URC

Sucralose: An Overview

Genevieve Frank
Penn State University


Abstract

Sucralose is an artificial sweetener derived from native sucrose that reached the American market in 1998. Sucralose efficacy, regulation, metabolism, toxicity, pharmacokinetics, and stability are explored and compared with current common artificial sweetening agents available to American consumers. Emphasis is given to product safety and industrial applications.

FDA approval supports claims of long-term sucralose safety, yet public concern remains. Evidence exists of public distrust of long-term usage of aspartame, a synthetic sweetener that has been on the market since 1981. Several non-clinical reports found on the Internet claim adverse long-term reactions to aspartame. Further literature research will need to be done in order to compare results from studies prior to 1989 with more recent long-term aspartame toxicity studies. Sucralose appears to be at the stage similar to where aspartame was in 1989. Public concern found in layperson Internet reports revolves around concern for long-term sucralose usage, despite clinical study findings that report no long-term adverse effects. The public is concerned that sucralose will prove to have long-term toxicity, as aspartame is now thought to do, according to personal testimonies from Internet publications. 

Substituting three chlorine ions for hydroxyl groups on an ordinary sucrose molecule makes Sucralose. Developers found that selective halogenations changed the perceived sweetness of a sucrose molecule, with chlorine and bromine being the most effective. Chlorine, as a lighter halogen, retains higher water solubility, so chlorine was picked as the ideal halogen for substitution. 

According to Dr. L. A. Goldsmith, Vice President, Product Safety and Regulatory Affairs, McNeil Specialty Products Company (the producing company of Splenda sucralose), 

The safety review of a new food additive is, in theory, a straightforward process.  Regulatory agencies will usually permit the use of a food additive when a predefined series of rigorous studies have shown no adverse effects at doses at least 100 times the anticipated level of human consumption in appropriate animal models. (2000)

Expected human daily intake is at a level of 1.1 mg/kg/day. In reality, the process is much more complicated. 

The sponsoring companies must first determine for themselves if the product is safe. This process often involves numerous outside experts, as it did with sucralose. Once that internal decision has been reached a comprehensive food additive petition, often tens of thousands of pages in length, is finalized. Usually the petition is submitted to numerous regulatory agencies for simultaneous review. 

Sucralose was approved in Canada in 1991 and is now approved in more than 40 countries, including the United States, which was granted FDA approval in April 1998.

A PubMed search was completed for keywords “aspartame, sucralose, aspartame toxicity, sucralose toxicity, aspartame, sucralose, and aspartame safety.” Articles from 1975 to 2000 were found.

Introduction

            According to the United States-based Calorie Control Council, 101 million Americans in the early 1990s were consumers of low-calorie foods and beverages” (Knight, 1994). Low- and no-calorie sweeteners have been developed to meet this demand since the discovery of saccharin in 1857. As public and food industry demand for low- and no calorie sweeteners grew, an increasing number of such products were and are being developed. 

            The most common of these products are saccharin, cyclamates, and aspartame. Canada banned saccharin in 1977 after discovering the product to be potentially oncogenic. A Food and Drug Administration (FDA) ban on saccharin in the United Sates was never enacted, due to a Congressional moratorium (Knight 1994). Similarly, both the United States and Canada banned cyclamates, due to the discovery of their carcinogenic properties. 

            Aspartame is still clinically considered to be safe, with the exception of minor side effects after prolonged dosage, such as headaches in some subjects (The Healing Arts Online Newsletter, 2001). Testimonials implicating long-term aspartame intake as the cause of conditions ranging from migraine headaches, epilepsy, bi-polar disorder, fibromyalgia, to chronic fatigue syndrome exist, yet clinical trials consistently verify aspartame’s safety after both short-term and long-term usage. Despite such consumer claims of aspartame toxicity, aspartame is commonly known within the food industry to have its downfalls. Aspartame lacks both high-temperature processing stability and a long shelf life under acidic conditions. Due to the inadequacies of previously developed artificial sweeteners, the demand for a non-toxic and highly stable synthetic sweetener came to the attention of the Tate & Lyle sweetener company in London.

            In the 1960s, Tate & Lyle Sweeteners Division, a division of the Tate & Lyle Company, was investigating the use of sugar in nontraditional areas. As part of this initiative, a 1989 collaborative study was undertaken at Queen Elizabeth College, University of London (Knight, 1994), which resulted in the 1989 discovery of a compound that was eventually called sucralose. Sucralose was the first non-calorie sweetener made from sugar, or natural sucrose.

Sucralose may have the strangest “accidental discovery” story of all the sweeteners. Tate & Lyle, a British sugar company, was looking for ways to use sucrose as a chemical intermediate. In collaboration with Prof. Leslie Hough’s laboratory at King’s College in London, halogenated sugars were being synthesized and tested. A foreign graduate student, Shashikant Phadnis, responded to “testing” of a chlorinated sugar as a request for “tasting,” leading to the discovery that many chlorinated sugars are sweet with potencies some hundreds or thousands of times as great as sucrose. (Walters, 2000)

            Compared to sucrose, sucralose has three key molecular differences that make it similar in structure, yet different in metabolism and function. These three differences are chlorine. Three chlorine atoms, in the form of chloride ions, replace three hydroxyl groups in native sucralose. The Tate & Lyle collaborative study was designed to investigate the sweetness functionality of sucrose derivatives, specifically those substituted with halogens. The study found that selective halogenations changed the perceived sweetness of the molecule. Derivatives substituted with the lighter halogens (i.e., chlorine, fluorine) retained a high water solubility, but fluorine, as well as being difficult to handle, had less effect than chlorine on sweetening power. It was determined that the tightly bound chlorine atoms created a stable molecular structure, approximately 600 times sweeter than sugar. 

            This drastically increased sweetness is due to the structure of the sucralose molecule. According to Deutsch and Hansch, the generation of a sweet taste comes from the hydrophobic bonding from one area on a molecule with electronic bonding from another area (Knight, 1994). Highly intense sweeteners are more hydrophobic and thus give rise to increased absorption to the taste buds, in contrast to more hydrophilic simple sugars. Two hydrophobic binding sites necessary for a sweet taste were denoted A and B. Although this mechanism was true for all sweet compounds, many other compounds filled these structure requirements, yet did not have the characteristic of a sweet taste. A later study conducted by Kier in 1972 recognized the influence of a third site, which was hydrophobic and bound the sweet compound to the receptor site (Knight, 1994; Lichtenthaler & Immel, 1993). This third site was denoted X.

            In the case of sucralose, the two chlorine atoms present in the fructose portion of the molecule comprise the hydrophobic X-site, which extends over the entire outer region of the fructose portion of the sucralose molecule. The hydrophobic and hydrophilic regions are situated on opposite ends of the molecule, similar to sucralose, apparently unaffected by the third chlorine on the C4 of the pyranose ring (Knight, 1994). The similar structure of sucralose to native sucrose is responsible for its remarkably similar taste to sugar. 

            Interestingly, according to the producers of Splenda, Wiet and Miller made an opposing assessment of taste (1997). At a sucrose equivalency of 8%, in a buffered system, sucralose was perceived as being primarily sweet with slight drying and sour characteristics as compared to sucrose. At a 12% sucrose equivalency, sucralose was again perceived to deliver some drying and sour attributes, with a very slight rubbery taste. Such differences in taste assessment indicate that an individual may find sucralose taste to resemble native sucrose, yet not be an exact match.

            Sucralose was originally approved in Canada on September 5, 1991. The United States FDA followed suit and granted approval on April 1, 1998 for sucralose applications in 15 food and beverage categories. In 1999, FDA approval expanded to classify sucralose as a “general purpose sweetener,” which removed the limitations of allowing sucralose only in the before mentioned 15 food and beverage categories. The compound is currently approved for use in over 23 countries, in addition to Canada and the United States. Johnson & Johnson purchased the rights to develop sucralose as a commercially available product, and then created an individual company to be retained within Johnson & Johnson, for the exclusive purpose of developing their sucralose product. McNeil Specialty Products now produces a commercially available sucralose product under the trade name Splenda. In the next sections, this paper will explore the topic of sucralose efficacy, regulation, metabolism, toxicity, pharmacokinetics, and stability. 

Animal and Clinical Studies

            Despite FDA approval after extensive clinical trials indicating sucralose safety, consumer concern remains high about long-term dosage safety, as a result of pre-existing concerns regarding long-term consumption of other synthetic sweeteners. Saccharin, cyclamates, and aspartame were granted FDA approval and reached the market, only to later be implicated as having carcinogenic, toxic, or minor side effects. Naturally, consumers of artificial sweeteners would have concern for the safety of a newly developed product. However, the extensive clinical trials that led to FDA approval verify sucralose safety both after short-term and long-term product intake. 

            The producers of commercial sucralose at McNeil Specialty claim the results of safety evaluation studies conducted on sucralose have shown it to be a remarkably safe and inert ingredient (McNeil Specialty). Goldsmith and Grice (2000) noted that over 100 studies showed no signs of carcinogenicity, reproductive toxicology, neurotoxicology, or genetic toxicology as a result of sucralose administration over all clinical study parameters. 

Toxicity

            Results from over 100 animal and clinical studies included in this FDA approval process unanimously indicated a lack of risk associated with sucralose intake. Acceptable human intakes across all populations have been pinpointed, as noted by Baird, Shephard, Merritt, and Hildick-Smith (2000). The estimated daily intake (EDI) for humans is 1.1mg/kg/day. The intakes acceptable daily intake (ADI) is 16 mg/kg/day. The highest no adverse effects limit (HNEL) is 1500 mg/kg/day (Baird et al., 2000).

            Sucralose administration to Sprague-Dawley and COBS CD (SD) BR rats, mice, beagle dogs, monkeys, and eventually humans showed no signs of toxicity, carcinogenicity, or other side effects. Studies ranged from single dose administration to eating trials of over two years. Common methods of administration included oral, gavage, and IV intakes. No adverse reactions were observed at intakes up to 16,000 mg/kg/day in mice or 10,000 mg/kg/day in rats—a dosage equivalent to 1,000 pounds of sucrose administered in a single day to a 165-pound adult (Goldsmith, 2000). 

            Clinical studies that monitored for chronic toxicity equally resulted in a lack of adverse effects (Goldsmith, 2000). Acute oral sucralose-in-water dosing of male and female COBS CD (SD) BR rats (n=30 per sucralose concentration) and ICI Alderly Park mice (n-10 male, 10 female) resulted in no toxicological effects at four and eight weeks, except for a decrease in food consumption for rats dosed at 5% dietary sucralose due to decreased palatiblity. Decreased palatability was exclusively observed across several studies involving high-level sucralose administration to rats. In a related study, 

Toxicologist Judith] Bellin reviewed studies on rats starved under experimental conditions, and concluded that their growth rate could be reduced by as much as a third without the thymus losing a significant amount of weight (less than 7 percent). The changes were much more marked in rats fed on sucralose. While the animals’ growth rate was reduced by between 7 and 20 percent, their thymuses shrank by as much as 40 percent. (Mercola, 1997)

Such negative animal study results were found to not apply to human sucralose consumption, as decreased palatability was found across several studies to only occur in rats. Decreased palatability led to decreased thymus weight only in rats. 

            A continuation of this Goldsmith study showed no chronic toxicity in beagle dogs (n=4 male, 4 female) over the course of 52 weeks. Comprehensive hematological parameters for toxicity indications included packed cell volume, hematoglobin, mean cell hemoglobin concentration, red blood cell count, mean corpuscular volume, reticulocytes, white blood cell count, alkaline phosphatase level and activity, platlets, prothrombin activity time, alanine amintotransferase, aspartate aminotransferase activity, urea, gluclose, total bilirubin, cholesterol, etc. Baird and colleagues (2000) demonstrated a lack of adverse effects from frequent or long-term sucralose administration at levels exceeding the maximum expected intake level of 1.1 mg/kg/day in two additional studies involving human subjects. 

            Animal studies indicated a lack of neurotoxic effects as a result of sucralose intake (McNeil Specialty). “No morphological or functional signs of neurotoxicity were seen in any study conducted. Additionally, neither light nor electron system tissues revealed any abnormalities. There was no evidence of clinical or pathological neurotoxicity.” Results of a neurotoxicity study performed by Finn and Lord (2000) of sucralose and its two constituent chlorinated monosaccharide hydrolysis products, 1,6-DCG and 4-CG, were compared for their neurotoxicity with a known non-sucralose monosaccharide called 6-CG. 6-CG previously was discovered to have neurotoxic effects in animal studies, as noted by Finn and Lord. Mice (n=30 male, 30 female) and Marmoset monkeys (n=12 male) were treated with sucralose, 1,6-DCG, 4-CG, and 6-CG by gavage at various single dose experiment rations and at various individual concentrations. Evaluation by clinical pathology, light microscopy, and electron microscopy showed an absence of neurotoxicity with sucralose or sucralose hydrolysis product administration, when compared with the 6-CG control.

            In addition to no sub chronic or chronic toxicological findings, sucralose was found to have no human genetic toxicity. “The potential for sucralose to induce heritable gene mutations was investigated in numerous studies on bacterial and mammalian cells and in whole animals. The results of these studies indicate[d] that mutagenicty is not a concern” (McNeil Specialty). According to the producers of Splenda, a two-generation rat reproduction study found no evidence of effects from sucralose on male or female mating performance. No effects on reproductive capability were found. “Similarly, there were no observed effects on gestation, litter size, or viability of progeny, even at maximum dietary concentrations” (McNeil Specialty). Gross, visceral, and skeletal examinations of sacrificed rat progeny showed that sucralose did not affect fetal development. 

Carcinogenicity

             Two studies performed by the producers of Splenda demonstrated the lack of toxic or carcinogenic effects due to sucralose product intake. In the first study, CD-1 mice (n=52 male, 52 female) received 0.3%, 1.0%, or 3.0% oral sucralose over 104 weeks. No effects upon survival or carcinogenicity were found. Sucralose administration resulted in no effect upon tumor frequency or type in comparison with controls. Sucralose was determined to not be carcinogenic in CD-1 mice at the maximum tolerated dose of 3% (Mann et al., 2000a).

            In the second study, Sprague-Dawley rats were exposed to dietary sucralose concentrations both in utero and up to 104 weeks after parturition (Mann et al. 2000b). Gavage study toxicity results (n=30 male, 30 female) and carcinogenicity results (n=50 male, 50 female) indicated no effects at dietary concentrations ranging from 0.3% - 3%, compared with the human sucralose highest-no-adverse-effect level of 1,500 mg/kg/day, estimated daily intake of 1.1 m g/kg/day, and acceptable daily intake of 15 mg/kg/day (Baird et al., 2000). A decrease in body weight was noted at 5%. (This decrease was attributed to decreased food consumption due to decreased palatability. Decreased consumption due to suspect decreased palatability was noted across multiple studies exclusively involving rats.) No difference in tumor type or frequency was found between experimental and control groups. There were no ophthalmologic changes found due to sucralose administration. All experimental groups had a decrease in blood glucose level. Sucralose did not adversely affect reproductive or developmental parameters and showed no toxic or carcinogenic effects. 

Teratogenicity

            Teratogenic potential of sucralose was studied in rats and rabbits during fetal organogenesis (Kille et al. 2000). McNeil Specialty research previously indicated the possibility that small amounts of sucralose could not cross the human placenta. The effects of this sucralose movement on fetal development were still unknown. Groups of 20 mated rats of 6 - 15 says of gestation and groups of 16 - 18 artificially inseminated rabbits were administered various experimental sucralose concentrations by gavage. Control animals received only the vehicle of administration. At 21 days of gestation, no anomalies related to sucralose were observed in the dams. Fetal and placental weights were comparable to those of the control. Pregnant female rats showed signs of gastrointestinal distress, due to undigested sucralose . No adverse affects were observed in the fetuses. The progress of pregnancy and fetal development in rats and mice were unaffected by sucralose up to levels exceeding maternally tolerant levels. 

Pharmacokinetics

        According to commercial sucralose promotional materials, results from numerous studies following sucralose pharmacokinetics confirmed that in humans, approximately 85% of ingested sucralose was excreted after intake and approximately 15% was absorbed. Studies with radiolabelled sucralose in rats, dogs, and humans have shown that sucralose was passively absorbed through the small intestine in limited amounts. Mean absorption in humans was approximately 15% of the ingested dose. The remainder of the ingested sucralose passed through the digestive system unchanged and was excreted in the feces, with no resulting gastro-intestinal effects. Of the small portion of the initial dose that was absorbed, most was eliminated unchanged via urine, with the majority being excreted within 24 hours after dosage. Total elimination was virtually complete within a few days (McNeil Specialty). Results from rat studies demonstrated that metabolic handling of sucralose was not altered over the course of long-term dosage when compared with short-term dosage. Results from human and animal studies showed that no bioaccumulation was found. 

            “The relatively small amount of sucralose that is absorbed is distributed to essentially all tissues. There is not active transport of sucralose across the blood-brain barrier to the central nervous system, across the placental barrier, or from the mammary gland into milk” (McNeil Specialty). “Although passive movement of sucralose across the placenta does occur, studies using radiolabelled sucralose in pregnant animals have shown that the levels of sucralose found in the placenta and fetus do not exceed those found in the maternal blood” (McNeil Specialty). The equimolar concentrations of labeled sucralose do not accumulate in the developing fetus. The consistency of studies indicating a lack of sucralose toxicity indicates that even if fetal accumulation were found, no toxicity would result.

            Doses of radioactive 14C-sucralose by IV and by oral gavage were administered to beagle dogs (n=2 male, 2 female) to study sucralose pharmacokinetics and metabolism (Wood, John, & Hawkins, 2000). Plasma, urine, and fecal samples were collected and monitored for radioactivity. Beagle urine samples were compared with samples from human males given a single oral dose of 14C-sucralose. Unchanged sucralose was the major component after either oral or IV administration. Significant small amount (2-8% of oral dose) of sucralose urinary metabolite glucuronic acid was detected by mass spectrometry. Glucuronic acid metabolite was resistant to hydrolysis. IV administration to dogs resulted mainly in urinary excretion. Oral gavage in dogs resulted mainly in fecal excretion. Fecal excretion accounted for a mean of 65.9% of dose during the first 24 hours, increasing to 68.4% after five days. Urinary excretion accounted for means of 13.8%, 22.3%, and 26.5% or oral dose after 6, 12, and 24 hours post dosing, respectively, increasing to 27.6% after five days. Over the course of five days, the mean total of urinary excretion, fecal excretion, and cage washings was 97.6%. The minor metabolite in human urine, glucuronic acid conjugate of sucralose, was co-chromatographed against one of the two minor radioactive components isolated from experimental beagle dog samples, relating this study to sucralose pharmacokinetics and metabolism in man. 

            Another classic example of a sucralose pharmacokinetics and metabolism animal study was a John et al. (2000a) study. Doses of radioactive 14C-sucralose (20 mg/kg body weight) by tail injection and by oral gavage in isotonic saline were administered to CD-1 mice. Isotonic saline IV sucralose solution was administered via tail injection (5ul/g body weight) (n=4 male, 4 female). Isotonic saline solution (20ul/g body weight) was administered by gavage to three groups of rats: 100 mg/kg body weight (n=4 male, 4 female), 1,500 mg/kg body weight (n=2 male, 2 female), and 3,000 mg/kg-body weight (n=2 male, 2 female). Reactivity in all samples was measured by liquid scintillation analysis. Urine and fecal samples were collected and monitored for radioactivity. The 20 mg/kg IV dose was rapidly excreted, primarily via urine at 80% after five days. The 100, 1,500, and 3,000 mg/kg oral doses resulted in urinary excretions of 23%, 15%, and 16%, respectively, after five days. Comparisons with the IV dose experimental results indicated that 20 - 30% of the oral dose was absorbed. Chromatographic urine sample analysis showed that unchanged sucralose was the main excretory form of sucralose in all samples. The minor metabolite in human urine, glucuronic acid conjugate of sucralose (originally identified in the dog) was co-chromatographed against one of the two minor radioactive components found in experimental urine samples. The other minor metabolite was hypothesized to be another glucuronide conjugate. These results indicated that the metabolism of orally dosed sucralose in the mouse is similar to the metabolism of orally dosed sucralose in humans.

            The purpose of the Roberts study (2000) was to apply results from previous animal studies and confirm that they hold true for humans. A preliminary and unpublished study of three males showed limited absorption, a peak plasma sucralose concentration after two hours of administration, and the absence of carbon from sucralose sources expelled in CO2. In this, study, highly purified radiolabelled 14C-sucralose was monitored for its metabolic and pharmacokinetic activity within a larger cohort.

            Two sub-studies comprised the Roberts study (2000). The first was an extension of the preliminary study. Healthy males, mean 39 years, 79 kg weight (n=8) received an oral sucralose dose of 1 mg/kg in water. Blood samples were collected in heparinized tubes immediately before dosing and at 19 proceeding intervals. Administration duration was 72 hours. The second sub-study (n=2 out of the original 8 subjects with higher than average 14C-sucralose excretion) involved an oral dose of 10 mg/kg body weight. Urine samples from subjects involved with both studies were collected prior to dosing and sequentially thereafter for a duration of 120 hours. Fecal material was collected for 120 hours. Concentration of radioactivity was monitored in all biological samples. Controls received non-radioactive sucralose. 

            Results from both studies indicated that radioactivity was mainly excreted in the feces over five days, with a mean recovery of 78.3% of the oral dose. Urinary excretion for low dose varied between 8.9 and 11.2%. The sum excretion by urine and feces over five days averaged 92.8%. Results indicated that essentially all recovered sucralose was excreted through the feces and confirmed the lack of sucralose accumulation within the body. 

            Animal studies have demonstrated that sucralose is not toxic or teratogenic, has virtually no effect on metabolism, and is rapidly eliminated from the body. A clinical study by John and colleagues (2000b) showed that being in the state of pregnancy does not alter sucralose pharmacokinetics or metabolism. Pregnant (n=3) and non-pregnant (n=3) New Zealand White rabbits were given a single oral 10 mg 14C-sucralose/kg dose by syringe in 15 - 20 ml distilled water. Radioactivity was measured by liquid scintillation analysis. Non-pregnant urinary excretion was 8% and fecal excretion was 17% of the oral dose after 24 hours. Urinary excretion increased to 22.3% and fecal excretion increased to 54.7% after five days. Pregnant urinary excretion was 9% and fecal excretion was 28% of the oral dose after 24 hours. Urinary excretion increated to 21.5% and fecal excretion increased to 65.2% after five days. Remaining 14C-sucralose was found in biliary excretion and in the enterhepatic circulation. These results indicate that pregnancy does not significantly influence sucralose pharmacokinetcs. 

Special Populations

        Although sucralose is derived from sucrose, the body does not recognize it as a carbohydrate, as it would for native sucrose. “Sucralose does not effect normal carbohydrate metabolism, including insulin secretion and glucose and fructose absorption” (McNeil Specialty). Sucralose is therefore suitable for consumption by the diabetic population.

            In a study performed by Mezitis, Maggio, Kock, Auddoos, Allison, & Pi-Sunyer (1996), the short-term glucose homeostatic effects of a single 1,000 mg sucralose (versus cellulose placebo) oral dose upon 13 insulin dependent diabetes mellitus (IDDM) and 13 non-insulin dependent diabetes mellitus (NIDDM) human subjects were observed. All subjects had initial blood glucose levels within normal ranges. The average sucralose dose was 13.8 mg/kg for IDDM subjects and 10.5 mg/kg for NIDDM subject. All doses were in excess of the estimated daily sucralose intake at the 90th percentile (2.3 mg/kg). Results indicated that sucralose had no short-term adverse effects on blood glucose control in both IDDM and NIDDM diabetics. Similarly, sucralose contains no phenylalanine or other amino acids. Unlike aspartame, sucralose poses no risk to phenylketonuria patients. 

            Despite indications of comprehensive sucralose safety, as indicated by animal and clinical trials, skepticism in regards to safety persists, especially in regards to diabetics. According to Dr. Joseph Mercola of the Optimal Wellness Center in Schaumburg, Illinois, few human studies of safety have been published on sucralose (Mercola, 1997). Mercola noted that one small study on diabetic patients using the sucralose “showed a statistically significant increase in glycosylated hemoglobin (Hba1C), which is a marker of long-term blood glucose levels and is used to assess glycemic control in diabetic patients. According to the FDA, “increases in glycosylation in hemoglobin imply lessening of control of diabetes.” Further study on sucralose in relation to diabetics will provide a more complete safety assessment in the future. Since sucralose has a high level of heat, acid, and long-term storage stability, its incorporation into many food and beverage products has the potential to make such products safely available to the diabetic community for the first time.  

            In addition to the general recognition of sucralose safety for diabetics and phenylkenonuria patients, this product was also found to be safe for children and pregnant women. “For example, a 20 pound child would have to drink more than 450, 12 ounce SPLENDA sweetened soft drinks every day to exceed the very high amount of SPLENDA shown to be harmless in animal studies (McNeil Specialty). Children should not be fed calorie-restricted diets for proper growth and development, however, so no- and low-calorie diets are not recommended for this segment of the population. Although sucralose is safe for children, it is not recommended in their diet for this reason. 

Industrial Applications

        Hallmark traits of sucralose are its safety, its almost identical taste to native sucrose, and its stability both in processing and in storage. The limited use of previously developed low-calorie sweeteners in commercial products is due primarily to the instability of aspartame both at high temperatures and over time, and the taste limitations of saccharin and acesulfame-K (McNeil Specialty). In contrast, foods made with Splenda maintain their sweetness during cooking and in storage for long periods.  

Processing

            The purpose of a Barndt and Jackson (1990) sucralose processing study was to demonstrate sucralose stability in a variety of common baked goods. Yellow cake, cookies, and graham crackers were selected because they represent a common cross section of common ingredients and typical process conditions used in the baking industry. The use of 14C-sucralose minimized difficulties and possibly error associated with the recovery and detection of low sucralose levels in the presence of other carbohydrates commonly found in baked goods. For each baked product, no TLC peaks other than sucralose would be detected. Aqueous/methanolic extracts of baked products indicated a 100% sucralose recovery. Complete recovery of 14C-sucralose in each food product after baking indicated that sucralose did not interact with ingredients and that the compound remained stable under baking conditions. 

Storage - Time

            Results of a study of carbonated cola at pH 3.1, sweetened with either Splenda or aspartame showed that after one year of storage at 73F, 99% of the Splenda remained unchanged compared to 29% of the aspartame (McNeil Specialty). The effect of storage on the flavor of cola drinks sweetened with sugar (control), sucralose, aspartame, and an aspartame/acesulfame-K blend was studied over a period of 6 months in 20 degrees C storage at pH 3 (Quinlan et al. 1999). Sucralose stability and flavor retention were of particular focus.  An expert sensory panel confirmed each sweetener system at study initiation to be of equal sweetness and comparable in flavor. Sucralose cola retained initial flavor, except for a slight increase in metallic flavor, and sweetness intensity over the duration of 6 months. In comparison, both other experimental sweetener systems decreased in sweetness intensity and increased in bitterness. Sucralose cola retained cola flavor over 6 months. Aspartame and aspartame/acesulfame-K blend colas decreased in cola flavor. Control sugar cola retained initial flavor and sweetness. Sucralose was found to consistently deliver a sugar-like taste, retain food system flavor, retain sweetness, and remain stable over 6 months.

            According to McNeil Specialty promotional materials, stability studies of other Splenda sweetened foods, including canned fruit chocolate syrup, and jams and jellies, have shown that aqueous based products retain their sweetness level and high quality taste over time. “Splenda Brand Sweetener is also stable in dry mix foods and instant powders. For example, no loss of Splenda was found to occur in ice tea, gelatin, or pudding mixes stored for six months at 95F” (McNeil Specialty).

Storage - Temperature

            “Baking studies have shown that Splenda is exceptionally heat-stable. No measurable breakdown of Splenda occurred in any of the baked goods tested” (McNeil Specialty). 100% of the sucralose was recovered from cakes, biscuits, and crackers after baking at typical temperatures of 350F, 410F, and 450F, respectively. 

            Effects of temperature (50 and 6 degrees C), pH (3.0, 4.0, 5.0, 6.0, and 7.0), and nonvalent and divalent cation addition (5 mM Na+, 5mM K+, and 5mM Ca 2+) on sweetness intensity ratings on various sweeteners were studied in a three-part experiment (Schiffman, Sattely-Miller, Grahm, Bennett, Booth, Desai, & Bishay, 2000). A panel trained to identify levels of sweetness tasted all samples (n=9 male, 9 female). Sweetener systems included three sugars (fructose, glucose, sucrose), three terpenoid glycosides (monoammonium glycyrhizinate, rebaudioside-A, stevioside), two dipeptide derivatives (alitame, aspartame), two N-sulfonylamides (acesulfame-K, sodium saccharin), two polyhydric alcohols (mannitol, sorbitol), one dihydrochalcone (neohesperidin dihydrochalcone), one protein (thaumatin), one sulfamate (sodium cyclamate), and one chlorodeoxysugar (sucralose). All compounds were dissolved in deionized water. The main finding from all three study sections was that temperature, pH, and ions had little effect upon perceived sweetness. The only change in taste related to sucralose was a slightly increased noticeable bitterness when KCl was added to the experimental deionized water solution. Addition of KCl slightly increased bitter ratings for acesulfame-K, aspartame, fructose, and sucralose. 

Implications

            Sucralose is a safe non-caloric sweetner derived from native sucrose. Sucralose has no demonstrated adverse effects on special populations within the consuming public, including phenylketonuria patients, diabetics, pregnant women, and children. The close taste to sucrose, high stability in processing, and high storage storage stability render sucralose more desirable in commercial, industrial, and household applications than other common artificial sweeteners. As concluded by Nabors and Gelardi (1991), 

            These characteristics provide the food and beverage industry with a unique opportunity to improve existing low-calorie products and develop totally new low-calorie/reduced-calorie product applications that will meet the ever-growing consumer demand for good tasting, high quality, low-calorie food and beverages. 

References

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Goldsmith, L. A. (2000). Acute and subchronic toxicity of sucralose. Food Chemical Toxicology, 38 (Supplement 2), S53-S69.

Grice, H. C., & Goldsmith, L. A. (2000). Sucralose - an overview of the toxicity data. Food Chemical Toxicology, 38 (Supplement 2), S1-S6.

The Healing Arts Online Newsletter. Wysiwyg://partner.38/http://swiftweb.com/ha/aspartame/html. Viewed 20, February 2001.

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