sucralose

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Sucralose (Splenda)

The comet assay with 8 mouse organs: results with 39 currently
used food additives.
1: Mutat Res. 2002 Aug 26;519(1-2):103-19.Click here to read .PMID:
12160896

Sucralose induces DNA damage in gastrointestinal organs.

Full Citation: "We determined the genotoxicity of 39 chemicals currently in use as food additives. They fell
into six categories-dyes, color fixatives and preservatives, preservatives, antioxidants, fungicides, and
sweeteners. We tested groups of four male ddY mice once orally with each additive at up to 0.5xLD(50) or
the limit dose (2000mg/kg) and performed the comet assay on the glandular stomach, colon, liver, kidney,
urinary bladder, lung, brain, and bone marrow 3 and 24h after treatment. Of all the additives, dyes were
the most genotoxic. Amaranth, Allura Red, New Coccine, Tartrazine, Erythrosine, Phloxine, and Rose
Bengal induced dose-related DNA damage in the glandular stomach, colon, and/or urinary bladder. All
seven dyes induced DNA damage in the gastrointestinal organs at a low dose (10 or 100mg/kg). Among
them, Amaranth, Allura Red, New Coccine, and Tartrazine induced DNA damage in the colon at close to
the acceptable daily intakes (ADIs). Two antioxidants (butylated hydroxyanisole (BHA) and butylated
hydroxytoluene (BHT)), three fungicides (biphenyl, sodium o-phenylphenol, and thiabendazole),
and four sweeteners (sodium cyclamate, saccharin, sodium saccharin, and sucralose) also
induced DNA damage in gastrointestinal organs. Based on these results, we believe that more
extensive assessment of food additives in current use is warranted."

Splenda alters gut microflora and increases intestinal
p-glycoprotein and cytochrome p-450 in male rats.
1: J Toxicol Environ Health A. 2008;71(21):1415-29. .PMID: 12160896

The administration of Splenda (sucralose) to rats at a dose far below the US FDA Acceptable Daily
intake for sucralose exhibited numerous adverse effects in the gastrointesintal tract of male rats.

Full Citation: "Splenda is comprised of the high-potency artificial sweetener sucralose (1.1%) and the
fillers maltodextrin and glucose. Splenda was administered by oral gavage at 100, 300, 500, or 1000
mg/kg to male Sprague-Dawley rats for 12-wk, during which fecal samples were collected weekly for
bacterial analysis and measurement of fecal pH. After 12-wk, half of the animals from each treatment
group were sacrificed to determine the intestinal expression of the membrane efflux transporter
P-glycoprotein (P-gp) and the cytochrome P-450 (CYP) metabolism system by Western blot. The
remaining animals were allowed to recover for an additional 12-wk, and further assessments of fecal
microflora, fecal pH, and expression of P-gp and CYP were determined. At the end of the 12-wk treatment
period, the numbers of total anaerobes, bifidobacteria, lactobacilli, Bacteroides, clostridia, and total
aerobic bacteria were significantly decreased; however, there was no significant treatment effect on
enterobacteria. Splenda also increased fecal pH and enhanced the expression of P-gp by 2.43-fold,
CYP3A4 by 2.51-fold, and CYP2D1 by 3.49-fold. Following the 12-wk recovery period, only the total
anaerobes and bifidobacteria remained significantly depressed, whereas pH values, P-gp, and CYP3A4
and CYP2D1 remained elevated. These changes occurred at Splenda dosages that contained
sucralose at 1.1-11 mg/kg (the US FDA Acceptable Daily Intake for sucralose is 5 mg/kg). Evidence
indicates that a 12-wk administration of Splenda exerted numerous adverse effects, including (1)
reduction in beneficial fecal microflora, (2) increased fecal pH, and (3) enhanced expression levels
of P-gp, CYP3A4, and CYP2D1, which are known to limit the bioavailability of orally administered
drugs."

Popular sweetner sucralose as a migraine trigger.
1: Headache. 2006 Sep;46(8):1303-4. PMID: 16942478

Sucralose may be a migraine trigger.

Full Citation: "Sucralose (trichlorogalactosucrose, or better known as Splenda) is an artificial sweetener
from native sucrose that was approved by the FDA on April 1, 1998 (April Fool's Day). This observation of
a potential causal relationship between sucralose and migraines may be important for physicians to
remember this can be a possible trigger during dietary history taking. Identifying further triggers for
migraine headaches, in this case sucralose, may help alleviate some of the cost burden (through
expensive medical therapy or missed work opportunity) as well as provide relief to migraineurs."

A combined chronic toxicity/carcinogenicity study of sucralose
in Sprague-Dawley rats.
1: Food Chem Toxicol. 2000;38 Suppl 2:S71-89. PMID: 10882819

Sucralose generates adverse changes in rats.

Full Citation: "The chronic toxicity and potential carcinogenicity of sucralose was evaluated by exposing
Sprague-Dawley rats to dietary concentrations of this low-calorie sweetener both in utero and for up to 104
weeks following parturition. The rats assigned to the toxicity phase of this investigation were administered
diets containing either 0% (control), 0.3% (3000 ppm), 1.0% (10,000 ppm) or 3.0% (30,000 ppm)
sucralose. Each treatment group comprised 30 male and 30 female rats, of which 15 males and 15
females were sacrificed after 52 weeks of treatment. The surviving rats were killed following 78 weeks of
sucralose administration. In the carcinogenicity phase of this investigation, groups of 50 male and 50
female rats were administered dietary sucralose at concentrations of 0% (control 1), 0% (control 2), 0.3%,
1.0% or 3.0% for 104 weeks. Evaluation of the data obtained from the two phases of this study showed
that sucralose was not carcinogenic. Sucralose did not adversely affect the survival or clinical condition of
the rats, and there were no toxicologically significant findings. Group mean body weight gain and food
consumption were significantly decreased in a dose-dependent manner in sucralose-treated rats
throughout the treatment period as compared to the controls. The primary effect of sucralose on food
consumption, and secondarily on body weight gain, was established in later studies to be due to the fact
that diets containing high concentrations of sucralose are unpalatable to rats. These subsequent studies
established that the reduction of body weight gain seen in previous rat studies using sucralose in the diet
at concentrations of 1% and below resulted from reduced food intake as a direct consequence of the
unpalatable nature of sucralose. Similarly, at concentrations of 3% in the diet, it was shown that
approximately 95% of the effect on body weight gain could be attributed to the reduction in food intake due
to the reduced palatability of the diet, the remainder apparently due to a physiologic response to the high
concentrations of non-digestible sucralose in the rats' diet. Complete toxicological evaluations of gavage
studies with histopathological evaluations demonstrated that even at the 3% dietary level, toxicity was not
responsible for the small body weight gain decrement. Gross and histopathologic examinations revealed
that the administration of sucralose affected neither the types nor incidence of the tumours observed. The
incidences of some non-neoplastic findings were statistically significantly increased in the
sucralose treated groups relative to the controls. These included: renal pelvic epithelial hyperplasia
in all female treatment groups, renal pelvic mineralization in females administered the intermediate
or highest dietary concentrations of sucralose, adrenal cortical haemorrhagic degeneration in
high-dose group female rats, and the histopathologic incidence of cataracts at necropsy in
high-dose group male rats. The non-neoplastic findings that occurred were of no toxicological
significance since they were either spontaneous findings commonly observed in aged rats of this strain or
the physiological response to high dietary levels of a poorly absorbed compound.."

Acute and subchronic toxicity of sucralose.
1: Food Chem Toxicol. 2000;38 Suppl 2:S53-69. PMID: 10882818

Sucralose reduces the weight of spleen and thymus in rats.

Full Citation: "The toxicity of sucralose has been evaluated in acute and subchronic toxicity studies.
Acute oral toxicity studies in male and female mice and male rats documented no deaths or
treatment-related signs at doses of 16g/kg for mice and 10g/kg for rats. Sucralose was administered to
male and female rats for 4 and 8 weeks at dietary concentrations of 1.0, 2.5 or 5.0%. Achieved dose
ranges (mg/kg/day) for the respective dietary levels were 737-1287, 1865-3218 and 2794-6406. There
were no toxicologically significant effects observed at the 1.0% or 2.5% dietary levels. However,
decreases in food consumption, body weight gain and selected organ weights and ratios as well as
splenic and thymic histopathologic changes occurred in rats administered 5.0% for 4 or 8 weeks. A
gavage study wherein doses of 0, 750, 1500 or 3000mg/kg/day were administered to male and female rats
for 26 weeks investigated further the observations from the dietary study as well as general subchronic
toxicity. The gavage study documented no sucralose-related toxicity. These results implicate the reduced
palatability and digestibility of diets containing high concentrations of sucralose seen in the diet study as
the cause for the decreased food consumption and other accompanying alterations. Dose selection for
chronic toxicity studies in rats took into consideration the effect of high concentrations of sucralose on
digestion and food consumption and the limitations that would be imposed on subsequent studies. In male
and female dogs, no sucralose-related adverse effects were observed following the dietary administration
of 0.3, 1.0 or 3.0% for 12 months achieving doses of approximately 90, 300 and 900mg/kg/day
respectively. These studies establish that sucralose is non-toxic in rodents following acute oral
administration. The rat no-observed-adverse-effect level ranged between 2.5 and 5.0% following
subchronic dietary administration. A 3.0% dietary concentration equivalent to a dose of 900mg/kg/day
produced no adverse effects in beagle dogs when fed for 12 months."

Renal mineralization--a ubiquitous lesion in chronic rat studies.
1: Food Chem Toxicol. 1990 Jun;28(6):449-55. PMID: 2210518

Sucralose causes bowel enlargement, kidney mineralization and abnormal pelvic tissue changes
in rats.

Full Citation: "Renal mineralization is a commonly encountered lesion in old rats and its presence at times
complicates the interpretation of data derived from chronic rat studies. The feeding of sucralose, a new
and high-intensity sweetener under regulatory review, resulted in caecal enlargement and an
increase in the incidences of renal mineralization and pelvic epithelial hyperplasia. These responses
prompted a review of the literature focusing on the relationships, if any, between the caecal and renal
changes. The literature supports the contention that caecal and renal changes occur frequently in
response to feeding poorly absorbed osmotically active substances to rats. Some possible mechanisms
that may be involved in the development of the renal lesion are discussed."

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