21).
Mannitol is used as a dusting agent for chewing gum and a bulking agent in powdered foods. Xylitol is approved as a GRAS food additive for use in chewing gums, candies, pharmaceuticals, and hygiene products. A petition for GRAS status has been accepted for filing by FDA for isomalt, lactitol, maltitol, hydrogenated starch hydrolysates (HSH), and erythritol. These polyols are used in confections and/or as bulking agents.
The United States leads the world in consumption of high-intensity sweeteners, consuming approximately 50% of the world demand (22). High-intensity sweeteners can offer consumers a way to enjoy the taste of sweetness with little or no energy intake or glycemic response. Nonnutritive sweeteners may assist in weight management, control of blood glucose, and prevention of dental caries.
The food industry evaluates these sweeteners for many attributes, including sensory qualities (eg, clean sweet taste, no bitterness, odorless), safety, compatibility with other food ingredients, and stability in different food environments. The trend in the food industry is to blend high-intensity sweeteners.
Blending can cause sweetness synergy (ie, the combination is sweeter than the individual components), which can decrease the amount of sweetener needed and can improve the overall sweet taste.
FDA has approved 4 nonnutritive sweeteners and regulates them as food additives: saccharin (on an interim basis pending additional study), aspartame, acesulfame potassium (or acesulfame-K), andsucralose.
Saccharin exceeds the sweetness of sugar 200 to 700 times (23). It provides no energy, as it is not metabolized by human beings (23), and it is not cariogenic. The FDA Center for Food Safety and Applied Nutrition estimates the daily use of saccharin at 50 mg per person per day.
The JECFA has set the ADI for saccharin at 5 mg/kg body weight per day (24). Despite the decline in use, saccharin is the largest-volume, lowest-cost high-intensity sweetener used in the world (nearly 62 million lb were used in 1995) (22). It is approved for use in more than 100 countries.
Saccharin was originally included on the GRAS listing. In 1977, FDA placed a ban on use of saccharin because it was reported to be a carcinogen in rats. In the same year, Congress, through the Saccharin Study and Labeling Act, imposed an 18- month moratorium on the FDA ban and required products containing saccharin to bear the following warning: "Use of this product may be hazardous to your health. This product contains saccharin which has been determined to cause cancer in laboratory animals."
Congress has extended this moratorium 7 times, the last to continue through May 2002. In 1991, FDA formally withdrew the proposed ban and considers saccharin to be a food additive on an interim basis for use in cosmetics, pharmaceuticals, foods and beverages, tabletop sugar substitutes, and chewing gum.
The amount of saccharin must appear on the food label and is limited to no more than 12 mg/oz in beverages, 20 mg per sweetening equivalent of 1 tsp sugar, or no more than 30 mg per food serving (21).
Since 1981, saccharin has been listed as an "anticipated" human carcinogen (25). Studies of high users (ie, persons with diabetes) do not support an association between saccharin and cancer (26,27). However, subgroups of persons (eg, male heavy smokers) may present increased risk (25).
The advisory board for the National Toxicology Program did not recommend removal of saccharin from the Report on Carcinogens, Ninth Edition (report in preparation).
Aspartame a dipeptide (methyl ester of l-aspartic acid and l-phenylalanine) is 160 to 220 times sweeter than sucrose. Intestinal esterases hydrolyze aspartame to aspartic acid, methanol, and phenylalanine (28). The amino acids are metabolized to provide 4 kcal/g. Thus, this sweetener does provide energy; however, because of the intense sweetness of aspartame, the amount of energy derived from it is negligible.
In 1981, FDA approved aspartame as a sweetener for a number of dry uses (eg, tabletop sweetener, cold breakfast cereal, gelatins, puddings) and in chewing gum and carbonated beverages. In 1985, the Council on Scientific Affairs of The American Medical Association concluded that "Available evidence suggests that consumption of aspartame by normal humans is safe and is not associated with serious adverse health effects" (29, p 400).
FDA has evaluated aspartame use in food and beverages 26 times since its original approval. In 1996, FDA approved aspartame as a general-purpose sweetener for use in all foods and beverages. Aspartame is also approved for use in more than 100 nations.
Demand for aspartame in the United States rose from 8.4 million lb in 1986 to 17.5 million lb in 1992, a figure that represents more than 80% of the world demand. Although soft drinks account for more than 70% of aspartame consumption, this sweetener is added to more than 6,000 foods, personal care products, and pharmaceuticals.
Aspartame is available in liquid, granular, encapsulated, and powder forms to extend its use in food and beverage products. The encapsulated form has made aspartame more heat stable and has extended its use in some commercially baked products.
Detailed studies have been conducted to determine how ingestion influences plasma levels of aspartic acid, phenylalanine, and methanol (or the by-product formate). In studies of healthy adults (30), a bolus load (up to 200 mg/kg) did not alter levels of plasma aspartate concentrations or blood levels of formate. Plasma phenylalanine response to aspartame varies genetically.
Persons with phenylketonuria, a homozygous recessive inborn error of metabolism, are unable to metabolize phenylalanine. In persons with this rare (frequency is approximately 1 in 10,000 whites) inborn error, excess intake of this amino acid causes higher plasma levels and altered synthesis of monoamine neurotransmitters (31) and adverse effects (32).
Thus, medical nutrition therapy for phenylketonuria involves the control of dietary sources of phenylalanine, including aspartame. Foods containing aspartame must, by FDA requirements, contain a label indicating that they contain phenylalanine.
Persons with phenylketonuria appear to tolerate the amount of phenylalanine in diet soda sweetened with aspartame (approximately 104 mg/12 oz) (33). Heterozygotes for phenylketonuria do not show changes in cognitive performance or in electroencephalograms after 12 weeks of consuming either 15 or 45 mg/kg aspartame per day (34).
In persons without phenylketonuria, single bolus studies of aspartame (up to 50 mg/kg body weight) or repeat dose studies show a plasma phenylalanine response near the normal postprandial range and considerably lower than that observed in persons with phenylketonuria or those with mild hyperphenylalanemia (30).
Aspartame breaks down to diketopiperazine in liquid systems with heat exposure and loses it sweetness. Animal toxicity studies show that even if all aspartame was converted to diketopiperazine in beverages, the amount would be well below the ADI of 3,000 mg/kg for diketopiperazine (35).
Some persons report allergic reactions to aspartame, including edema of the lips, tongue, and throat; dermatologic reactions; and respiratory problems (36). However, 2 double- blind challenge studies report difficulty recruiting persons who claim an allergic response to aspartame and failure to reproduce the allergic reaction in controlled experiment conditions (37,38).
FDA increased ADI for aspartame to its current level of 50 mg/kg body weight when it was approved for use in carbonated beverages. Post market assessment of aspartame shows that estimated daily intake of aspartame is below this ADI (39): aspartame eaters (at least 90th percentile of consumption) in the general population consume 6% of the ADI (3.0 mg/kg per day) and those aged 1 to 5 years consume 10.4% of the ADI (5.2 mg/kg per day).
Food labels can help consumers identify foods and beverages that contain aspartame, although the amount is not generally labeled. Consumers would need to contact the companies to determine the amount of aspartame in each product. Nonetheless, the amount in some common foods is: up to 225 mg in a 12-oz diet soda, 100 mg in an 8-oz drink made from powder, 80 mg in an 8-oz yogurt or a 4-oz gelatin dessert, up to 32 mg in 3/4 c sweetened cereal, and up to 47 mg in 1/2 c frozen dairy dessert.
As a tabletop sweetener, packets contain 37 mg aspartame and are equivalent to the sweetness of 2 tsp sugar. In the granular form, 1 tsp contains 16 mg aspartame and equals the sweetening of 1 tsp sugar. To reach the ADI, an 18 kg (nearly 40 lb) child would need to consume 900 mg aspartame per day, which translates to 24 packets of sweetener (equivalent to 48 tsp sugar), four 12-oz cans of diet soda, or nine 8-oz glasses of fruit drink made from a powder.
Acesulfame-K (5,6-dimethyl-1,2,3-oxathiazine-4(3H)-one-2,2-dioxide) is approximately 200 times sweeter than sucrose. The "K" refers to potassium. Acesulfame-K can withstand high cooking/baking temperatures. Blends of acesulfame-K with other nutritive and nonnutritive sweeteners can synergize the sweetness potential and decrease the bitter taste. This sweetener does not provide any energy; it is not metabolized by the body and is excreted in the urine unchanged.
This sweetener was evaluated for safety by JECFA in 1983 (40,41). FDA approved acesulfame-K in 1988. Both regulatory groups have set an ADI of 15 mg/kg body weight. In the United States, acesulfame-K is approved for use as a tabletop sweetener and as an additive in chewing gum, confections, desserts, yogurt, sauces, and alcoholic beverages (21).
FDA is reviewing acesulfame-K for use in nonalcoholic beverages. The tabletop sweetener contains approximately 0.4 g acesulfame-K per packet. The amount of acesulfame-K added to food products is very small because of its intense sweetening power and because it is often used in combination with other sweeteners.
Sucralose (trichlorogalactosucrose) is 600 times sweeter than sucrose. Sucralose provides no energy; it is not well absorbed and is excreted in the urine essentially unchanged. This sweetener is heat stable in cooking and baking.
Sucralose was approved in April 1998 as a tabletop sweetener and for use in a number of desserts, confections, and nonalcoholic beverages. FDA concluded from a review of more than 110 studies in human beings and animals that this sweetener did not pose carcinogenic, reproductive, or neurologic risk to human beings. In 1990, JECFA increased the temporary ADI from 0 to 3.5 mg/kg body weight to 0 to 15 mg/kg body weight (42).
Nonnutritive Sweeteners Not Yet Approved In The United States
A petition for alitame as a tabletop sweetener and for use in a range of products including baked goods, beverages, and confections was submitted to FDA in 1986. Alitame is composed of l-aspartic acid, d-alanine, and a novel C-terminal amide moiety and is 2,000 times sweeter than sucrose without the bitter or metallic qualities of high-intensity sweeteners (43).
This sweetener blends with other high-intensity sweeteners to maximize the quality of sweetness. From an oral load of alitame, 7% to 22% is unabsorbed and excreted in the feces. The remaining amount (78% to 93%) is hydrolyzed to aspartic acid and alanine amide.
The aspartic acid is metabolized normally and the alanine amide is excreted in the urine as a sulfoxide isomer, sulfone, or conjugated with glucuronic acid. The incomplete absorption and metabolism results in a core value of 1.4 kcal/g.
In 1995, JEFCA concluded that alitame was not carcinogenic and did not show reproductive toxicity (44). However, recommendations on an ADI await further research on its safety. In the FDA petition, the estimated daily intake is 0.34 mg/kg body weight, which represents the amount if alitame was used as the only sweetener in a person's diet.
The level at which no observed adverse effects occurred in animals was 100 mg/kg (43). Alitame is approved for use in food and beverages in Australia, New Zealand, Mexico, and the People's Republic of China.
FDA banned this sweetener as a food ingredient in 1969 because the saccharin/cyclamate mixture was shown to cause cancer in laboratory mice (45). The primary concern was that it could be carcinogenic to some persons who appear to metabolize cyclamate to cyclohexylamine (46). To support a petition for use of cyclamate in 1982, the Cancer Assessment Committee of FDA reviewed the scientific evidence and concluded that cyclamate was not carcinogenic.
This was reaffirmed in 1985 by the National Academy of Sciences (47). The petition to reapprove cyclamate in the United States is still under review by FDA. This sweetener is more than 30 times sweeter than sucrose and is approved for use by more than 50 countries.
Sweetener Use In Segments Of The Population
Because of their size and relatively high food and fluid intakes compared with adults, children will have the highest intake of nutritive and nonnutritive sweeteners as calculated by milligram intake per kilogram body weight. Children can safely consume nutritive sweeteners within a diet consistent with the Dietary Guidelines.
Children have shown a substantial increase in intake of fructose, presumably through intake of sweetened drinks and fruit drinks (5). Healthy young children (aged 6 to 18 months) can exhibit carbohydrate malabsorption (eg, fructose and sorbitol) with ingestion of common fruit juices (eg, apple juice) (48). (One cup apple juice can contain 14 g fructose and 2.5 g sorbitol.)
Children who exhibit nonspecific diarrhea may benefit from a reduction in fructose and products containing polyols.
It has been suggested that caregivers may want to limit intake of saccharin by young children because of the limited amount of data available for its use in children (49). The estimated daily intake of aspartame in children ranges from 8 to 17 mg/kg body weight in children aged 2 to 5 years, which is below the acceptable daily intake of 50 mg/kg body weight. Intakes of acesulfame-K in children are also below ADI (ranges from 3 to 9 mg/kg body weight).
Use of nutritive sweeteners that have GRAS status is acceptable during pregnancy. Recommendations for nonnutritive sweetener use during pregnancy must be based on well-designed and approved clinical investigations to ensure a healthy pregnancy and healthy babies. Saccharin can cross the placenta and may remain in fetal tissues because of slow fetal clearance (50). It has been suggested that women consider careful use of saccharin during pregnancy (49).
The issue with aspartame in pregnancy relates to fetal exposure to aspartic acid, phenylalanine, or methanol. In animals, an aspartame load does not change fetal exposure to aspartic acid (51). Fetal circulation levels of phenylalanine exceed maternal levels because of concentration across the placental barrier (52).
A bolus of aspartame (34 mg/kg or the 99th percentile of estimated daily intake) results in a peak plasma level of phenylalanine in normal subjects (112 micromol/L)1 and phenylketonuric heterozygotes (162 micromol/L) below the level that would cause neurological problems in the fetus (1,090 micromol/L) (53).
Plasma response of methanol and formate were not significant after an aspartame load. Thus, if placental transport of these compounds occurs, the amount is not clinically harmful (54). Use of aspartame within FDA guidelines appears safe for pregnant women.
Safety of acesulfame-K use during pregnancy has been determined with rat studies. (JECFA has determined that rats are an appropriate model for human beings.) At high levels (3% of the diet), there was no change observed in fertility, size of litter, body weight, growth, or mortality (55). Thus, use of acesulfame-K within FDA guidelines appears safe for pregnant women.
1 To convert micromol/L phenylalanine to mg/dL, multiply micromol/L by 0.01652.
To convert mg/dL phenylalanine to micromol/L, multiply mg/dL by 60.54.
Phenylalanine of 300 micromol/L=4.96 mg/dL.
Sweetener Use In Chronic Conditions
Claims of an association between sugar and hyperactivity have not been supported (56), even in those children who, by report, are sensitive to sugar (57). In fact, some research supports that persons with negative mood states (eg, seasonal affective disorders, alcohol withdrawal) should consume carbohydrate-rich foods, including sweets, as a way of alleviating their condition (58).
The mechanism by which carbohydrate, including sugars, may affect mood is not certain, but may involve the synthesis and release of serotonin in the brain. Serotonin controls functions such as temperature regulation, sensory perception, onset of sleep, and appetite. Control of brain levels of serotonin is of current interest for the management of depression, mood disorders, and appetite.
The alleged association between hyperactivity and aspartame is not scientifically supported (56,57). Some consumers report behavioral side-effects of aspartame (eg, headache, dizziness, mood alteration) related to the central nervous system. The Centers for Disease Control and Prevention reviewed 600 of these behavior complaints and concluded that there was no association (59).
Controlled clinical studies do not show an association between aspartame intake and seizures in sensitive children (60) or difficulties with cognitive and behavioral tasks in children with attention deficit disorder (61).
The association claimed between aspartame intake and risk of brain tumors has not been supported. A recent report hypothesized that aspartame use since its approval in 1981 had contributed to an increased incidence of brain tumors (61,62). However, FDA, using data from an analysis of the National Cancer Institute's database on cancer incidence in the United States (63), found a flattening of the rate of brain cancer since 1985 with a slight decrease from 1991 to 1993.
With consideration of these findings with other data reviewed at the time of approval, FDA continues to support the original approval of aspartame.
Risk of dental caries increases with intake of nutritive sugars, however, this risk does not work independently from factors such as oral hygiene and fluoridation (64). Use of polyol-based gum can reduce the risk of dental caries compared to sucrose-sweetened gum, with the greatest benefit from xylitol-based gums (65).
FDA authorizes use of the health claim in food labeling that sugar alcohols (eg, sorbitol, mannitol, xylitol) do not promote tooth decay (66). Nonnutritive sweeteners do not promote dental caries.
The primary goal for disease management in persons with diabetes mellitus is to maintain near-normal blood glucose levels. Nutritive sweeteners do not produce greater increase in blood glucose response than complex starches, as was previously believed (67). Intake as high as 60 g fructose or sucrose per day may not adversely affect glycemic or lipid response in persons with type 2 diabetes (68).
Although it is recognized that carbohydrate sources provide different glycemic responses, the clinical perspective is that attention should be given first to the total amount of carbohydrate consumed rather than the source of carbohydrate (69).
The selection of healthful foods within the context of the Food Guide Pyramid and with attention to energy intake and blood glucose control is recommended for the management of diabetes (69).
Nonnutritive sweeteners are also appropriate in meal plans for persons with diabetes and may help control of energy intake. Dietetics practitioners can help persons with diabetes incorporate nutritive and nonnutritive sweeteners into their individual meal plans.
Usual intakes of sucrose or fructose do not elevate plasma triglycerides in most persons, including those with diabetes, provided that energy balance is unchanged (13). However, very high intakes of dietary fructose and sucrose (approximately 2 to 3 times usual consumption) can result in elevations of plasma triglycerides (12). At this time there is no evidence that current levels of fructose intake contribute tohyperlipidemia.
Excess body fat (obesity) arises from the energy imbalance caused by taking in too much energy and using too little. Perhaps because sugar adds hedonic value to many foods and beverages it has been hypothesized that sugar plays a major role in the etiology of obesity. There are several arguments against this hypothesis. First, sugars suppress appetite to the same extent as other carbohydrates (4).
Second, there is no relationship between the per capita amount of sugar available in the food supply and the incidence of obesity in the population (70). Third, epidemiologic studies show an inverse relationship between sugar intake and obesity (71) and a direct relationship between obesity and fat intake (72) and the ratio of fat to sugar in the diet (16). Obesity is a complex problem and its cause cannot be simply attributed to any 1 component of the food supply.
The contribution of nonnutritive sweeteners to obesity management is unclear. The original motivation for their development was based on the goal of providing a sweet taste without added energy to persons with diabetes and those wanting to control energy intake. Nonnutritive sweeteners can save the consumer up to 16 kcal/tsp sweetening.
Theoretically, if total intake of sugars (estimated at 95 g or approximately 24 tsp/day) were replaced by nonnutritive sweeteners, this could result in a deficit of 380 kcal/day or a 1 lb weight loss in 9 to 10 days. One study has shown that the addition of aspartame- sweetened foods and beverages to a multidisciplinary weight-control program facilitated long-term maintenance of reduction in body weight in obese women (73).
However, obesity prevalence has increased substantially at the same time as the consumption of nonnutritive sweeteners has increased. The rise in prevalence clearly relates to all factors that cause an energy imbalance.
Therefore, persons who wish to lose weight may choose to use nonnutritive sweeteners but should do so within the context of a sensible weight management program including a sensible diet and enjoyable exercise.
Implications For Dietetics Professionals
Sweetness can add pleasure to eating, and today consumers can enjoy a wide range of sweeteners in a wide variety of foods and beverages. Both food labeling and the range of nutritive and nonnutritive sweeteners allow choice in the type and amount of sweeteners to include in the diet.
Consumers can incorporate nutritive sweeteners into a healthful eating plan and meet the Dietary Guidelines for Americans. The food label also provides information to consumers on types and amounts of nutritive sweeteners in food and beverages.
Nonnutritive sweeteners are safe for use by most persons within the approved guidelines. The trend in sweetener blending will maximize sweetener potential and help to support intakes of nonnutritive sweeteners well within the acceptable levels. As new nonnutritive sweeteners emerge, the safety of these substitutes used alone or in combination with other nutritive and nonnutritive sweeteners and macronutrient substitutes, such as fat replacers, will need to be examined.
Additionally, national surveillance of intake of both nutritive and nonnutritive sweeteners is important to determine if they help consumers meet the recommended dietary goals.
- Bartoshuk LM, Beauchamp GK. Chemical senses. Ann Rev Psychol. 1994;45:419-449.
- Anderson G. Sugars and health: a review. Nutr Res. 1997;17:1485-1498.
- Toxicological Principles for the Safety Assessment of Direct Food Additives and Color Additives Used in Food. Washington, DC: Food and Drug Administration, Bureau of Foods (now Center for Food Safety and Applied Nutrition); 1982. National Technical Information Order No. PB83-170696.
- Glinsmann W, Park Y. Perspective on the 1986 Food and Drug Administration assessment of the safety of carbohydrate sweeteners: uniform definitions and recommendations for future assessments. Am J Clin Nutr. 1995;62(suppl):161S-169S.
- Gibney M, Sigman-Grant M, Stanton J, Keast D. Consumption of sugars. Am J Clin Nutr. 1995;62(suppl):178S-194S.
- Food labeling: mandatory status of nutrition labeling and nutrient content revision, format for nutrition label. Federal Register. January 6, 1993;58:2079-2173.
- Davis E. Functionality of sugars: physicochemical interactions in foods. Am J Clin Nutr. 1995;62(suppl):170S-177S.
- National Academy of Sciences, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. Washington, DC: National Academy Press; 1997.
- Hanover L, White J. Manufacturing, composition, and applications of fructose. Am J Clin Nutr. 1993;5 (suppl):724S-732S.
- Shi X, Schedl H, Summers R, Lamber G, Chang R, Xiz T, Gisolfi G. Fructose transport mechanisms in humans. Gastroenterology. 1997;113:1171-1179.
- Rumessen J. Fructose and related food carbohydrates: sources, intake, absorption, and clinical implications. Scand J Gastroenterol. 1992;27:819-828.
- Uusitupa M. Fructose in the diabetic diet. Am J Clin Nutr. 1994;59(suppl):753S-757S.
- Truswell A. Food carbohydrates and plasma lipids--update. Am J Clin Nutr. 1994;59(suppl):710S-718S.
- Food Guide Pyramid: A Guide to Daily Food Choices. Washington, DC: US Dept of Agriculture, Human Nutrition Services;1992. Home and Garden Bulletin No. 252.
- Nutrition and Your Health: Dietary Guidelines for Americans. 4th ed. Washington, DC: US Depts of Agriculture and Health and Human Services; 1995. Home and Garden Bulletin DHHS (PHS) publication No. 88-50210.
- Bolton-Smith C, Woodward M. Dietary composition and fat to sugar ratios in relation to obesity. Int J Obes. 1994;18:820-828.
- Lewis C, Park Y, Dexter P, Yetley E. Nutrient intakes and body weights of persons consuming high and moderate levels of added sugars. J Am Diet Assoc. 1992;92:708-713.
- McNutt K, Sentki A. Sugar replacers: a growing group of sweeteners in the United States. Nutr Today. 1996;31(6):255-261.
- Dills W. Sugar alcohols as bulk sweeteners. Ann Rev Nutr. 1989;9:161-186.
- Senti FR. Health Aspects of Sugar Alcohols and Lactose. Bethesda, Md: Federation of American Societies for Experimental Biology;1986:85.
- Food and Drug Administration. Code of Federal Regulations: Food and Drugs. The Office of the Federal Register: April 1, 1996: Parts 170 to 199.
- Bizzari S, Jackel M, Yoshida Y. High intensity sweeteners. In: Chemical Economics Handbook. Menlo Park, Calif: SRI Consulting; 1996.
- Mitchell M, Pearson R. Saccharin. In: Nabors L, Gelardi R, eds. Alternative Sweeteners. New York, NY: Marcel Dekker; 1991:127-156.
- Joint FAO/WHO Expert Committee on Food Additives. Evaluation of Certain Food Additives and Contaminants: Saccharin. Geneva, Switzerland: World Health Organization; 1993:17-19. WHO Technical Report Series.
- National Toxicology Program. Seventh Annual Report on Carcinogens: Saccharin. Washington, DC: Dept of Health and Human Services/National Institutes of Health;1994. CAS No. 128-44-99.
- Morgan R, Wong O. A review of epidemiological studies on artificial sweeteners and bladder cancer. Food Chem Toxicol. 1985;23:529-533.
- Risch H. Dietary factors and the incidence of cancer of the urinary bladder. Am J Epidemiol. 1988;127:1179-1191.
- Ranney R, Oppermann J, Muldoon E, McMahon FG. Comparative metabolism of aspartame in experimental animals and humans. J Toxicol Environ Health. 1976;2:441-451.
- Council on Scientific Affairs. Aspartame: review of safety issues. JAMA. 1985;254:400-402.
- Stegink L, Filer LJ. Effects of aspartame ingestion on plasma aspartate, phenylalanine, and methanol concentrations in normal adults. In: Tschanz C, Butchko H, Stargel W, Kotsonis F, eds. The Clinical Evaluation of a Food Additive. New York, NY: CRC Press; 1996.
- Maher T, Wurtman R. Possible neurological effects of aspartame, a widely used food additive. Environ Health Perspect. 1987;75:53-57.
- Wolf-Novak L, Stegink L, Brummel M, Person TJ, Filer LT Jr, Bell EF, Ziegler EE, Krause WL. Aspartame ingestion with and without carbohydrate in phenylketonuric and normal subjects: effect on plasma concentrations of amino acids, glucose, and insulin. Metabolism. 1990;39:391-396.
- Mackey S, Berlin CJ. Effect of dietary aspartame on plasma concentrations of phenylalanine and tyrosine in normal and homozygous phenylketonuric patients. Clin Pediatr. 1992;31:394-399.
- Trefz F, De Sonneville L, Matthis P, Benninger C, Lanz-Englert B, Bickel H. Neuropsychological and biochemical investigations in
heterozygotes for phenylketonuria during ingestion of high dose aspartame (a sweetener containing phenylalanine). Hum Genet. 1994;93:369-374.
- Food and Drug Administration. Food additives permitted for direction addition to food for human consumption: aspartame. Federal Register. 1983;48:31376-31382.
- Health Hazard Evaluation. Summary of Adverse Reactions Attributed to Aspartame. Washington, DC: US Dept of Health and Human Services; 1995.
- Garriga M, Berkebile C, Metcalfe D. A combined single-blind, double-blind, placebo-controlled study to determine the reproducibility of hypersensitivity reactions to aspartame. J Allergy Clin Immunol. 1991;87:821-827.
- Geha R, Buckley C, Greenberger P, Patterson R, Polmar S, Saxon A, Rohr A, Yang W, Drouin M. Aspartame is no more likely than placebo to cause urticaria/angioedema: results of a multicenter, randomized, double-blind, placebo-controlled crossover study. J Allergy Clin Immunol. 1993;92:513-520.
- Food and Drug Administration. Food additives permitted for direct addition to food for human consumption: aspartame. (21 CFR Part 172). Federal Register. 1996;61:33654-33656.
- FAO/WHO Expert Committee on Food Additives. Toxicological Evaluations of Certain Food Additives. Acesulfame Potassium. Geneva, Switzerland: World Health Organization; 1981;10-27. WHO Food Additive Series vol 16.
- FAO/WHO Expert Committee on Food Additives. Toxicological Evaluations of Certain Food Additives and Food Contaminants. Acesulfame Potassium. Geneva, Switzerland: World Health Organization; 1983;12-20. WHO Food Additive Series vol 18.
- FAO/WHO Expert Committee of Food Additives. Trichlorogalactosucrose. Geneva, Switzerland: World Health Organization; 1991;21-23. WHO Technical Report Series.
- Hendrick M. Alitame. In: Nabors L, Gelardi R, eds. Alternative Sweeteners. New York, NY: Marcel Dekker; 1991:29-38.
- Joint FAO/WHO Expert Committee of Food Additives. Sweetening Agent: Alitame. 1995;23-27.WHO Technical Report Series vol 44.
- Price J, Blava B, Oser B, Steinfield J, Ley H. Bladder tumors in rats fed cyclohexylamine or high doses of a mixture of cyclamate and saccharin. Science. 1970;167:1131-1132.
- Kojima S, Ichibagase H. Cyclohexylamine, a metabolite of sodium cyclamate. Chem Pharm Bull. 1966;14:971-974.
- Committee on the Evaluation of Cyclamate and Carcinogenicity. Evaluation of Cyclamate for Carcinogenicity. Washington, DC: National Academy of Science, National Resource Council; 1985.
- Smith M, Davis M, Chasalow F, Lifshitz F. Carbohydrate
absorption from fruit juice in young children. Pediatrics. 1995;95:340-344.
- Council on Scientific Affairs, American Medical Association. Saccharin: review of safety issues. JAMA. 1985;254:2622-2624.
- Pitkin RM, Reynolds W, Filer LJ, et al. Placental transmission and fetal distribution of saccharin. Am J Obstet Gynecol. 1971;111:280-286.
- Stegink L, Pitkin R, Reynolds W, Brummel M, Filer LJ. Placental transfer of aspartate and its metabolites in the primate. Metabolism. 1979;28:669-676.
- Pueschel S, Boylan J, Jackson B, Piasecki G. A study of placental transfer mechanisms in nonhuman primates using [14C] phenylalanine. Obstet Gynecol. 1982;59:182-188.
- Levy H, Waisbren S. Effects of untreated maternal phenylketonuria and hyperphenylalaninemia on the fetus. N Engl J Med. 1983; 309:1269-1274.
- London R. Saccharin and aspartame. Are they safe to consume during pregnancy? J Reprod Med. 1988;33(1):17-21.
- Toxicological Evaluation of Certain Food Additives. Geneva, Switzerland: World Health Organization; 1980;11.WHO Food Additives Series vol 16.
- Kanarek R. Does sucrose of aspartame cause hyperactivity in children? Nutr Rev. 1994;52:173-175.
- Wolraich M, Lindgren S, Stumbo P, Stegink L, Appelbaum M, Kiritsy M. Effects of diets high in sucrose or aspartame on the behavior and cognitive performance of children. N Engl J Med. 1994;330:301-307.
- Christensen L. Effects of eating behavior on mood: a review of the literature. Int J Eat Disord. 1992;14:171-183.
- Bradstock M, Serdula M, Marks J, Barnard RJ, Crane NT, Remington RL, Trowbridge FL. Evaluation of reactions to food additives: the aspartame experience. Am J Clin Nutr. 1986;43:464-469.
- Rowan A, Shaywitz B, Tuchman L, French J, Luciano D, Sullivan C. Aspartame and seizure susceptibility: results of a clinical study in reportedly sensitive individuals. Epilepsia. 1995;36:270-275.
- Shaywitz B, Sullivan C, Anderson G, Gillespie S, Sullivan B, Shaywitz S. Aspartame, behavior, and cognitive function in children with attention deficit disorders. Pediatrics. 1994;93:70-75.
- Olney J, Faber N, Spitznagel E, Robins L. Increasing brain tumor rates: is there a link to aspartame? J Neuropathol Exp Neurol. 1996; 55:115-123.
- FDA Statement on Aspartame. Rockville, Md: Food and Drug Administration. FDA Talk Paper. November 18, 1996.
- Navia J. Dietary carbohydrates and dental health. Am J Clin Nutr. 1994;59(suppl):719S-727S.
- Makinen K, Bennett C, Hujoel P, Isokangas P, Isotupa K, Pape HJ. Xylitol chewing gums and caries rates: a 40-month cohort study. J Dent Res. 1995;74:1904-1913.
- Food and Drug Administration. Health claims: dietary sugar alcohols and dental caries. Federal Register. August 23, 1996:61:43433-43445.
- Wolever T, Brand J. Sugars and blood glucose control. Am J Clin Nutr. 1995;62(suppl):212S-227S.
- Malerbi D, Paiva E, Duarte A, Wajchenberg B. Metabolic effects of dietary sucrose and fructose in type II diabetic subjects. Diabetes Care. 1996;19:1249-1256.
- Position of The American Diabetes Association: nutrition recommendations and principles for people with diabetes mellitus. Diabetes Care. 1997;1(suppl):S14-S17.
- Anderson G. Sugars, sweetness and food intake. Am J Clin Nutr. 1995;62(suppl):195S-202S.
- Hill J, Prentice A. Sugar and body weight regulation. Am J Clin Nutr. 1995;62(suppl):264S-274S.
- Prentice A, Poppitt S. Sugar and body weight regulation. Int J Obes. 1996;20 (suppl):S18-S23.
- Blackburn G, Kanders B, Lavin P, Keller S, Whatley J. The effect of aspartame as part of a multidisciplinary weight-control program on short- and long-term control of body weight. Am J Clin Nutr. 1997; 65:409-418.
ADA position adopted by the House of Delegates on October 18, 1992, and reaffirmed on September 6, 1996. This position will be in effect until December 31, 2001. This position was reaffirmed; an update paper will be published in 2002. ADA authorizes republication of the position statement/support paper, in its entirety, provided full and proper credit is given. Requests to use portions of the position must be directed to ADA Headquarters at 312/899-0040, ext 4896 or email@example.com. Positions may be accessed directly at www.eatright.org/positions.html.
Recognition is given to the following for their contributions:
Valerie B. Duffy, PhD, RD, and G. Harvey Anderson, PhD
ADA Government Relations Team; Carolyn D. Berdanier, PhD; Marion J. Franz, MS, RD; Marsha Hudnall, MS, RD; Lisa H. McKee, PhD; Margaret A. Powers, MS, RD; Claire Regan, MS, RD; Phyllis J. Stumbo, PhD, RD; Susan K. Taylor, MS, RD.
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