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