International Journal of Pediatric Obesity, 2010; 5: 305–312
ISSN Print 1747-7166 ISSN Online 1747-7174 © 2010 Informa UK Ltd. (Informa Healthcare, Taylor & Francis AS)
DOI: 10.3109/17477160903497027
Correspondence: Rebecca J. Brown, Building 10, Room 7C-432A, 9000 Rockville Pike, Bethesda, MD 20892, USA. Fax: 301 402 8573. Email: brownrebecca@
mail.nih.gov
(Received 27 May 2009; accepted 30 October 2009)
REVIEW ARTICLE
Artiﬁcial Sweeteners: A systematic review of metabolic effects in youth
REBECCA J. BROWN, MARY ANN DE BANATE & KRISTINA I. ROTHER
National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
Abstract
Epidemiological data have demonstrated an association between artiﬁcial sweetener use and weight gain. Evidence of a
causal relationship linking artiﬁcial sweetener use to weight gain and other metabolic health effects is limited. However,
recent animal studies provide intriguing information that supports an active metabolic role of artiﬁcial sweeteners. This
systematic review examines the current literature on artiﬁcial sweetener consumption in children and its health effects.
Eighteen studies were identiﬁed. Data from large, epidemiologic studies support the existence of an association between
artiﬁcially-sweetened beverage consumption and weight gain in children. Randomized controlled trials in children are very
limited, and do not clearly demonstrate either beneﬁcial or adverse metabolic effects of artiﬁcial sweeteners. Presently, there
is no strong clinical evidence for causality regarding artiﬁcial sweetener use and metabolic health effects, but it is important
to examine possible contributions of these common food additives to the global rise in pediatric obesity and diabetes.
Key words: Acesulfame-K, artiﬁcial sweetener, aspartame, neotame, obesity, saccharine, sucralose, weight gain
Introduction
Artiﬁcial sweeteners and the obesity epidemic
As a means to help curtail the obesity epidemic,
small dietary changes to prevent weight gain in children
and adolescents have been encouraged (1).
Artiﬁcial sweeteners have gained attention as
dietary tools (2) that provide sweet taste without
the extra energy derived from foods and drinks containing
caloric sugars (3–7), and thus may assist in
weight-loss plan adherence (8). A key question is
whether replacement of sugar-sweetened products
with those containing artiﬁcial sweeteners is truly
beneﬁcial.
Since their FDA approval, artiﬁcial sweeteners
and their beneﬁts on metabolic health have been
questioned (9,10). An association between artiﬁcial
sweetener intake and weight gain was ﬁrst observed
in epidemiological studies with adults. Several largescale
studies, including the National Health and
Nutrition Examination Survey (NHANES) and the
San Antonio Heart Study, have shown a positive
association between artiﬁcial sweetener use and
increases in weight and/or BMI (11–14). Other large,
prospective cohort studies in adults have shown
associations between artiﬁcial sweetener intake and
incidence of the metabolic syndrome and its components,
including waist circumference, blood pressure,
and fasting blood glucose (15–18). Some studies in
adults have demonstrated links between artiﬁcial
sweetener consumption and insulin resistance, incidence
of type 2 diabetes, and poor glucose control
in patients with pre-existing diabetes (19,20), while
others have found no association with diabetes incidence
or glycemia control (21,22).
Beneﬁcial effects of artiﬁcial sweeteners have
been shown in adults, as well. For example, the
Nurses Health Study II found decreased weight
gain among adults who consumed artiﬁcially-sweetened
beverages (23). More importantly, randomized
controlled studies in adults have shown mildly
beneﬁcial results of artiﬁcial sweetener use, including
decreased weight regain after dieting (24),
and weight-stability or minimal short-term weight
loss compared with caloric-sweetener supplementation
(25,26). In response to these conﬂicting data,
several reviews were conducted (27,28). The consensus
in the early 1990s was that artiﬁcial sweeteners
had not been found to increase weight in
humans (29,30).
306 R. J. Brown et al.
Mechanism of action of artiﬁcial sweeteners
Multiple behavioral mechanisms have been proposed
to account for the epidemiologic association
between artiﬁcial sweetener use and weight gain. It
has been suggested that the dissociation of the sensation
of sweet taste from caloric intake may promote
appetite, leading to greater food consumption
and weight gain. In addition, increased consumption
of added caloric sweeteners has been associated
with lower diet quality in children (31), perhaps by
altering taste preferences toward sweetened foods in
place of more healthful foods, such as fruits and
vegetables; this mechanism could apply to artiﬁcial
sweeteners as well.
New data from both humans and animal models
have provided convincing evidence that artiﬁcial
sweeteners play an active role in the gastrointestinal
tract, thus providing a mechanistic explanation for
observed metabolic effects. Sweet-taste receptors,
including the taste receptor T1R family and
α-gustducin, respond not only to caloric sugars, such
as sucrose and glucose, but also to artiﬁcial sweeteners,
including sucralose (Splenda™) and acesulfame-K
(32,33). In both humans and animals, these receptors
have been shown to be present not only in lingual
taste buds, but also in glucagon-like peptide-1 (GLP-1)
secreting L cells of the gut mucosa (34–36), where
they serve as critical mediators of GLP-1 secretion
(36). Mace et al. showed in rat studies that stimulation
of intestinal taste receptors with sucralose led to more
rapid absorption of sugars from the intestine into
the bloodstream (32). We have demonstrated in
young healthy volunteers that consumption of diet
soda before an oral glucose challenge potentiates
GLP-1 secretion, thus potentially altering both gastric
emptying and insulin secretion (62).Translating
these results into the clinical realm, consumption of
an artiﬁcial sweetener in conjunction with a sugarcontaining
food or drink could lead to more rapid
sugar absorption, as well as increased GLP-1 and
insulin secretion, potentially affecting weight, appetite,
and glycemia.
In light of this new information regarding the
metabolic activity of artiﬁcial sweeteners, we have
conducted a systematic review of the effects of artiﬁcial
sweeteners on food intake, weight, and metabolic
health in children.
Commonly used artiﬁcial sweeteners
Currently, the FDA has approved ﬁve artiﬁcial sweeteners
for consumption: acesulfame-K, aspartame,
neotame, saccharin, and sucralose (Table I). In addition,
the FDA has determined that a new sugar
substitute, stevia, is a dietary supplement “generally
recognized as safe” (GRAS). Artiﬁcial sweeteners are
known by several names, which include: low-calorie
sweeteners, high intensity sweeteners, non-sucrose
sweeteners, intense sweeteners, non-nutritive sweeteners,
sugar substitutes, and sugar-free sweeteners
(37). For the purposes of this review, we will use the
term “artiﬁcial sweeteners.”
Artiﬁcial sweetener intake in children
Beverages have been identiﬁed as a major source of
artiﬁcial sweeteners in the diet (38,39), hence estimates
of artiﬁcial sweetener consumption are typically
based on artiﬁcially-sweetened drinks or sodas.
Nationally representative surveys from the 1990s
estimatedthatartiﬁcially-sweetenedsodasaccounted
for approximately 4–18% of total carbonated beverage
intake in children (40,41).Artiﬁcially-sweetened
soft drink consumption appears to be increasing in
children, both with age and over time (40–43).
Methods
Search strategy
Eligible studies were identiﬁed by searching the following
electronic databases: PubMed, Web of Science,
and EMBASE.The following terms were used:
artiﬁcial sweeteners, sweetening agent, sweetener,
sugar substitute, nonnutritive sweetener, intense
sweetener, sucralose, aspartame, saccharin, sugar
free, diabetes, weight, obesity, obese, metabolic syndrome,
cholesterol, and blood pressure. The year of
publication was not restricted. Additional studies
were identiﬁed by manual search of reference lists of
key original and review articles.
Study selection
For inclusion, studies were required to: (a) be published
in peer reviewed journals in the English language,
(b) include pediatric subjects age 0 to 18;
(c) speciﬁcally address artiﬁcial sweetener consumption
in association with metabolic health effects, such
as food intake, weight change, diabetes, and metabolic
syndrome components; and (d) provide original
data. Articles published solely in abstract form
were omitted.
Data extraction
Two authors (RJB and MAdB) independently identiﬁed
potentially relevant articles based on titles and
abstracts. A full text record was retrieved when articles
met eligibility criteria or when reviewers disagreed.
Artiﬁcial sweeteners in youth 307
A third reviewer (KIR) with no involvement in the
initial search process resolved disagreements.
Data extracted from eligible articles included
author, date and duration of study, study design,
characteristics of the participants (sample size, age,
gender), outcome measures and results.
Results
The initial literature search produced 116 potentially
eligible articles. Of these articles, 111 were excluded
as they did not meet requirements. An additional 13
articles were identiﬁed based on a reference list
search of review articles. Our search yielded a total
of 18 human studies, summarized in Table II.
Effects of artiﬁcial sweeteners on food intake in children
Several studies have looked at the effect of caloric
versus artiﬁcial sweetener preloads on subsequent ad
libitum food intake in children. In two experiments,
boys aged 9–14 with a wide range of body mass indices
(BMIs) exhibited complete caloric compensation
in ad libitum lunch intake 30 minutes following a
Table I. FDA-approved artiﬁcial sweeteners.
Chemical Name Trade Names
Sweetness (compared
with sucrose)
Acceptable Daily
Intake (ADI) Structure
Saccharin (C7H5NO3S) Sweet N’ Low 300x 5 mg/kg
S
NH
O
O
O
Aspartame (C14H18N2O5) NutraSweet, Equal 160–220x 50 mg/kg
OCH3
O
N
H
O
NH2
OH
O
Acesulfame-Potassium
(C4H4KNO4S)
Sunett, Sweet & Safe,
Sweet One
200x 15 mg/kg
-HN
S
O
O
K+
O
O
Sucralose (C12H19Cl3O8) Splenda 600x 5 mg/kg
O
Cl
HO
OH
HO
O
Cl
O
HO
OH
Cl
Neotame (C2OH3ON2O5) Made by NutraSweet 7 000–13 000x 0.10 mg/kg
308 R. J. Brown et al.
Table II. Review of pediatric studies on the effects of artiﬁcial sweeteners on weight gain and glucose metabolism.
Study Subjects Age Duration Result
Acute effects on food intake
Anderson et al. (48) 20 healthy children 9–10 years – 6% compensation∗ in ad lib lunch intake 90 min
after aspartame vs. sucrose-sweetened preload.
Bellissimo et al. (45) 14 boys 9–14 years – 94% compensation in ad lib lunch intake 30 min
after sucralose vs. glucose-sweetened preload.
Bellissimo et al. (44) 14 boys 9–14 years – 112% compensation in ad lib lunch intake 30
min after sucralose vs. glucose-sweetened
Kool-Aid preload (only 66% compensation if
watching TV during lunch).
Birch et al. (49) 18 children 3–5 years – 90% compensation in ad lib snack intake 20 min
after aspartame vs. maltodextrin-sweetened
pudding. When subsequently given
intermediate caloric density pudding, children
who previously had aspartame-sweetened
pudding ate 50 kcal more ad lib snack than
those previously given maltodextrin-sweetened
pudding.
Birch et al. (46) 22 children
26 adults
2.5–5 years
25–35 years
– Children showed 109% compensation in ad lib
snack intake 20 min after aspartame vs.
maltodextrin-sweetened pudding, while adults
showed 0% compensation.
Birch et al. (47) 24 children 2–5 years – 60%, 1% and 11% compensation in ad lib snack
intake 0, 30 and 60 min after aspartame vs.
sucrose-sweetened preload. Children reduced
ad lib snack intake 30 min after aspartamesweetened
preload (compared with water), but
not after 0 or 60 minutes.
Interventional studies: randomized controlled trials
Knopp et al. (56) 55 children and young adults 10–21 years 13 wk No signiﬁcant differences in weight loss between
2.7 g/day encapsulated aspartame vs. placebo
Ebbeling et al. (57) 103 children (56♀ 47♂) 13–18 years 25 wk No signiﬁcant difference in BMI between those
in intervention (replacing SSBs with ASBs) vs.
control group except among heaviest subjects
Williams et al. (3) 32 overweight girls 13.2Ϯ1.4 years 12 wk No signiﬁcant difference in BMI between those
permitted sugar-sweetened soda vs. those only
artiﬁcially-sweetened soda
Observational studies: cross-sectional studies
Forshee et al. (52) 3 311 children (1 624♀
1 687♂); USDA CSFII
1994–6, 1998
6–19 years – BMI positively associated with ASB
consumption
Giammattei et al. (53) 385 children (199♀ 186♂) 11–13 years – Higher BMI z-score in those consuming Ն3
servings per day of SSBs and ASBs
O'Connor et al. (54) 1 160 children (581♀ 579♂);
NHANES 1999–2002
2–5 years – No association between ASB consumption and
BMI
Observational studies: prospective cohort studies
Ludwig et al. (55) 548 children (263♀ 285♂);
Planet Health Project
11.7Ϯ0.8 years 2 yr Obesity positively associated with SSB intake
but negatively associated with ASB intake
Berkey et al. (50) 11 654 children (6 636♀
5 067♂); Growing Up
Today study
9–14 years r 3 yr ASB intake associated with weight gain in boys,
but not in girls
Blum et al. (43) 166 (92♀ 74♂) 9.3Ϯ1 years 2 yr Increased ASB intake associated with BMI
z-score at end of study
Striegel-Moore et al. (41) 2 371 girls 9–10 years 10 yr Diet soda intake signiﬁcantly associated with
total daily energy intake
Johnson et al. (51) 1 203 children 5–7 years 9 yr ASB consumption associated with baseline
BMI and fat mass at age 9
Kral et al. (42) 177 children 3–6 years 3 yr No association between ASB consumption and
obesity risk status
∗Compensation after a preload is deﬁned as the difference in subsequent ad libitum caloric intake between two conditions, divided by the
calories in the preload.
BMI: Body mass index; SSB: sugar-sweetened beverage; ASB: artiﬁcially-sweetened beverage; USDA CSFII: United States Department
of Agriculture Continuing Survey of Food Intake by Individuals; NHANES, National Health and Nutrition Examination Survey.
Artiﬁcial sweeteners in youth 309
sucralose versus sugar-sweetened drink, meaning
that they reduced their intake at lunch by the number
of calories contained in the preload (44,45). In
another study, 2.5 to 5-year-old children showed
complete caloric compensation 20 minutes after a
low-calorie, aspartame-sweetened pudding preload
versus high-calorie, maltodextrin-sweetened pudding
(46). Interestingly, adults participating in the same
experiment showed no caloric compensation, meaning
they ate the same number of calories at lunch
regardless of which preload they received.
The timing of artiﬁcial sweetener consumption
with respect to meals may also affect food intake.
Children who consumed sugar-sweetened beverages
immediately prior to a test meal ate less than those
who consumed artiﬁcially-sweetened beverages
before the meal (47). However, no compensation in
meal intake was observed when sugar- versus artiﬁcially-sweetened
beverages were given 30, 60, or 90
minutes prior to the test meal (47,48). In addition,
children reduced ad libitum lunch intake 30 minutes
after an aspartame-sweetened preload (compared
with water), but not after 0 or 60 minutes (47).
These studies, of course, do not describe the
effect of chronic consumption of artiﬁcial sweeteners
on food intake. Birch et al. explored this idea by
giving 3 to 5-year-old children an ad libitum snack
20 minafter either low-calorie (aspartame-sweetened)
or high-calorie (maltodextrin-sweetened) pudding
during multiple trials (49). With each trial, children
consistently showed complete caloric compensation
for the preload. However, when subsequently given
an intermediate caloric density pudding of the same
ﬂavor they had received previously, children who had
eaten low-calorie pudding beforehand ate signiﬁcantly
more snack than those previously given highcalorie
pudding, by approximately 50 kcal.
Observational studies of artiﬁcial sweeteners and weight
gain in children
The majority of pediatric epidemiologic studies have
found a positive correlation between weight gain and
artiﬁcially-sweetened beverage intake. Blum et al.
examined beverage consumption and BMI Z-scores
in 164 elementary school-aged children (43). This
longitudinal study found that increased diet soda
consumption was positively correlated with followup
BMI Z-score after two years. Comparable results
were found by Berkey et al., who examined the relationship
between BMI and diet soda consumption in
over 10 000 children (aged 9 to 14 years) of Nurses’
Health Study II participants over the course of one
year (50). Artiﬁcially-sweetened beverage intake was
signiﬁcantly correlated with weight gain in boys, but
not in girls, during the study period. A long-term
prospective study of 1 203 children in England found
that artiﬁcially-sweetened beverage consumption at
ages 5 and 7 was correlated both with baseline BMI
and fat mass at age 9 (51). Another longitudinal
study of 2 371 girls (aged 9 and 10) participating in
the National Heart,Lung and Blood Institute Growth
and Health Study showed that diet soda consumption
was signiﬁcantly associated with higher daily
caloric intake, but not with BMI (41).A much smaller
study of 177 children aged 3 to 6 years showed no
association between diet soda consumption and risk
of obesity (42).
Several cross-sectional studies in children have
added to the association between artiﬁcially-sweetened
beverage use and adverse health effects.
Forshee et al. analyzed data from the US Department
of Agriculture’s Continuing Survey of Food
Intake by Individuals from 1994–96 and 1998.This
nationally representative sample of US children
between 6 and 19 years of age found that BMI was
positively correlated with diet soda consumption
(52). These results were consistent with Giammattei
et al.’s ﬁndings in 385 sixth and seventh graders,
which showed that both diet and sugar-sweetened
soda intake were positively correlated with BMI
z-score and percent body fat (53). However, a study
of 2 to 5-year-old children using NHANES data
did not show an association between artiﬁciallysweetened
beverage consumption and BMI in this
age group (54).
To date, only one observational study has shown
an inverse association between artiﬁcial sweetener use
and weight gain. In this study of 548 ethnically diverse
school children (mean age 11.7 years) in Massachusetts,
Ludwig et al. found that increased diet soda
consumption over a 19-month time period was associated
with decreased incidence of obesity, whereas
the odds ratio of becoming obese increased 1.6 fold
for each sugar-sweetened drink consumed (55).
Interventional studies of artiﬁcial sweeteners and weight
gain in children
Three small interventional studies that manipulated
artiﬁcial sweetener intake have been conducted in children,
and have failed to show metabolic effects. Shortly
after the approval of aspartame by the FDA, its effects
during active weight reduction and its role in glucoregulatory
hormone changes were studied in 55 overweight
children and young adults, aged 10 to 21,
during a 13-week 1 000 kcal/day diet (56).There were
no differences in weight loss for subjects receiving 2.7
g/day of encapsulated aspartame versus placebo.
A randomized, controlled pilot study of 103 adolescents,
aged 13 to 18 years, examined the effect of
replacing sugar-sweetened drinks with artiﬁcially-
310 R. J. Brown et al.
sweetened beverages or water during a 25-week
period (57). Changes in BMI for intervention versus
control (no replacement of sugar-sweetened drinks)
were not signiﬁcant for the entire group, although an
exploratory post-hoc analysis showed that the intervention
made the greatest difference in the heaviest
subjects, whose BMIs declined by 0.63 Ϯ 0.23 kg/
m2, compared with a 0.12 Ϯ 0.26 kg/m2 gain in the
control group. However, the authors did not separately
report consumption of water versus artiﬁciallysweetened
beverages during the intervention, and
thus the effect of artiﬁcial sweeteners in this study
could not be isolated.
In the third randomized, controlled trial, girls
aged 11 to 15 years consumed a 1500 kcal/day diet
for 12 weeks. In one group, sugar-sweetened soda was
permitted as a snack, while in the other group, only
diet sodas were permitted.There were no differences
between groups for BMI change, and reported intake
of either sugar-sweetened or artiﬁcially-sweetened
soda did not affect BMI change (3).
Artiﬁcial sweeteners and the metabolic syndrome
Components of the metabolic syndrome have been
assessed in two pediatric studies.The previously discussed
study of encapsulated aspartame versus placebo
in young people found no differences in blood
pressure, glucose, or lipid proﬁles between groups
(56). Similarly, in the study in which teenage girls
were permitted either sugar-sweetened or artiﬁciallysweetened
soda as a snack during weight loss, there
were no differences between groups in blood pressure,
waist circumference, or lipid proﬁle (3).
Discussion
Recent epidemiological, clinical and laboratory ﬁndings
question whether recommendations for the use
of artiﬁcial sweeteners are indeed appropriate. A
careful review of this literature by health professionals
including physicians, epidemiologists, and dietitians is
necessary to help consumers make well-informed
decisions about their health. In this review, we have
examined the existing evidence supporting or refuting
a link between artiﬁcial sweetener use and weight
change and other metabolic effects in children.
Epidemiologic studies of artiﬁcial sweetener use
in children have generally shown a positive association
between artiﬁcial sweetener intake (most commonly
as diet soda) and weight gain. In interpreting
such studies, it is critical to consider the conditions
required to support causality in such studies, including
the strength of the association, consistency in
ﬁndings, temporality, biological gradient, plausibility,
coherence between epidemiological and laboratory
ﬁndings, and strength of the dose-response relationship
(58). Based on these criteria, causality is far
from established with regard to artiﬁcial sweetener
use and weight gain in children. It is particularly difﬁcult
to establish causality between artiﬁcial sweetener
consumption, weight gain, and metabolic
abnormalities, as artiﬁcial sweetener intake is likely
to be an indicator for other variables. For example,
the decision to consume artiﬁcial sweeteners is often
made by individuals who are concerned about their
weight in an effort to reduce their caloric intake. In
the case of children, this decision is frequently made
by parents who are concerned about their own weight
and consequently the weight of their offspring, thus
further confounding the choice to use artiﬁcial sweeteners
with genetic and behavioral variables.
Studies of artiﬁcial sweeteners and food intake
demonstrate that caloric compensation is more complete
in children than in adults, in whom food intake
is substantially inﬂuenced by social cues and learned
behaviors. However, even in children the degree of
caloric compensation depends on the timing of the
preload relative to the ad libitum meal, as well as the
age of the child and other experimental circumstances.
Although not all studies agree, the general
trend is that artiﬁcial sweeteners may reduce total
caloric intake when consumed between meals, but
when consumed with meals, children may compensate
for low-calorie snacks or drinks by increasing
meal-associated calories. One study (49) supported
the hypothesis that training children to associate
sweet taste with low caloric density may result in
overeating. Such studies, while not realistically mimicking
actual human behavior, may provide insight
into underlying mechanisms.
The strongest evidence for causation between
artiﬁcial sweetener use and either adverse or beneﬁcial
health effects comes from randomized controlled
trials. The few small, randomized controlled trials
conducted in children did not ﬁnd an association
between artiﬁcial sweetener consumption and weight
change. However, these studies were not speciﬁcally
designed to look for effects of artiﬁcial sweeteners on
weight change, and were presumably underpowered
to ﬁnd such effects. Currently, several trials are in
progress to study the effects of artiﬁcially-sweetened
carbonated soft drinks on body weight and other metabolic
parameters in both children and adults (59,60),
and studies of mechanisms underlying metabolic
effects of artiﬁcial sweeteners are ongoing as well
(61). These studies, and other similar investigations,
will be critical for advancing understanding of the
role of artiﬁcial sweeteners in metabolic health.
At the current time, the jury remains out regarding
a possible role of increased artiﬁcial sweetener use in
the obesity and diabetes epidemics, whether adverse,
Artiﬁcial sweeteners in youth 311
beneﬁcial or neutral. In particular, very little data exist
regarding the role of artiﬁcial sweeteners in glucose
metabolism in children. Our growing understanding
of the active metabolic role played by such chemicals
in animal models should spur further research into the
effects of these common food additives in humans.
Acknowledgements
This work was supported by the intramural research
program of the National Institute of Diabetes, Digestive
and Kidney Diseases.
Declaration of interest: The authors report no
conﬂicts of interest. The authors alone are responsible
for the content and writing of the paper.
References
Rodearmel SJ, Wyatt HR, Stroebele N et al. Small changes1.
in dietary sugar and physical activity as an approach to
preventing excessive weight gain: the America on the Move
family study. Pediatrics. 2007;120(4):e869–79.
Benton D. Can artiﬁcial sweeteners help control body weight2.
and prevent obesity? Nutr Res Rev. 2005;18(1):63–76.
Williams CL, Strobino BA, Brotanek J.Weight control among3.
obese adolescents: A pilot study. Int J Food Sci Nutr. 2007;
58(3):217–30.
Bellisle F, Altenburg de Assis MA, Fieux B et al. Use of4.
‘light’ foods and drinks in French adults: biological, anthropometric
and nutritional correlates. J Hum Nutr Diet.
2001;14(3):191–206.
Husoy T, Mangschou B, Fotland TO et al. Reducing added5.
sugar intake in Norway by replacing sugar sweetened beverages
with beverages containing intense sweeteners - A risk beneﬁt
assessment. Food Chem Toxicol. 2008;46(9): 3099–105.
Guthrie JF, Morton JF. Food sources of added sweeteners6.
in the diets of Americans. J Am Diet Assoc. 2000;100(1):
43–51, quiz 49–50.
Bellisle F, Drewnowski A. Intense sweeteners, energy intake7.
and the control of body weight. Eur J Clin Nutr. 2007;
61(6):691–700.
Morris D, Cuneo P, Stuart M et al. High-intensity sweetener,8.
energy and nutrient intakes of overweight women and men
participating in a weight-loss program. Nutr Res. 1993;13:
123–32.
Friedhoff R, Simon JA, Friedhoff AJ. Sucrose solution vs.9.
no-calorie sweetener vs. water in weight gain. J Am Diet
Assoc. 1971;59(5):485–6.
Blundell JE, Hill AJ. Paradoxical effects of an intense10.
sweetener (aspartame) on appetite. Lancet. 1986;1(8489):
1092–3.
Fowler SP, Williams K, Resendez RG et al. Fueling the11.
obesity epidemic? Artiﬁcially sweetened beverage use and
long-term weight gain. Obesity. 2008;16(8):1894–900.
Stellman SD, Garﬁnkel L. Artiﬁcial sweetener use and one-12.
year weight change among women. Prev Med. 1986;15(2):
195–202.
Colditz GA, Willett WC, Stampfer MJ et al. Patterns of13.
weight change and their relation to diet in a cohort of healthy
women. Am J Clin Nutr. 1990;51(6):1100–5.
Duffey KJ, Popkin BM. Adults with healthier dietary14.
patterns have healthier beverage patterns. J Nutr. 2006;136
(11):2901–7.
Lutsey PL, Steffen LM, Stevens J. Dietary intake and the devel-15.
opment of the metabolic syndrome: the Atherosclerosis Risk in
Communities study. Circulation. 2008;117(6):754–61.
Dhingra R, Sullivan L, Jacques PF et al. Soft drink consump-16.
tion and risk of developing cardiometabolic risk factors and
the metabolic syndrome in middle-aged adults in the community.
Circulation. 2007;116(5):480–8.
Winkelmayer WC, Stampfer MJ, Willett WC et al. Habitual17.
caffeine intake and the risk of hypertension in women. JAMA.
2005;294(18):2330–5.
Nettleton JA, Lutsey PL,WangY et al. Diet soda intake and18.
risk of incident metabolic syndrome and type 2 diabetes in
the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes
Care. 2009;32(4):688–94.
Mackenzie T, Brooks B, O’Connor G. Beverage intake,19.
diabetes, and glucose control of adults in America. Ann
Epidemiol. 2006;16(9):688–91.
McNaughton SA, Mishra GD, Brunner EJ. Dietary patterns,20.
insulin resistance, and incidence of type 2 diabetes in the
Whitehall II study. Diabetes Care. 2008;31(7):1343–8.
Palmer JR, Boggs DA, Krishnan S et al. Sugar-sweetened21.
beverages and incidence of type 2 diabetes mellitus in
African American women. Arch Intern Med. 2008;168
(14):1487–92.
Grotz VL, Henry RR, McGill JB et al. Lack of effect of22.
sucralose on glucose homeostasis in subjects with type
2 diabetes. J Am Diet Assoc. 2003;103(12):1607–12.
Schulze MB, Manson JE, Ludwig DS et al. Sugar-sweetened23.
beverages, weight gain, and incidence of type 2 diabetes in
young and middle-aged women. JAMA. 2004;292(8):
927–34.
Blackburn GL, Kanders BS, Lavin PT et al. The effect of24.
aspartame as part of a multidisciplinary weight-control program
on short- and long-term control of body weight. Am J
Clin Nutr. 1997;65(2):409–18.
Tordoff MG, Alleva AM. Effect of drinking soda sweetened25.
with aspartame or high-fructose corn syrup on food intake
and body weight. Am J Clin Nutr. 1990;51(6):963–9.
Raben A, Vasilaras TH, Moller AC et al. Sucrose compared26.
with artiﬁcial sweeteners: different effects on ad libitum food
intake and body weight after 10 wk of supplementation in
overweight subjects. Am J Clin Nutr. 2002;76(4):721–9.
Drewnowski A. Intense sweeteners and the control of27.
appetite. Nutr Rev. 1995;53(1):1–7.
Blackburn GL. Sweeteners and weight control. World Rev28.
Nutr Diet. 1999;85:77–87.
Rolls BJ. Effects of intense sweeteners on hunger, food29.
intake, and body weight: a review. Am J Clin Nutr. 1991;
53(4):872–8.
Renwick AG. Intense sweeteners, food intake, and the weight30.
of a body of evidence. Physiol Behav. 1994;55(1):139–43.
Libuda L, Alexy U, Buyken AE et al. Consumption of sugar-31.
sweetened beverages and its association with nutrient intakes
and diet quality in German children and adolescents. Br J
Nutr. 2009;101(10):1549–57.
Mace OJ, Afﬂeck J, Patel N et al. Sweet taste receptors in rat32.
small intestine stimulate glucose absorption through apical
GLUT2. J Physiol. 2007;582(Pt 1):379–92.
Nelson G, Hoon MA, Chandrashekar J et al. Mammalian33.
sweet taste receptors. Cell. 2001;106(3):381–90.
Dyer J, Salmon KS, Zibrik L et al. Expression of sweet34.
taste receptors of the T1R family in the intestinal tract and
enteroendocrine cells. Biochem Soc Trans. 2005;33(Pt 1):
302–5.
312 R. J. Brown et al.
Margolskee RF, Dyer J, Kokrashvili Z et al. T1R3 and gust-35.
ducin in gut sense sugars to regulate expression of
Na+-glucose cotransporter 1. Proc Natl Acad Sci USA.
2007; 104(38):15075–80.
Jang HJ, Kokrashvili Z,Theodorakis MJ et al. Gut-expressed36.
gustducin and taste receptors regulate secretion of glucagonlike
peptide-1. Proc Natl Acad Sci USA. 2007;104(38):
15069–74.
Duffy VB, Sigman-Grant M. Position of the American37.
Dietetic Association: use of nutritive and nonnutritive
sweeteners. J Am Diet Assoc. 2004;104(2):255–75.
Morgan KJ, StultsVJ, Zabik ME.Amount and dietary sources38.
of caffeine and saccharin intake by individuals ages 5 to 18
years. Regul Toxicol Pharmacol. 1982;2(4):296–307.
Ilback NG, Alzin M, Jahrl S et al. Estimated intake of the39.
artiﬁcial sweeteners acesulfame-K, aspartame, cyclamate
and saccharin in a group of Swedish diabetics. Food Addit
Contam. 2003;20(2):99–114.
French SA, Lin BH, Guthrie JF. National trends in soft drink40.
consumption among children and adolescents age 6 to 17
years: prevalence, amounts, and sources, 1977/1978 to
1994/1998. J Am Diet Assoc. 2003;103(10):1326–31.
Striegel-Moore RH, Thompson D, Affenito SG et al. Cor-41.
relates of beverage intake in adolescent girls: the National
Heart, Lung, and Blood Institute Growth and Health Study.
J Pediatr. 2006;148(2):183–7.
KralTV, Stunkard AJ, Berkowitz RI et al. Beverage consump-42.
tion patterns of children born at different risk of obesity.
Obesity (Silver Spring). 2008;16(8):1802–8.
Blum JW, Jacobsen DJ, Donnelly JE. Beverage consumption43.
patterns in elementary school aged children across a two-year
period. J Am Coll Nutr. 2005;24(2):93–8.
Bellissimo N, Pencharz PB, Thomas SG et al. Effect of tele-44.
vision viewing at mealtime on food intake after a glucose
preload in boys. Pediatr Res. 2007;61(6):745–9.
Bellissimo N, Thomas SG, Goode RC et al. Effect of45.
short-duration physical activity and ventilation threshold on
subjective appetite and short-term energy intake in boys.
Appetite. 2007;49(3):644–51.
Birch LL, Deysher M. Caloric compensation and sensory46.
speciﬁc satiety: evidence for self regulation of food intake by
young children. Appetite. 1986;7(4):323–31.
Birch LL, McPhee L, Sullivan S. Children’s food intake47.
following drinks sweetened with sucrose or aspartame: time
course effects. Physiol Behav. 1989;45(2):387–95.
Anderson GH, Saravis S, Schacher R et al. Aspartame: effect48.
on lunch-time food intake, appetite and hedonic response in
children. Appetite. 1989;13(2):93–103.
Birch LL, Deysher M. Conditioned and Unconditioned49.
Caloric Compensation: Evidence for Self-Regulation of
Food Intake in Young Children. Learn Motiv. 1985;16:
341–55.
Berkey CS, Rockett HR, Field AE et al. Sugar-added50.
beverages and adolescent weight change. Obes Res. 2004;12
(5):778–88.
Johnson L, Mander AP, Jones LR et al. Is sugar-sweetened51.
beverage consumption associated with increased fatness in
children? Nutrition. 2007;23(7–8):557–63.
Forshee RA, Storey ML. Total beverage consumption and52.
beverage choices among children and adolescents. Int J Food
Sci Nutr. 2003;54(4):297–307.
Giammattei J, Blix G, Marshak HH et al.Television watching53.
and soft drink consumption: associations with obesity in 11to
13-year-old schoolchildren. Arch Pediatr Adolesc Med.
2003;157(9):882–6.
O’Connor TM,Yang SJ, Nicklas TA. Beverage intake among54.
preschool children and its effect on weight status. Pediatrics.
2006;118(4):e1010–8.
Ludwig DS. Relation between consumption of sugar sweet-55.
ened drinks and childhood obesity: a prospective, observational
analysis. Lancet. 2001;357(9255):505–8.
Knopp RH, Brandt K, Arky RA. Effects of aspartame in56.
young persons during weight reduction. J Toxicol Environ
Health. 1976;2(2):417–28.
Ebbeling CB, Feldman HA, Osganian SK et al. Effects of57.
decreasing sugar-sweetened beverage consumption on body
weight in adolescents: a randomized, controlled pilot study.
Pediatrics. 2006;117(3):673–80.
Hill AB. The Environment and Disease: Association or58.
Causation? Proc R Soc Med. 1965;58:295–300.
Richselsen B, Nielsen M. Effect of carbonated soft drinks59.
on the body weight. In: ClinicalTrials.gov [Internet].
Bethesda (MD): National Library of Medicine (US).
2000-[cited 2008 Nov 20] Available from http://clinicaltrials.gov/ct2/show/locn/NCT00777647
NLM Identiﬁer:
NCT00777647.
Antonelli T. Reducing sugar-sweetened beverage consump-60.
tion in overweight adolescents (BASH). In ClinicalTrials.gov
[Internet]. Bethesda (MD): National Library of Medicine
(US). 2000-[cited 2008 Nov 20] Available from http://clinicaltrials.gov/ct2/show/locn/NCT00381160
NLM Identiﬁer:
NCT00381160.
DiSabatino A. Zero calorie drink products. In ClinicalTrials.61.
gov [Internet]. Bethesda (MD): National Library of Medicine
(US) 2000-[cited 2008 Nov 20] Available from http://
clinicaltrials.gov/ct2/show/locn/NCT00525694 NLM Identiﬁer:
NCT00525694.
Brown RJ,Walter M, Rother KI. Ingestion of diet soda before62.
a glucose load augments glucagon-like peptide-1. Diab care.
2009;32(12):2184–6.
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