Edulcorantes Artificiales en el Tratamiento de la Obesidad: Qué dice

Edulcorantes Artificiales en el Tratamiento
de la Obesidad:
Qué dice la evidencia??
Dra. Catalina Fuentes G
Nutrióloga Hospital Clínico FACh
Clínica las Lilas
Placer por lo dulce, azúcar y obesidad
Edulcorantes artificiales: no tan rápido!
Mecanismos propuestos para el “daño”
Evidencia actual
Conclusiones
El ser humano nace con una fuerte preferencia por
el sabor dulce….
Se estima que..
•  La ingesta promedio de azúcar agregada en USA,
corresponde a un 15.8% de las calorías totales.
•  47% de esas calorías viene dado por bebidas
azucaradas
•  El consumo de este tipo de bebidas aumentó 135%
entre 1977 y 2001
•  Si se agrega a la dieta 1 lata de bebida
azucarada=150 kcal (40-50g azúcar)por día (sin
modificar el resto)------ +6.75 kg/año
Am J Clin Nutr 2006;84:274–88 will reduce the prevalence of obesity
Pro v Con Debate: Role of sugar sweetened beverages in
obesity
obesity-related
diseases
F. B. Hu
Resolved: there is sufficient scientific evidence
that
decreasing sugar-sweetened beverage consumption
will reduce the prevalence of obesity and
obesity-related diseases
1,2
1
Departments of Nutrition and Epidemiology,
Harvard School of Public Health, Boston, MA,
USA; 2Channing Division of Network
Medicine, Department of Medicine, Brigham
and Women’s Hospital, Harvard Medical
School, Boston, MA, USA
F. B. Hu1,2
1
Departments of Nutrition and Epidemiology,
Harvard School of Public Health, Boston, MA,
USA; 2Channing Division of Network
Medicine, Department of Medicine, Brigham
and Women’s Hospital, Harvard Medical
School, Boston, MA, USA
Received 17 March 2013; revised 1 April
2013; accepted 1 April 2013
Address for correspondence: FB Hu,
Department of Nutrition, Harvard School of
Public Health, 665 Huntington Ave, Boston,
MA 02115, USA.
E-mail: frank.hu@channing.harvard.edu
Summary
Received 17 March 2013; revised 1 April
2013; accepted 1 April 2013
Sugar-sweetened beverages (SSBs) are the single largest source of added sugar and
Address
for correspondence:
Hu,
the top source of energy intake in the U.S. diet. In this
review,
we evaluate FB
whether
Department
of
Nutrition,
Harvard
School
there is sufficient scientific evidence that decreasing SSB consumption will reduceof
Public Health, 665 Huntington Ave, Boston,
the prevalence of obesity and its related diseases.
Because prospective cohort
02115, USA.
studies address dietary determinants of long-termMAweight
gain and chronic disE-mail: frank.hu@channing.harvard.edu
eases, whereas randomized clinical trials (RCTs) typically evaluate short-term
effects of specific interventions on weight change, both types of evidence are
critical in evaluating causality. Findings from well-powered prospective cohorts
have consistently shown a significant association, established temporality and
demonstrated a direct dose–response relationship between SSB consumption and
long-term weight gain and risk of type 2 diabetes (T2D). A recently published
meta-analysis of RCTs commissioned by the World Health Organization found
that decreased intake of added sugars significantly reduced body weight (0.80 kg,
95% confidence interval [CI] 0.39–1.21; P < 0.001), whereas increased sugar
intake led to a comparable weight increase (0.75 kg, 0.30–1.19; P = 0.001). A
parallel meta-analysis of cohort studies also found that higher intake of SSBs
among children was associated with 55% (95% CI 32–82%) higher risk of being
overweight or obese compared with those with lower intake. Another metaanalysis of eight prospective cohort studies found that one to two servings per day
of SSB intake was associated with a 26% (95% CI 12–41%) greater risk of
developing T2D compared with occasional intake (less than one serving per
month). Recently, two large RCTs with a high degree of compliance provided
convincing data that reducing consumption of SSBs significantly decreases weight
gain and adiposity in children and adolescents. Taken together, the evidence that
decreasing SSBs will decrease the risk of obesity and related diseases such as T2D
is compelling. Several additional issues warrant further discussion. First, prevention of long-term weight gain through dietary changes such as limiting consumption of SSBs is more important than short-term weight loss in reducing the
Summary
Sugar-sweetened beverages (SSBs) are the s
the top source of energy intake in the U.S. d
there is sufficient scientific evidence that de
the prevalence of obesity and its related
studies address dietary determinants of lo
eases, whereas randomized clinical trials
effects of specific interventions on weigh
critical in evaluating causality. Findings fr
have consistently shown a significant ass
demonstrated a direct dose–response relati
long-term weight gain and risk of type 2
meta-analysis of RCTs commissioned by t
that decreased intake of added sugars signi
95% confidence interval [CI] 0.39–1.21;
intake led to a comparable weight increa
parallel meta-analysis of cohort studies a
among children was associated with 55% (
overweight or obese compared with tho
analysis of eight prospective cohort studies
of SSB intake was associated with a 26%
developing T2D compared with occasion
month). Recently, two large RCTs with a
convincing data that reducing consumption
gain and adiposity in children and adolesc
decreasing SSBs will decrease the risk of ob
is compelling. Several additional issues wa
tion of long-term weight gain through diet
tion of SSBs is more important than sh
prevalence of obesity in the population.
individual becomes obese, it is difficult to l
should consider the totality of evidence r
(e.g. from short-term RCTs only). Finally,
harm on health against SSBs is strong, we
absolute proof before allowing public hea
Keywords: Diabetes, nutrition, obesity, su
obesity reviews (2013) 14, 606–619
Fácil: cambiemos las bebidas por agua!
The negative impact of consuming sugar-sweetened
beverages on weight and other health outcomes has
been increasingly recognized; therefore, many people
have turned to high-intensity sweeteners like aspartame, sucralose, and saccharin as a way to reduce the
risk of these consequences. However, accumulating evidence suggests that frequent consumers of these sugar
substitutes may also be at increased risk of excessive
weight gain, metabolic syndrome, type 2 diabetes, and
cardiovascular disease. This paper discusses these findings and considers the hypothesis that consuming
sweet-tasting but noncaloric or reduced-calorie food
and beverages interferes with learned responses that
normally contribute to glucose and energy homeostasis.
Because of this interference, frequent consumption of
high-intensity sweeteners may have the counterintuitive
effect of inducing metabolic derangements.
body weight, and other related co-morbidities. A secon
goal is to identify and examine the types of physiologic
mechanisms that could underlie such adverse health co
sequences. A third aim is to consider factors that can ma
studies into the effects of artificial sweeteners on ener
and body weight regulation difficult to interpret.
•  Potencial valor de reemplazar la sacarosa de
bebidas y otros alimentos por endulzantes no
calóricos…
Sweeteners and health
Consumption of sugar-sweetened beverages (SSB; see
Glossary) has been increasingly associated with negative
health outcomes such as being overweight, obesity, type 2
diabetes (T2D), and metabolic syndrome, for reviews, see
[1–5]. Based largely on these associations, many researchers and healthcare practitioners have proposed that noncaloric, high-intensity sweeteners provide a beneficial
alternative in foods and beverages [6–10].There is no
doubt that replacing caloric with noncaloric sweeteners
reduces the energy density of foods and beverages. However, whether reducing energy density in this manner
always translates into reduced energy intake, lower body
weight, and improved metabolic health is much less certain. Recent reviews of studies spanning at least the past
40 years have concluded that high-intensity sweeteners
are potentially helpful [11], harmful [12], or have as yet
unclear effects [9,13–15] with regard to regulation of
energy balance or other metabolic consequences. One
purpose of this opinion paper is to summarize and evaluate recent research that is consistent with the rather
counterintuitive claim that consuming high-intensity
sweeteners may promote excess energy intake, increased
Corresponding author: Swithers, S.E. (swithers@purdue.edu).
Keywords: obesity; diabetes; sweeteners.
1043-2760/$ – see front matter
! 2013 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.tem.2013.05.005
Glossary
Artificially sweetened beverages (ASB): also known as ‘diet’ soft drinks
beverages manufactured with one or more high-intensity sweeteners in plac
of energy-yielding sugars like sucrose or high-fructose corn syrup with th
purpose of reducing or eliminating calories.
Body mass index (BMI): used as an index of risk for weight-related healt
outcomes and is calculated as (kg/m2). In adults BMIs of 18.5–24.9 ar
considered to be within the normal range, whereas BMIs from 25 to 29.9 ar
classified as overweight and a BMI greater than 30 is classified as obese.
Hazard ratio (HR) and odds ratio (OR): statistical measures of how often a
event occurs in one group compared to another. A HR or OR of 1 means there i
no difference between the groups and an HR or OR >1 means there is a
increased likelihood that the event will occur in the group of interest relative t
the comparison group.
High-intensity sweeteners: also known as low-calorie sweeteners, artificia
sweeteners, non-nutritive sweeteners, or noncaloric sweeteners are chemical
that produce the perception of sweet taste at very low concentrations. High
intensity sweeteners currently used commonly in foods and beverages includ
sucralose, aspartame, saccharin, and acesulfame potassium, as well as newl
approved extracts from the plant Stevia rebaudiana. Although some high
intensity sweeteners can be metabolized by the body, foods and beverage
typically contain them in such small quantities that even those that can b
metabolized contribute minute amounts of energy to the diet.
Incretin hormones: hormones such as glucagon-like peptide-1 (GLP-1) an
glucose-dependent insulinotropic peptide (GIP) that are released from L cell
and K cells in the intestine, respectively, and serve to enhance the release o
insulin from beta cells, slow the rate of gastric emptying, and may contribute t
satiety.
Metabolic syndrome: a group of factors that occur together and contribute t
increased risk for coronary artery disease, stroke, and type 2 diabetes (T2D
Typical definitions require three or more of the following: blood pressure >130
85 mmHg; fasting blood glucose >100 mg/dl; large waist circumference (me
>102 cm, women >89 cm); low high-density lipoprotein (HDL) cholestero
(men <40 mg/dl; women <50 mg/dl); triglycerides >150 mg/dl.
Post-prandial glucose homeostasis: following meals (post-prandial) levels o
glucose in the blood are tightly regulated by the release of a variety o
hormones that contribute to clearance of glucose. For example, release o
insulin from the beta cells of the pancreas is required to move sugar from th
blood into cells.
Sugar-sweetened beverages (SSB): also known as ‘regular’ soft drinks
manufactured with one or more caloric sweeteners such as sucrose or high
fructose corn syrup.
Thermic effect of food: increase in metabolic rate after consumption of a mea
related to energy required to process and metabolize the consumed food.
Type 2 diabetes: chronic elevation of blood glucose due to insulin resistanc
that is also characterized by impaired incretin secretion.
Trends in Endocrinology and Metabolism, September 2013, Vol. 24, No. 9
4
El valor de los endulzantes para disminuir el
aporte total de calorías es mayor en
productos líquidos
Intense sweeteners, energy intake and the control of body weight
F Bellisle and A Drewnowski
Table 2 Comparison of sugar-reduced and regular foods and drinks
Type of food or drink
Cola drinks
Fruit drinks
Cocoa
Hard candies
Drinking yogurt
Yogurt nonfat
Fruit Pie
Gelatin
Pudding
RTE cereal
Muesli
Cookies
Chocolate syrup
Chocolate
Chewing gum
Regular
Sugar-reduced or sugar-free
CHO content (per 100 g)
Energy content (kcal per 100 g)
CHO content (per 100 g)
Energy content (kcal per 100 g)
10.2
14
10.9
100
12.8
13.8
33.6
13.6
21.2
90
68
33
61
59
120
40
56
50
375
72
75
237
57
131
360
380
445
261
513
500
0
1.9
4.4
93
4.0
4.9
26
0
8.6
90
69
32.5
32.9
49
60
2
11
25
253
42
44
171
8
64
360
344
445
140
510
300
energy density of beverages; the reduction is smaller for
semi-liquid food products, and can be very small for solid
foods. The impact of intense sweeteners on energy intakes
may, therefore, largely depend on the energy density of the
1998b). Typically, preload volume is adjusted by the addition
of water preload and energy is adjusted by the addition of
non-caloric components (intense sweeteners or fat replacements), whereas preload nutrient
composition is determined
European Journal of Clinical Nutrition (2007) 61, 691–700
Placer por lo dulce, azúcar y obesidad
Edulcorantes artificiales: no tan rápido!
Mecanismos propuestos para el “daño”
Evidencia actual
Conclusiones
Key:
SSB
30
150
100
50
0
ASB
SSB
100
80
20
10
60
40
Change in per capita soda
availability since 1962 (litres)
Change in overweight and obesity
prevalence since 1962 (Percent)
ASB
Overweight and obesity
Per capita consump!on
in 2000 (litres)
Aumento de la prevalencia de obesidad y
sobrepeso a pesar de la incorporación de
Opinion
Trends in Endocrinology an
[(Figure_1)TD$IG]
edulcorantes
no calóricos
cross-sectionally, b
study, SSB intake
males only in the
were no increased
body fat percentag
ferences in outcom
Fowler et al. stud
younger subjects, a
However, neither s
sumption was ass
weight gain or incr
Metabolic syndrom
A number of studie
20
ic syndrome for c
cohorts [6,20–22] (
0
0
increase in the risk
1974
1980
1994
2000
Year
consuming ASB ra
TRENDS in Endocrinology & Metabolism
ratios (HRs) and o
(e.g., those consum
Figure 1. Beverage consumption and the prevalence of obesity. Line graph illustrates
Trends in Endocrinology and M
etabolism 013, Vol. 24, Ncom
o. bolic 2syndrome
changes in per capita consumption of artificially
sweetened
beverages
(ASB;
red September Estudios de Cohorte Prospectivos/
observacionales
Dietary Intake and the Development of the
Metabolic Syndrome
The Atherosclerosis Risk in Communities Study
Pamela L. Lutsey, MPH; Lyn M. Steffen, PhD, MPH, RD; June Stevens, PhD, MS, RD
•  “… Diet Soda también se asoció positivamente con la
incidencia de SM. Aquellos en el tercil más alto de
consumo con 34% mayor riesgo que el tercil más bajo. La
fuerza de esta asociación es sorprendente. Sin embargo es
consistente con datos recientes del Estudio Framingham,
que encontró 56% aumento del riesgo de SM entre quienes
consumían una porción de diet soda por día…”
ackground—The role of diet in the origin of metabolic syndrome (MetSyn) is not well understood; thus, we sough
evaluate the relationship between incident MetSyn and dietary intake using prospective data from 9514 participants (a
45 to 64 years) enrolled in the Atherosclerosis Risk in Communities
(ARIC)Intake
study. and the Development o
Dietary
ethods and Results—Dietary intake was assessed at baseline via a 66-item food
frequency Syndrome
questionnaire. We u
Metabolic
principal-components analysis to derive “Western” and “prudent” dietary
patterns from 32Risk
foodingroups
and evalua
The Atherosclerosis
Communities
St
10 food groups used in previous studies of the ARIC cohort.
MetSyn was defined by American Heart Associat
Pamela L. Lutsey, MPH; Lyn M. Steffen, PhD, MPH, RD; June Steven
guidelines. Proportional-hazards regression was used. Over 9 years of follow-up, 3782 incident cases of MetSyn w
Background—The role of diet in the origin of metabolic syndrome (MetSyn) is not well un
identified. After adjustment for demographic factors, smoking,
physical activity, and energy intake, consumption o
evaluate the relationship between incident MetSyn and dietary intake using prospective data
45 to 64with
years) incident
enrolled in the
Atherosclerosis
Riskfurther
in Communities
(ARIC) study.
Western dietary pattern (Ptrend!0.03) was adversely associated
MetSyn.
After
adjustment
for int
Methods and Results—Dietary intake was assessed at baseline via a 66-item food freque
of meat, dairy, fruits and vegetables, refined grains, and whole
grains, analysis
of individual
groups
revealed
principal-components
analysis to derive
“Western” and food
“prudent”
dietary patterns
from 3
10
food
groups
used
in
previous
studies
of
the
ARIC
cohort.
MetSyn
was
defined
meat (Ptrend"0.001), fried foods (Ptrend!0.02), and diet soda (Ptrend!" 0.001) also were adversely associatedbyw
guidelines. Proportional-hazards regression was used. Over 9 years of follow-up, 3782 in
incident MetSyn, whereas dairy consumption (Ptrend!0.006)
was
No associations
were
observed
betw
identified.
Afterbeneficial.
adjustment for demographic
factors, smoking,
physical
activity, and
ene
Western dietary pattern (P !0.03) was adversely associated with incident MetSyn. After
incident MetSyn and a prudent dietary pattern or intakesof of
whole grains, refined grains, fruits and vegetables, n
meat, dairy, fruits and vegetables, refined grains, and whole grains, analysis of individu
meat (P "0.001), fried foods (P !0.02), and diet soda (P !" 0.001) also wer
coffee, or sweetened beverages.
incident MetSyn, whereas dairy consumption (P !0.006) was beneficial. No associat
onclusions—These prospective findings suggest that consumption
ofanda aWestern
dietary
meat,grains,
andrefined
friedgrains
fo
incident MetSyn
prudent dietary
pattern orpattern,
intakes of whole
coffee, orprovides
sweetened beverages.
promotes the incidence of MetSyn, whereas dairy consumption
some protection. The diet soda association w
Conclusions—These prospective findings suggest that consumption of a Western dietary p
not hypothesized and deserves further study. (Circulation.
2008;117:754-761.)
promotes
the incidence of MetSyn, whereas dairy consumption provides some protection. T
trend
trend
trend
trend
trend
not hypothesized and deserves further study. (Circulation. 2008;117:754-761.)
Key Words: dairy products ! diet ! food habits Key
metabolic
syndrome
! meat
Words:!
dairy
products ! diet
! food habitsX! meat ! metabolic s
O R I G I N A L
A R T I C L E
Diet Soda Intake and Risk of Incident
Metabolic Syndrome and Type 2 Diabetes
in the Multi-Ethnic Study of Diet
Atherosclerosis
Soda Intake and Risk of In
(MESA)*
Metabolic Syndrome
and
Type
Nettleton and
Associates
residual confounding by other dietary beJ
A. N
,
J
A. L ,
in
the
Multi-Ethnic
Study
of Ath
E D. M
,
haviors,
lifestyle
factors, or demographic
P
L. L
,
Table
2—Risk
of
incident
metabolic
syndrome
and
type
2
diabetes
according
to
diet
soda
consumption
categories
in
participants
from
MESA
Y
W
,
D
R. J
, J .,
characteristics (1,2). Biological mecha(MESA)*
nisms possibly explaining these associaCardiovascular and Metabolic Risk
O R I G I N A L
ENNIFER
AMELA
OUFA
ETTLETON PHD
2
UTSEY PHD
3
ANG MD, PHD
1
OÃO
RIN
AVID
A R T I C L E
4
IMA PHD
4
ICHOS MD
ACOBS
R
PHD
2,5
tions are few and largely focus on artificial
# rare/never but !1
!1 serving/week
to !1 increasing
in beverages/foods
OBJECTIVE — We determined associations between diet soda consumption and riskJENNIFER
of sweeteners
A. NETTLETON
, PHD1
JOÃO A. LIMA, PHD4
Rare
or
never
serving/week
serving/day
!1
serving/day 4
2
of)
incident metabolic syndrome, its components, and type 2 diabetes in the Multi-Ethnic Study
of the
RIN D. MICHOS, MD
PAMELA
L. Ldesire
UTSEY, for
PHD (and consumption E
Atherosclerosis.
Ptrend*
YOUFA sugar-sweetened,
WANG, MD, PHD3 energy-dense beveragDAVID R. JACOBS, JR., PHD2,5
Metabolic syndrome
es/foods (3) or disrupting consumers’
RESEARCH
DESIGN AND METHODS
was assessed by food ability to accurately
n
2,288 — Diet soda consumption367
722
estimate energy in- 501
frequency questionnaire at baseline (2000 –2002). Incident type 2 diabetes was identified at
take
and
remaining
energy
needs (4).
Cases
478
95
169
129
OBJECTIVE — We determined
associations
between
diet soda consumption and risk of
three follow-up examinations (2002–2003, 2004 –2005, and 2005–2007) as fasting glucose
Thus,
diet
soda
consumption
may
result
incident
metabolic
syndrome,
its
components,
and
type
2 diabetes in the Multi-Ethnic
Study of
!126
type 2 diabetes,1.00†
or use of diabetes medication.
Metabolic syndrome
HRmg/dl,
(95%self-reported
CI)
1.34 (1.07–1.67)
1.20 (1.00–1.43)
1.31 (1.07–1.60)
0.003
in overconsumption, increased body
Atherosclerosis.
(and components) was defined by National
Cholesterol
Education
Program
Adult
Treatment
1.00‡
1.42 (1.14–1.78)
1.28 (1.06–1.53)
1.36 (1.11–1.66)
!0.001
Panel III criteria. Hazard ratios (HRs) with 95% CI for type 2 diabetes, metabolic syndrome, and weight, and consequent metabolic dysRESEARCH
DESIGN
AND
METHODS
—
Diet
soda
consumption
was
assessed
1.00§ adjusting for1.31
(1.05–1.64)
1.13 (0.94–1.37)
0.06 by food
If true, such relations 1.18
have (0.96–1.44)
metabolic syndrome components were estimated,
demographic,
lifestyle, and function.
frequency
questionnaire
at
baseline
(2000
–2002).
Incident
type
2
diabetes
was
identified at
important
implications for dietary coundietary confounders.
1.00!
1.30 (1.04–1.62)
1.15examinations
(0.95–1.38)
1.17
(0.96–1.44)
0.06
three follow-up
(2002–2003,
2004
–2005, and 2005–2007) as fasting glucose
seling,
given
the
high
frequency
of
diet
Type 2 diabetes
!126 mg/dl, self-reported type 2 diabetes, or use of diabetes medication. Metabolic syndrome
RESULTS
— At least daily consumption of diet soda was associated with a 36% greater relative
beverage consumption
by those at high
(and components) was
by National Cholesterol
Education Program Adult Treatment
455 type 2 diabetes
914defined
681
risknof incident metabolic syndrome 2,961
and a 67% greater relative risk of incident
risk
for
metabolic
dysfunction
(5).
Panel
III
criteria.
Hazard
ratios
(HRs)
with
95%
CI
for
type
2 diabetes, metabolic syndrome, and
compared
and
Cases with nonconsumption (HR 1.36
221 [95% CI 1.11–1.66] for metabolic
33 syndrome metabolic
84
75 for demographic, lifestyle, and
Replication
of previously
observedadjusting
syndrome
components
were estimated,
1.67 [1.27–2.20] for type 2 diabetes). Of metabolic syndrome components, only high waist
soda–metabolic
HR (95%(men
CI) !102 cm and women !88
1.00†
1.06
(0.73–1.52)
1.39
(1.07–1.80)syndrome associa1.63 (1.24–2.13)
!0.001
dietary diet
confounders.
circumference
cm) and high fasting
glucose
(!100 mg/dl) were
tions
in
a
distinct cohort would bolster
prospectively associated with diet soda consumption.
between
diet soda consump1.00‡ Associations1.10
(0.76–1.59)
1.46 (1.12–1.89)
1.67 (1.27–2.20)
!0.001
RESULTS
At least daily
of diet soda
their—credibility
andconsumption
provide further
in- was associated with a 36% greater relative
tion and type 2 diabetes were independent 1.00§
of baseline measures of1.00
adiposity
or
changes
in
these
(0.69–1.45)
(0.94–1.60)
(1.06–1.84)
0.01
risk of incident
metabolic
syndrome
a 67%1.40
greater
relative risk of incident type
2 diabetes
sight1.23
into
the nature
of theand
relationship.
measures, whereas associations between diet soda and metabolic syndrome were not indepencompared
with
nonconsumption
(HR
1.36
[95%
CI
1.11–1.66]
for
metabolic
syndrome
and
1.00!
0.98
(0.68–1.42)
1.25
(0.96–1.62)
1.38
(1.04–1.82)
0.01
Previous
studies
have
not
addressed
assodent of these factors.
Los sujetos en el percen.l más alto de consumo de diet soda tenían mayor IMC y circunferencia de cintura basales 1.67 [1.27–2.20] for type 2 diabetes). Of metabolic syndrome components, only high waist
between
dietrace/ethnicity,
soda and individual
n " 5,011. *Ptrend with categorical variable modeled continuously. †Model 1 adjusted
forciations
study(men
site,
age, sex,
‡Model(!100
2 adjusted
circumference
!102
cm and women !88and
cm) energy
and highintake.
fasting glucose
mg/dl) were
CONCLUSIONS
—
Although
these
observational
data
cannot
establish
causality,
consumpmetabolic
syndrome
components
or risk
for the variables in model 1 above plus education, physical activity, smoking status,prospectively
pack-years,associated
and weekly
ordiet
more
supplement
use.
§Adjustedbetween
for thediet
variables
in
with
soda
consumption.
Associations
soda consumption of diet soda at least daily was associated with significantly greater risks of select incident of type 2 diabetes nor have they fully admodel
2
above
$
waist
circumference
(centimeters).
!Adjusted
for
the
variables
in
model
2
above
$
waist
circumference
(centimeters)
and
BMI
(weight
in
kilograms
tion
and
type
2
diabetes
were
independent
of
baseline
measures
of
adiposity
or
changes
in these
metabolic syndrome components and type 2 diabetes.
dressed
potential
longitudinal
mediators
measures,
whereas
associations
between diet
soda and metabolic syndrome were not independivided by the square of height in meters).
these
relationships, i.e., changes in addent of of
these
factors.
Diabetes Care 32:688–694, 2009
iposity status (body weight and or waist
CONCLUSIONS
thesewe
observational
2 — Although
circumference).
Therefore,
evaluated data cannot establish causality, consump4.51]
with considBMI
If
excludedcohort
fromstudies
our analyses
parMetabolic
syndrome
and
wowe
longitudinal
have such
as diet1.10
soda,–are
commonly
tion!25
of associations
diet kg/m
soda at least
daily was
with
significantlycomponent
greater risks of select incident
between
diet associated
soda consump2
ticipants
with
any
metabolic
syndrome
Compared
with
metabolic
syndrome
type 2 diabetes.
1.48
[1.07–2.05]
with
!25
shown positive associations be- ered “benign”
because
they contribute
noBMI
tion
and kg/m
riskcomponents
of )incidentand
metabolic
syn- nonconsumers, individtween dietatsoda
consumption
and a energy
few nutrients
diet. Concomponent
baseline
(leaving
muchandand
uals consuming
drome
(and
metabolic
syndrome !1 daily serving of diet
for typeto2the
diabetes
(1.94
[0.87–
4.35]
Diabetes Care 32:688–694, 2009
incident
metabolic
syndrome
indepensequently,
the
previously
observed
diet
2
components) as well soda
as incident
2
smaller sample of 1,078 participants and
had atype
significantly
greater risk of de-
T
re
ha
ch
ni
tio
sw
th
su
es
ab
ta
Th
in
w
fu
im
se
be
ri
di
tio
th
si
Pr
ci
m
of
dr
of
ip
Causalidad Reversa??
Confundentes Residuales??
•  Podría ser el consumo de diet soda un marcador de otros
estilos de vida poco saludables o a algún patrón
alimentario que derive en riesgo metabólico??
REVIEW
Does low-energy sweetener consumption affect energy intake
and body weight? A systematic review, including metaanalyses, of the evidence from human andLow-energy
animalsweeteners
studies systematic review
PJ Rogers et al
PJ Rogers1, PS Hogenkamp2, C de Graaf3, S Higgs4, A Lluch5, AR Ness6, C Penfold6, R Perry6, P Putz7, MR Yeomans8 and DJ Mela9
By reducing energy density, low-energy sweeteners (LES) might be expected to reduce energy intake (EI) and body weight (BW). To
assess the totality of the evidence testing the null hypothesis that LES exposure (versus sugars or unsweetened alternatives) has no
effect on EI or BW, we conducted a systematic review of relevant studies in animals and humans consuming LES with ad libitum
access to food energy. In 62 of 90 animal studies exposure to LES did not affect or decreased BW. Of 28 reporting increased BW, 19
compared LES with glucose exposure using a specific ‘learning’ paradigm. Twelve prospective cohort studies in humans reported
inconsistent associations between LES use and body mass index (−0.002 kg m−2 per year, 95% confidence interval (CI) −0.009 to
0.005). Meta-analysis of short-term randomized controlled trials (129 comparisons) showed reduced total EI for LES versus sugarsweetened food or beverage consumption before an ad libitum meal (−94 kcal, 95% CI −122 to −66), with no difference versus
water (−2 kcal, 95% CI −30 to 26). This was consistent with EI results from sustained intervention randomized controlled trials
(10 comparisons). Meta-analysis of sustained intervention randomized controlled trials (4 weeks to 40 months) showed that
consumption of LES versus sugar led to relatively reduced BW (nine comparisons; −1.35 kg, 95% CI –2.28 to −0.42), and a similar
relative reduction in BW versus water (three comparisons; −1.24 kg, 95% CI –2.22 to −0.26). Most animal studies did not mimic LES
consumption by humans, and reverse causation may influence the results of prospective cohort studies. The preponderance of
evidence from all human randomized controlled trials indicates that LES do not increase EI or BW, whether compared with caloric or
non-caloric (for example, water) control conditions. Overall, the balance of evidence indicates that use of LES in place of sugar, in
children and adults, leads to reduced EI and BW, and possibly also when compared with water.
International Journal of Obesity (2016) 40, 381–394; doi:10.1038/ijo.2015.177
INTRODUCTION
Low-energy sweeteners (LES), such as acesulfame-K, aspartame,
saccharin, stevia and sucralose are consumed throughout the
world.1 The history of their use has been accompanied by debate
and disagreements, not least about their potential nutritional
impact. The use of LES to replace or partially replace added sugar
in foods and beverages might well be expected to reduce energy
intake (EI),2–4 yet over recent years there has been widely reported
speculation that consumption of LES might increase the risk of
becoming overweight and obese.5–7
Studies covertly manipulating energy density show higher EI
after consumption of a reduced-energy food or beverage, but that
the degree of energy ‘compensation’ is variable.8 Crucially, energy
compensation is usually lower than the difference in energy
content of the comparison foods/beverages, seemingly being
lowest of all for liquids.8 This suggests that consuming LES in place
of sugar-sweetened products should reduce overall EI, and
particularly so for consumption of beverages, the most popular
OPEN
vehicles for LES.1 The question also arises whether the presence of
LES in beverages affects appetite and EI relative to plain water.1,9
Although the imprecise control of short-term energy balance
predicts that LES consumption should help reduce EI and
therefore reduce risk of overweight and obesity,3,10 it is possible
that, as consumed in everyday life, other effects of LES balance or
even outweigh the energy dilution effect. For example, a low
calorie or ‘diet’ label may cause the consumer to eat a larger
portion of the product or eat more of accompanying foods in the
meal, or eat more later.11–14 More simply, adding sweetness to a
product may increase intake owing to increased palatability.15,16
Or, by ‘uncoupling’ the relationship between sweetness and
energy content, the consumption of LES may undermine the
usefulness of sweetness as a cue in the control of energy
balance.5,17–20
The effects of LES consumption on EI and body weight (BW)
have been the subject of many studies over the past 30 years;
nonetheless there is no clear consensus about this body of
evidence. Taken together, a number of narrative reviews1–4,21–25
and systematic reviews of some types of studies26–30 lead to the
International Journal of Obesity (2016) 40, 381–394
consistent but guarded conclusion that substitution of LES for
© 2016 Macmillan Publishers Limited All rights reserved 0307-05
sugar, especially in beverages, can help reduce EI, but that fully
orest plot showing individual and combined effect sizes for prospective cohort studies reporting the association betw
n and change in BMI over the follow-up period. Effect sizes have been standardised to a 1 year follow-up period. Negativ
Placer por lo dulce, azúcar y obesidad
Edulcorantes artificiales: no tan rápido!
Buscando Causalidad: Plausibilidad Biológica
Evidencia actual
Conclusiones
–  El hecho de agregar sabor a un “vehículo” no calórico
podría aumentar el apetito posterior.
–  Estudios no han demostrado efectos en apetito cuando
edulcorantes se han administrado a través de SNG o en
cápsulas
Am J Clin Nutr 2009;89:1–14. Hambre, Apetito y Saciedad
Respuestas Digestivas
Preabsortivas
El sabor dulce de la sacarina promovería una aumento del hambre e ingesta a través de esKmulación de secreción de insulina (preabsorKva) Efectos Nutritivos y Osmóticos
Bebidas con mayor densidad energéKca u osmolaridad son vaciadas más lentamente del estómago Hambre, Apetito y Saciedad
Respuesta de Péptidos
Intestinales
•  Macronutrientes en la dieta
estimulan la liberación de
péptidos intestinales.
•  CH estimula secreción de
GLP-1, potente incretina y
factor de saciedad
Am J Clin Nutr 2009;89:1–14. Aumento de ingesta y Balance
Uso informado produciría
sobrecompensación
Disrupción del aprendizaje de
asociación
Placer por lo dulce, azúcar y obesidad
Edulcorantes artificiales: no tan rápido!
Mecanismos propuestos para el “daño”
Evidencia actual
Conclusiones
F Bellisle and A Drewnowski
694
Estudios de “precarga”
Table 3 The impact of intense sweetener aspartame on hunger and energy intakes compared to the control conditions
Study
Subjects
Dose (mg)
Volume
(ml)
Vehicle
Control
condition(s)
Delay
(min)
Meal
Hunger
Consumption
Blundell and Hill (1986)
Rogers et al. (1988)
95
8M, 4F
162
162
200
200
Water
Water
—
60
—
Lunch
Birch et al. (1989)
Rodin (1990)
24 (4–5 years) 140
24
250
205
500
Fruit drink
Water
0–60
38
Snacks
Lunch
Increased
Higher
No effect
—
—
—
No
No
No
No
Rolls et al. (1990)
42M
0,30, 60
Lunch
Decreased
No effect
20 M
Soft drink
Water
60
Lunch
No effect
No effect
Canty and Chan (1991)
2M, 18F
240
480
280
560
200
Lemonade
Black et al. (1991)
110
220
160
320
112
Water
Water
Glucose
Water
Water
Fructose
Glucose
Water
Fruit drink
60
Lunch
Black et al. (1993)
18M
340
280
560
65
Lunch
No effect
No effect
No effect
No effect
No effect
No effect
DiSogra et al. (1990)
6M, 6F
10M, 5F
Water
Water
60
60
Lunch
Lunch
Tordoff and
Alleva (1990a)
Anderson et al. (1989)
Rolls et al. (1989)
60M, 60F
234
235
470
0.05–1%
Capsule
Water
Soft drink
Capsules
Capsules
Water
Sucrose
Water
—
—
Decreased
Decreased
Decreased
—
20 (9–10 years) 10 mg/kg
16M, 16F
211–391
300
Ad lib
90
120
Lunch
Lunch
—
Decreased
Decreased
Higher
Higher
No effect
No effect
No effect
No effect
Mattes (1990a)
12M, 12F
70g
180
Drewnowski et al. (1994b)
12M, 12F
0.16% by
weight
500
Decreased
Decreased
No effect
No effect
No effect
No effect
Drewnowski et al. (1994b)
24F
500
500
No effect
No effect
Lavin et al. (1997)
14F
Not
reported
330
No effect
No effect
Increased
No effect
Beridot-Therond et al. (1998) 12M, 12F
50 mg/l
Ad lib
B15
B6.5hr
No effect
No effect
Melanson et al. (1999b)
10M
B100
350
Variable
Lunch
—
No
No
No
No
King et al. (1999)
16M
Not
reported
790
Water
Unsweetened
Sucrose
Lemon Water Carbohydrate
Fat
Fruit drink
Water
Lunch
Dinner
Lunch
Snack
Dinner
Lunch
Snack
Dinner
Snack
Lunch
Dinner
Lunch
Dinner
B15
Lunch
No effect
Increased
Wilson (2000)
135 (2–5 years) Not
reported
Ad lib
Milk
Sucrose
Milk
0
Lunch
No effect
—
Increased
No effect
Van Wymelbeke
et al. (2004)
12M, 12F
2000
Fruit drink
Sucrose milk
Sucrose
Varibale
Lunch No effect
Dinner
40
—
500
Chewing gum Plain gum
No gum
Fruit drink
Sucrose
Pudding/
Sucrose
Gelatin
Cereal
Plain
Sucrose
Soft white
Plain
cheese
Sucrose
Maltodextrin
Soft white
Plain
cheese
Sucrose
Maltodextrin
Lemonade
Sucrose
Water
Fruit drink
3h
6.5h
9.5h
3h
6.5h
9.5h
Variable
effect
effect
effect
effect
effect
effect
effect
effect
No effect
No effect
Adelaide Hospital, North Terrace, Adelaide, South Australia 5000 Australia.
and GIP, the so-called incretin hormones, from the gut in healthy
E-mail: chris.rayner@adelaide.edu.au.
humans (3). In patients with type 2 diabetes, the incretin effect is
4
Abbreviations used: GIP, glucose-dependent insulinotropic polypeptide;
impaired (4). Incretin-based therapies for diabetes have focused
GLP-1, glucagon-like peptide 1; iAUC, incremental AUC; SGLT1, sodiumon GLP-1 rather than on GIP, because the insulinotropic action
glucose cotransporter-1; T50, half-emptying time;
TIM, tagatose/isomalt mix1–3
of the latter is diminished in these patients (5). Other actions of
ture; 3OMG, 3-O-methyglucose.
GLP-1 include slowing of gastric emptying (6) and reduction of
Received June 11, 2011. Accepted for publication October 11, 2011.
published
online
December
7, 2011; doi: 10.3945/ajcn.111.021543.
energy
intakeJ(7).
Tongzhi Wu,appetite
Beiyi Rand
Zhao,
Michelle
Bound, Helen L Checklin, Max Bellon, First
Tanya
J Little,
Richard
L Young,
Karen L Jones, Michael Horowitz, and Christopher K Rayner
Effects of different sweet preloads on incretin hormone secretion,
gastric emptying, and postprandial glycemia in healthy humans
78
Am J Clin Nutr 2012;95:78–83. Printed in USA. ! 2012 American Society for Nutrition
ABSTRACT
One promising strategy to stimulate endogenous GLP-1 is the
Background: Macronutrient “preloads” can stimulate glucagon“preload” concept, in which a small load of macronutrient is given
like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypepa fixed interval before a meal, to induce the release of gut peptides
tide (GIP), slow gastric emptying, and reduce postprandial glycemic
such as GLP-1 and GIP to slow gastric emptying and stimulate
excursions. After sweet preloads, these effects may be signaled by
insulin secretion in advance of the main nutrient load. We have
sodium-glucose cotransporter-1 (SGLT1), sweet taste receptors,Appetite
or
shown
both fat and protein preloads markedly reduce post55
(2010)that
37–43
both.
prandial glycemic excursions in patients with type 2 diabetes by
Objective: We determined the effects of 4 sweet preloads on GIP
these mechanisms (8, 9). However, a potential disadvantage is that
Contents
lists available at ScienceDirect
and GLP-1 release, gastric emptying, and postprandial
glycemia.
the preload could increase overall energy intake; preloads that
Design: Ten healthy subjects were studied on 4 separate occasions
entail minimal additional energy would be advantageous.
each. A preload drink containing 40 g glucose, 40 g tagatose/isoIncretin stimulation by carbohydrates may be signaled by
Appetite
malt mixture (TIM), 40 g 3-O-methylglucose (3OMG; a nonmetasweet taste receptors and/or SGLT1. Data from in vitro, animal,
bolized substrate of SGLT1), or 60 mg sucralose was consumed 15
and human studies in this area have been inconsistent. For example,
j o u r n apotato
l h o mmeal.
e p a gBlood
e: www.elsevier.com/locate/appet
min before a 13C-octanoic acid–labeled mashed
stimulation of sweet taste receptors by sucralose (a noncaloric
glucose, plasma total GLP-1 and GIP, serum insulin, and gastric
artificial sweetener) was reported to release GLP-1 from enteroemptying were determined.
endocrine L cells in vitro (10, 11) but has no effect on GLP-1
Research
report
Results: Both glucose and 3OMG stimulated GLP-1 and GIP resecretion and gastric emptying in humans (12). It has also been
lease in advance of the meal (each P , 0.05), whereas TIM and
postulated
that intake,
SGLT1 maysatiety,
be involved and
in incretin
hormone seEffects
and
sucrose
on food
postprandial
sucralose
did of
not.stevia,
The overallaspartame,
postprandial GLP-1
response
was
cretion (13). Monosaccharides that are substrates for SGLT1, in§
greater
after glucose,
and TIM
than after sucralose (P ,
glucose
and3OMG,
insulin
levels
cluding glucose, galactose, and 3OMG, stimulate GLP-1 release in
0.05), albeit later after TIM than the other preloads. The blood
vitro anda in perfused ileum in aanimal studies (14–16), ana effect
a,b,d,
a
glucose
and insulin
responses in*the
first 30 min
after the meal
were
, Corby
K. Martin
Stephen
D. Anton
, Hongmei
Han by
, Sandra
, William
T. Cefalu
inhibited
phloridzin,Coulon
which blocks
SGLT1 (13).
Similarly, ,in ob/
a,cP , 0.05). Gastric emptying was aslower
greatest
glucose (each
, Donald A. Williamson
Paulaafter
Geiselman
ob mice,
GIP is37–43
secreted in response to glucose, galactose, and
Appetite
55 (2010)
after both 3OMG and TIM than after sucralose (each P , 0.05).
a
3OMG (17), but not to fructose and mannose, which are not
Pennington
Biomedical
Research
Center,
Baton
Rouge,
LA,
United
States
Conclusions:
In healthy humans, SGLT1 substrates stimulate GLP-1
b
Department of Aging and Geriatric Research, University of Florida, United States
SGLT1 substrates (18, 19). 3OMG is a glucose analog that is aband
GIP
and
slow
gastric emptying, regardless of whether they
are lists available at ScienceDirect
c
Contents
Department of Psychology, Louisiana State University, United States
sorbed from the small intestine via SGLT1, but it is not metabod
metabolized,
whereas
the
artificial
sweetener
sucralose
does
not.
Institute on Aging, University of Florida, 210 E Mowry Rd., Gainesville, FL 32611, United States
lized and makes no contribution to energy intake. Whether 3OMG
Poorly absorbed sweet tastants (TIM), which probably expose
stimulates GIP and GLP-1 secretion in humans is unknown.
a greater length of gut to nutrients, result in delayed GLP-1 secretion
but
A Rnot
T Iin
C delayed
L E I N FGIP
O release. These observations
A B have
S T Rthe
A Cpotential
T
1
to optimize the use of preloads for glycemic control. This trial was
From the Discipline of Medicine, University of Adelaide, Royal Adejournal homepage: www.elsevier.com/locate/appet
Article history:
Consumption of Am
sugar-sweetened
beverages
may Australia
be one of(TW,
the dietary
causes
of metabolic
disorders,
laide Hospital,
Adelaide,
BRZ, MJB,
HLC,
TJL, KLJ, MH,
registered
at www.actr.org.au as ACTRN12611000775910.
J
Received 30 September 2009
such as obesity. Therefore,and
substituting
sugar
with low calorie
sweeteners
may(MB)
be anand
efficacious
weight
CKR), and
the Department
of Nuclear
Medicine
the Nerve
Clin
Nutr 2012;95:78–83.
Downloaded from ajcn.nutrition.org by guest on May 3, 2016
•  No hubo incremento de niveles de insulina después de la carga de sucralosa ni de tagatosa a diferencia de glucosa •  No hubo incremento de los niveles de GLP-­‐1 después de carga de sucralosa •  No hubo diferencia significaKva en el Kempo de vaciamiento gástrico después de la carga de sucralosa o glucosa •  La sensación de saciedad fue mayor después de la carga de glucosa que sucralosa, sin embargo no hubo diferencias en apeKto ni en ingesta posterior •  Menor aumento de glucosa post carga de stevia y aspartame en relación Appetite
a sacarosa •  Menor aumento de insulina post carga de stevia en relación a aspartame y sacarosa Gut Laboratory (RLY), Royal Adelaide Hospital, Adelaide, Australia.
Research report
Supported by a grant awarded by the National Health and Medical ReINTRODUCTION
search
Council (NHMRC)
of Australia (grant no. 627139). TJL was sup• 
Sin d
iferencias e
n a
peKto n
i i
ngesta posterior MajorEffects
determinants
postprandial
blood glucose include
ofofstevia,
aspartame,
andthesucrose on food intake, satiety, and postprandial
Received in revised form 1 December 2009
Accepted 10 March 2010
management strategy. We tested the effect of preloads containing stevia, aspartame, or sucrose on food
2
intake, satiety, and postprandial
glucose and insulin levels. Design: 19 healthy lean (BMI = 20.0–24.9)
and 12 obese (BMI = 30.0–39.9) individuals 18–50 years old completed three separate food test days
Keywords:
during which they received
preloads
containing
stevia Clinical
(290 kcal),
aspartame
(290 kcal),
or sucrose
ported
by an NHMRC
Overseas
Postdoctoral
Training
Fellowship
Stevia
(493 kcal)
before the
and dinner
meal. The preload order was balanced, and food intake (kcal) was
no. 519349).
rate
of gastric emptying (1, 2) and the postprandial
re-lunch(grant
§insulin
Aspartame
3
4
directly calculated. Hunger
and
satiety
levels were reported
beforeDiscipline
and afterofmeals,
and Royal
every hour
Address
correspondence
to CK Rayner,
Medicine,
Sucrose of which !50% is stimulated by the secretion of GLP-1
sponse,
throughout
the
afternoon.
Participants
provided
blood
samples
immediately
before and
min after the
FoodGIP,
intake
Adelaide Hospital,
North
Terrace,
Adelaide,
South Australia
500020
Australia.
and
the so-called incretin hormones,
from
the
gut
in
healthy
a,b,d,
a
a in preloads (290 kcal a
lunch preload. Despite
the caloric difference
vs. 493 kcal), participants dida not
glucose and insulin levels
RCT Largo Plazo
Intense sweeteners, energy intake and the control of body weight
F Bellisle and A Drewnowski
69
Table 4 Long-term studies of the impact of intense sweetener aspartame on body weight
Study
Subjects
Design
Period
Weight loss diet
Products
Body weight loss
Tordoff and Alleva (1990b)
21M,9F Normal wt.
Xover
3 ! 3 weeks
No
0.5 kg loss M, F
Kanders et al. (1988)
13M,46F Obese
2arm
12 weeks
Yes
Soda, 1150 g reg. or
diet (aspartame)
Aspartame vs not
Blackburn et al. (1997)
163F Obese
2arm
19 weeks þ 1 year
Yes
Aspartame vs not
Raben et al. (2002)
6M,35F
2arm
10 weeks
No
Sucrose vs Aspartame
Aspartame lost,
sucrose gained
Porikos et al. (1977)
Overwt.
6F, 2M Obese
Xover
3 ! 6 ! 6 days
No
Sucrose vs Aspartame
No change
All lost, non-Asp F lost
least
Both lost B10%, Asp
regained less
Asp ¼ Aspartame.
reduction in sugar intake. On the other hand, Bellisle et al.
1977, 1982; Tordoff and Alleva, 1990b; Kanders et al., 1990;
Tate J
F /
2012) 318 a
dultos 2 b
razos +
6 m
eses No and
Cambio de b1995;
ebidas Blackburn
regulares et al.,
Sin diferencias (2001) found, in a cohort of 4278 French adults, aged 45–60
Naismith
Rhodes,
1997;
Gatenby
sobrepeso y
control por d
iet o
a
gua -­‐2% d
el p
eso years, that about 30% of women and 22% of men were at
et al., 1997; Reid and Hammersley, 1998; Raben et al.,
2002).
obesos least occasional users of intense sweeteners. As expected,
These RCTs showed considerable variations in their design,
higher body mass index (BMI) values and higher waist/hip
study population, duration and type of control. In addition,
Peters JC (2014) 303 adultos 2 brazos 12+40 semanas Si 24 onzas de diet soda/24 onzas -­‐5.95 kg asp, ratios were associated with more frequent use, suggesting
certain studies compared dietary conditions that did not
sobrepeso y de agua por día menos hambre that overweight persons were using intense sweeteners as a
only differ by the presence or absence of intense sweeteners.
obesos -­‐4.09 kg agua strategy for weight control. Users had lower energy intakes
For example the Foltin et al. (1988, 1992) studies did not
(significant difference in men only) and consumed less
focus specifically on intense sweeteners but compared diets
carbohydrate than did nonusers. In a Spanish study of 2450
varying in fat as well as carbohydrate contents, thereby
persons (Serra-Majem et al., 1996), about 18% of the
making it impossible to single out the contribution of
population used cyclamate. Within the user group, higher
sweeteners in the reported effects. The meta-analysis re-
a 12-week
loss treatment
program. treatment but was not significantly difWing examined the use of NNS beveragesduring
by those
in the behavioral
National weight
a function
of the behavioral
Methods: An equivalence trial design with water or NNS beverages as the main factor in a prospective
Weight Control Registry and found that successful weight losers ferent between groups. Sedentary behavior actually decreased signifrandomized trial among 303 men and women was employed. All participants participated in a behavioral
drank three times the NNS beverages compared
to those who had icantly
in the Waterweight
grouploss
overphase
time (12
but weeks)
not theofNNS
group. The
weight
loss treatment program.
The results of theBeverages
an ongoing trial (1
The
Effects
of
Water
and
Non-Nutritive
Sweetened
never lost weight (24).
changes
time two
weretreatments
not significant
between
groups. Taken
year) that is also evaluating the
effectsover
of these
on weight
loss maintenance
were
together,
changes
in
physical
activity
and
sedentary
behaviors
cannot
on Weight Loss During areported.
12-week Weight Loss Treatment
We chose 12 weeks as the weight loss phase
because
mosttreatments
studies were
account
for the difference
weight
loss observed.
Results:
The two
not equivalent
with the in
NNS
beverage
treatment group losing signifiProgram
weightofcompared
show
that weight loss slows considerablycantly
after more
6 months
treat- to the water group (5.95 kg versus 4.09 kg; P < 0.0001) after 12 weeks.
1
2 occurring in
1theNNS
2on reported
2
Participants
beverage
group
greater
subjective
feelings
ment
with
more
thanR.half
of1,the
weight
loss
inthe
firstC.
12Wojtanowski
Based
the design
of thisVeur
study
are unablein to
say, what
is theof
John C.
Peters
, Holly
Wyatt
Gary
D. Foster
, Zhaoxing Pan
, Alexis
, Stephanie
S.significantly
Vander
, wereductions
2
1
1
hunger
than
those
in
the
water
group
during
12
weeks.
weeks
(25,26),
probably
owing
to
difficulty
with
longer
term
adhermechanism
for
the
greater
weight
loss
in
the
NNS
group
compared
Sharon J. Herring , Carrie Brill and James O. Hill
Conclusion:
These
results show
that water
water group.
is not superior
NNS beverages
for significantly
weight loss during
ence to a hypocaloric regimen. Furthermore,
it is now
recognized
to the
Weekly tohunger
scores were
lower a
comprehensive behavioral weight loss program.
that weight loss is a different process from weight maintenance, among the NNS group than the water group although the absolute
Objective:
To compare
efficacy of non-nutritive
sweetened
or water
for weight
lossit is plausible that the NNS participants
22, 1415–1421.
doi:10.1002/oby.20737
both
behaviorally
and the
physiologically,
soObesity
it is(2014)
important
tobeverages
study (NNS)
changes
were small.
While
during a 12-week behavioral weight loss treatment program.
treatment effects on these two processes separately (27). The benefit were more likely to adhere to the dietary recommendations due to
Methods: An equivalence trial design with water or NNS beverages as the main factor in a prospective
of the current 1 year trial is that we will be able to compare both less hunger than the Watera beneficial
group we
cannot
conclude
this
based and
on energy
effect
or no effect
of NNS
on appetite
randomized trial among 303 men and women
was employed. All participants participated in a behavioral
Introduction
weight
and weight
loss maintenance
within
same
study.
Some
authors
(3,5,6)Other
havestudies
suggested
that use
of of
NNS
have reported
findings
increased
weight loss
loss treatment
program.
The results Beverage
of the the
weight
lossgroup
phaseof(12 this
weeks)
of an
ongoing
trial (7-11).
(1
consumption
recommendations
(1) suggest
water
as the
with
consumption
ofand
NNS disrupt
(11) but generally
withoutofan acco
participants.
The
trial
was
designed
to
allow
preplanned
analysis
of
may
increase
appetite
for
sweet
foods
regulation
year) that is also evaluating the effects ofgold-standard
these twobeverage
treatments
on weight
lossUSmaintenance
for optimal
health. The
Dietary Guide- were
ing increase in caloric intake.
the
treatment effects after just the 12-week
weight
phasebeverages
as energy
balance.sweeteners
Weight loss results for the present study suggest
lines (2)
suggestloss
that while
with non-nutritive
reported.
(NNS)
are preferable
to those
with caloric
there is still a did not increase energy intake from other
well
as after
months
of weight
(still
which
that sweeteners,
NNSgroup
consumption
Results:
The 9two
treatments
weremaintenance
not equivalent
withunderway)
the NNS
beverage
treatment
losing signifiquestion about whether they are beneficial for weight management. Several observational studies have reported a positive asso
will
bemore
reported
separately.
foods
compared
to12water.
This isNNS
consistent
with
that
cantly
weight
compared to the water group
(5.95
kg
versus
4.09
kg;
P
<
0.0001)
after
weeks.
between
consumption
and other
greater studies
body weight
and weig
While numerous clinical trials have examined the effects of nutritive
over
time
(4,12).
Determining
causality
is
not
possible
wit
Participants in the NNS beverage group reported
significantly
greater
reductions
in
subjective
feelings
of
have
not
found
increased
consumption
of
sweet
or
high
energy
sugar sweetened beverages (NS) compared to NNS beverages on
studies but it is possible that they represent “reverse ca
weight
loss,
few
studies
have
directly
compared
water
and
NNS
hunger
than
those
in
the
water
group
during
12
weeks.
While most secondary outcomes were not different between the foods while using NNS (28,29).
Further studies will be needed to
obesity may cause people to seek diet beverages (10
on weight to
lossNNS
usingbeverages
an equivalence
design.loss duringwhereby
Conclusion:
These group
results showed
show that
waterbeverages
is
not superior
fortrial
weight
groups,
the NNS
greater
reductions
in totaland
ascertain
the
mechanism(s)athat may be responsible for the weight
comprehensive behavioral
weight
losstoprogram.
LDL-cholesterol.
This may
be due
the NNS
greater
loss
thefood loss
wereweight
introduced
intointhe
supplyresults.
over 50 years ago and The largest and most recent randomized trial (14) to compare
•  Objetivo: comparar la eficacia de ENC o agua para la pérdida de peso
durante un programa de tratamiento de obesidad
•  303 adultos obesos de ambos sexos, todos participaron del programa de
manejo conductual.
•  Al grupo ENC se le pidió consumir al menos 24 onzas de bebidas con ENC
por día+ consumo libre de agua
•  Al grupo agua, se le pidió consumir al menos 24 onzas de agua por día y no
diet beverages
and an attention
control for their effects on
being used
of different food
and beverage products.
consumir ni agregar are
ENC
enin hundreds
cualquier
producto
líquido.
Sí podían
consumir
Despite the long history of usage there continues to be considerable loss used a superiority trial design. The authors found that
otros alimentos con controversy
ENC. concerning their role in the diet, particularly whether beverage treatment, but not water, significantly increased the
they are a useful tool as an aid in weight loss and weight loss main- bility of losing 5% of body weight over the 6-month study d
Obesity (2014) 22, 1415–1421. doi:10.1002/oby.20737
Introduction
tenance (3-6). NNS provide sweetness equivalent to NS but contrib- compared to a standard weight loss education and monitori
TABLE 3 Absolute weight loss (kg) for completers
(7-11). Other studies have reported findings of increased hunger
a beneficial effect or no effect of NNS on appetite and energy intake
essentially
energy. Since the 1980s a number of short-term gram. Subjects in both treatment groups lost a significant am
Beverage consumption recommendations (1) suggestute
water
as the zero
with consumption of NNS (11) but generally without an accompanyexperimental
have compared NNS to NS and several com- weight but the amount of weight lost compared to the cont
gold-standard beverage for optimal health. The US Dietary
Guide-studies
ing increase
in caloric intake.
Baseline
Week
90% CL
mean
between
treatment groups. P value
prehensive
reviews 12
haveclinic
concluded that the evidence supports either not different
lines (2) suggest that while beverages with non-nutritive
sweeteners
Group
(kg)
(kg)
Change
for change
for change
(NNS) are preferable to those withweight
caloric sweeteners,
there is still weight
a
Several observational studies have reported a positive association
1
question about whether they are beneficial for weight management.
Anschutz Health and Wellness Center, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA. Correspondence: John C. Peters
between
NNS
consumption
and
greater
body weight
andand
weight
gain Department
2
Temple
University,
Center
for
Obesity
Research
Education,
PA, USA
While(nnumerous
examined
the effects(john.c.peters@ucdenver.edu)
of nutritive87.11
NNS
5 142)clinical trials have93.56
(13.23)
(12.85)
26.45
(3.68)*
25.94,
26.96 of Medicine, Philadelphia,
<0.0001
over
time
(4,12).
Determining
causality
is
not
possible
with
these
sugar sweetened beverages (NS) compared to NNS beverages on
Water (n 5 134)
93.88 (12.99) Funding Agencies:
89.33
(13.07)
24.55
(3.67)*
24.03, 25.08
<0.0001
studies
but fully
it funded
is possible
that theyBeverage
represent
“reverse causality”
study was
by The American
Association.
weight loss, few studies have directly compared water
and NNS The
whereby
obesity may
causeThe
people
to(3.67)*
seek
diet beverages
Disclosure: JCP,
JOH
received
consulting
fees from
Coca-Cola
Company
outside of the(10,13).
submitted
The remaining co-authors declared
no conflict of in
NNS—water
(13.12)
22.22
(12.96)
21.90
21.16,work.
22.63
<0.0001
beverages on weight loss using an20.32
equivalence
trial design.
Author contributions: JP, HW, GF, ZP, JH, were involved in study design, data analysis and data interpretation; CB, SH, SV, AW were involved in data collection
authors were involved in writing the manuscript and approved the final submission.
The
largest
and 7most
recent
randomized
trial27(14)
to
compare
water,
NNS were introduced into the food supply over 50 Received:
years ago16and
2014;
Accepted:
March
2014;
Published
online
May
2014.
doi:10.1002/oby.20737
Analysis including participants who completed 12 weeks
of theJanuary
trial. Although
equivalence
cannot
be established
participants
lost more weight in the NNS group as comdiet
beverages
and
an
attention
control
for
their effects on weight
are being used in hundreds of different food and beverage
products.
This
is
an
open
access
article
under
the
terms
of
the
Creative
Commons
Attribution-NonCommercial-NoDerivs
License,
whichStatistically
permits use and
distribution in any
pared to the water group. All analyses were completed using a Satterthwaite two sample t test. All values are Mean (SD) unless otherwise
noted.
significant
the original work
properly
cited, the usetrial
is non-commercial
no modifications
or adaptations
loss isused
a superiority
design. The and
authors
found that
the diet are made.
Despite the long history of usage there continues to beprovided
considerable
values (P < 0.05) are shown by an asterisk (*) and statistically significant P values are shown in bold.
controversy concerning their role in the diet, particularly whether beverage treatment, but not water, significantly increased the probawww.obesityjournal.org
they are a useful tool as an aid in weight loss and weight loss main- bility of losing 5% of body weight over the 6-month study duration
Obesity | VOLUME 22 | NUMBER 6 | JUNE 2014
REVIEW
Does low-energy sweetener consumption affect energy intake
and body weight? A systematic review, including metaanalyses,
of the evidence
from human and animal studies
Low-energy sweeteners
systematic review
PJ Rogers et al
PJ Rogers1, PS Hogenkamp2, C de Graaf3, S Higgs4, A Lluch5, AR Ness6, C Penfold6, R Perry6, P Putz7, MR Yeomans8 and DJ Mela9
By reducing energy density, low-energy sweeteners (LES) might be expected to reduce energy intake (EI) and body weight (BW). To
Internation
OPEN
assess the totality of the evidence testing the null hypothesis that LES exposure (versus sugars or unsweetened alternatives) has no
© 2016 Mac
effect on EI or BW, we conducted a systematic review of relevant studies in animals and humans consuming LES with ad libitum
www.natu
access to food energy. In 62 of 90 animal studies exposure to LES did not affect or decreased BW. Of 28 reporting increased BW, 19
compared LES with glucose exposure using a specific ‘learning’ paradigm. Twelve prospective cohort studies in humans reported
−2
inconsistent associations between LES use and body mass index (−0.002 kg m
per year, 95% confidence interval (CI) −0.009 to
REVIEW
0.005). Meta-analysis of short-term randomized controlled trials (129 comparisons) showed reduced total EI for LES versus sugarsweetened food or beverage consumption before an ad libitum meal (−94 kcal, 95% CI −122 to −66), with no difference versus
water (−2 kcal, 95% CI −30 to 26). This was consistent with EI results from sustained intervention randomized controlled trials
(10 comparisons). Meta-analysis of sustained intervention randomized controlled trials (4 weeks to 40 months) showed that
consumption of LES versus sugar led to relatively reduced BW (nine comparisons; −1.35 kg, 95% CI –2.28 to −0.42), and a similar
relative reduction in BW versus water (three comparisons; −1.24 kg, 95% CI –2.22 to −0.26). Most animal studies did not mimic LES
consumption by humans, and reverse causation may influence the results of prospective
cohort studies. The preponderance of
PJ Rogers1, PS Hogenkamp2, C de Graaf3, S Higgs4, A Lluch5, AR Ness6, C Pen
evidence from all human randomized controlled trials indicates that LES do not increase EI or BW, whether compared with caloric or
non-caloric (for example, water) control conditions. Overall, the balance of evidence indicates that use of LES in place of sugar, in
By reducing
energy density, low-energy sweeteners (LES) might be expected t
children and adults, leads to reduced EI and BW, and possibly also when compared
with water.
Does low-energy sweetener consump
and body weight? A systematic revie
analyses, of the evidence from huma
assess the totality of the evidence testing the null hypothesis that LES exposu
effect on EI or BW, we conducted a systematic review of relevant studies in
International Journal of Obesity (2016) 40, 381–394; doi:10.1038/ijo.2015.177
access to food energy. In 62 of 90 animal studies exposure to LES did not affe
compared LES with glucose exposure using a specific ‘learning’ paradigm. Tw
inconsistent associations between LES use and body mass index (−0.002 kg
0.005). Meta-analysis of short-term randomized controlled trials (129 compar
sweetened food or beverage consumption before an ad libitum meal (−94 k
INTRODUCTION
Although thewater
imprecise
of toshort-term
balance
(−2 kcal, control
95% CI −30
26). This wasenergy
consistent
with EI results from su
predicts that(10LES
consumption
should
help
reduce
EI and
Low-energy sweeteners (LES), such as acesulfame-K, aspartame,
comparisons). Meta-analysis of sustained intervention
randomized contro
3,10
therefore reduce
risk of overweight
it is reduced
possibleBW (nine compar
consumption
of LES versus and
sugarobesity,
led to relatively
saccharin, stevia and sucralose are consumed throughout the
that, as consumed
everyday
life,versus
otherwater
effects
of LES
balance −1.24
or kg, 95% CI –2
relativein
reduction
in BW
(three
comparisons;
world.1 The history of their use has been accompanied by debate
consumption
by humans,
reverseFor
causation
may ainfluence
even outweigh
the energy
dilutionandeffect.
example,
low the results o
and disagreements, not least about their potential nutritional
evidence
human randomized
controlled
trials
calorie or ‘diet’
labelfrom
mayall cause
the consumer
to eat
a indicates
larger that LES do no
impact. The use of LES to replace or partially replace added sugar
non-caloric
(for
example,
water)
control
conditions.
Overall,
portion of the product or eat more of accompanying foods in thethe balance of ev
in foods and beverages might well be expected to reduce energy
2–4
and11–14
adults,
leadssimply,
to reduced
EI and
BW, and possibly
meal, or eat children
more later.
More
adding
sweetness
to a also when co
intake (EI), yet over recent years there has been widely reported
Efecto en el peso: edulcorantes v/s azúcar speculation that consumption of LES might increase the risk of
5–7
product may increase intake owing to increased palatability.15,16
International
of Obesity between
(2016) 40, 381–394;
doi:10.1038/ijo.2015.177
Or, by ‘uncoupling’
theJournal
relationship
sweetness
and
Placer por lo dulce, azúcar y obesidad
Edulcorantes artificiales: no tan rápido!
Mecanismos propuestos para el “daño”
Evidencia actual
Conclusiones
Conclusiones
•  Se ha establecido una relación de causalidad entre el
consumo de azúcar y bebidas azucaradas con el
aumento de la prevalencia de sobrepeso y obesidad a
nivel mundial
•  Los edulcorantes artificiales no calóricos representan
una alternativa de valor al disminuir el aporte de azúcar
de alimentos y sobre todo bebidas
•  Estudios observacionales han reportado asociación
entre el uso de edulcorantes no calóricos y riesgo de
obesidad
•  No se ha encontrado causalidad para esta relación
•  De la gran cantidad de estudios, de diferente diseño,
publicados, se puede desprender que el uso de
edulcorantes no tendría efectos adversos en baja de
peso ni su mantención.
•  No se ha demostrado beneficio significativo en la baja
de peso con el uso de edulcorantes artificiales.
•  Por qué habría de esperarse que sólo por el hecho de
consumir edulcorantes no calóricos alguien pudiera
perder peso??...
•  Los edulcorantes no calóricos podrían promover la baja
de peso en el contexto de una “dieta” o cambios activos
en la conducta alimentaria.