IUBMB Life, 63(1): 7–13, January 2011

Critical Review

The Application of the Glycemic Index and Glycemic

Load in Weight Loss: A Review of the Clinical Evidence
Amin Esfahani1,2,3, Julia M.W. Wong4,5, Arash Mirrahimi1,2, Chris R. Villa2 and
Cyril W.C. Kendall1,2,6
1
Clinical Nutrition & Risk Factor Modification Center, St. Michael’s Hospital, Toronto, Ontario, Canada
2
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
3
School of Medicine, New York Medical College, Valhalla, NY
4
Division of Endocrinology, Children’s Hospital Boston, Boston, MA
5
Department of Pediatrics, Harvard Medical School, Boston, MA
6
College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada

Summary
Obesity is rapidly becoming a global epidemic. As it is a
significant risk factor for several chronic diseases, including
type 2 diabetes and cardiovascular disease, it is imperative
to study dietary and lifestyle approaches that help reduce its
prevalence. Recently, due to its possible link to appetite control
and metabolism, several clinical studies have assessed the effect
of low glycemic index (GI) and glycemic load (GL) diets on
weight loss. To determine the application of GI/GL in the pre-
vention and treatment of obesity, we searched several databases
and identified 23 clinical trials that examined low GI/GL diets
and weight loss as the primary outcome measure. In general,
these studies showed much inconsistency in their findings. While
a few studies found significantly greater weight loss on the low
GI/GL diets, most of the other studies showed a non-significant
trend that favored low GI/GL diets; suggesting that factors
other than GI/GL may play a role. It would be helpful if a
pooled analysis were undertaken to clarify the current findings
and outline the limitations of these studies. There is also a need
for more long-term randomized, controlled trials that not only
focus on weight loss but also on weight maintenance and body
composition. Ó 2011 IUBMB
IUBMB Life, 63(1): 7–13, 2011
Keywords glycemic index; glycemic load; obesity; weight loss.
Received 8 September 2010; accepted 13 December 2010
Address correspondence to: Cyril W. Kendall, Department of Nutri-
tional Sciences, Faculty of Medicine, University of Toronto, Toronto,
Ontario, Canada M5S 3E2. Tel: 1416-978-6527. Fax: 1416-978-5310.
E-mail: cyril.kendall@utoronto.ca
ISSN 1521-6543 print/ISSN 1521-6551 online
DOI: 10.1002/iub.418
INTRODUCTION
Over the past two decades, the rate of obesity has reached
epidemic proportions in developed nations and is increasing in
developing countries. For instance, in 2008, more than 60%
of adults in the United States were categorized as either
overweight or obese (1). Because of numerous complications
associated with obesity and the consequent burden on the
healthcare system, numerous attempts have been made to reduce
its rate. However, there is a lack of consensus as to what consti-
tutes an ideal diet for achieving and maintaining a healthy body
weight. One thing that is accepted, however, is that the best
dietary approaches are those that not only reduce the rate of
obesity but also the risk of the associated complications through
mechanisms that are independent of weight loss.
The glycemic index (GI) (2) is a physiological assessment of
a food’s carbohydrate content through its effect on postprandial
blood glucose concentrations. Evidence suggests that low GI
and low glycemic load (GL) diets may be protective against the
development of chronic and obesity related diseases (e.g., type
2 diabetes and coronary heart disease [CHD]) (3). More
recently, because of the possible link to satiety and metabolism,
a number of studies have focused on the role of GI/GL in
weight loss. However, there has been much controversy with
respect to their possible benefit (4). Despite the academic
debate, popular books and programs devoted to weight loss use
the glycemic index concept as justification for their approach to
body weight control (Atkins, Zone, South Beach, Montignac).
We, therefore, undertook a review of the scientific literature to
identify and summarize the clinical studies that have assessed
the application of GI/GL diets in weight loss as a primary
outcome. Using the broad search terms ‘‘glycemic index OR
8 ESFAHANI ET AL.
glycemic load’’ across MEDLINE (1950 to June 2009 Week 4),
EMBASE (1980 to June 2009 Week 4), All EBM Reviews—
Cochrane DSR, ACP Journal Club, DARE, CCTR, CMR, HTA,
and NHSEED, we identified all clinical trials that used dietary
interventions of different glycemic indices with weight loss as
the primary outcome. The trials were at least 7 days in duration
and did not include studies with exercise as a cointervention.
DIET AND WEIGHT REDUCTION
The concept that ‘‘a calorie is a calorie’’ is the underlying
principle of conventional weight loss diets and is supported by
the majority of the clinical trials in the area. A recent study of
over 800 subjects who were randomized to one of four diets
with different compositions in fat, protein, and carbohydrate
demonstrated that equal clinically meaningful weight loss and
maintenance was achieved over a 2-year period regardless of
the macronutrient distribution (5). Similarly, other trials
comparing different diets of varying macronutrient distribution
have supported these findings, suggesting that adherence is an
important predictor of successful weight loss (6). Beyond
weight reduction, obesity is also associated with the metabolic
syndrome and a number of chronic diseases. Therefore, it may
be of even greater importance that the optimal diet not only
decrease body weight but also promote a metabolic profile
associated with reduced risk of developing chronic diseases.
Low-carbohydrate and high-protein diets, which are heavily
based on animal products, have fallen short in this respect
(6–10). However, a recent study of a diet high in vegetable
proteins and oils resulted in greater improvements in CHD risk
factors, including serum lipids and blood pressure, despite
similar weight reduction in the conventional low-fat control diet
(11). Similarly, a diet low in GI/GL may have added value in
reducing body weight, while also improving risk factors for
CHD independent of the reduction in body weight.
THE GLYCEMIC INDEX AND GLYCEMIC LOAD
The GI is determined by comparing the postprandial glyce-
mic response of a food with the postprandial glycemic response
to the same amount of available carbohydrate from a standard
food (white bread or glucose) in the same individual (2). The
actual GI value is the area under the blood glucose curve
(AUC) for the test food, expressed as a percentage of that of
the standard control and therefore, the value depends on the
food rather than on characteristics of the individual that con-
sumes it (2, 12). The GI of a food is impacted by the nature of
the starch, particle size, pH, the amount of fiber, fat, and
protein, in addition to cooking method and time (12). To
convert the GI values from glucose scale to bread scale, the
glucose scale value is multiplied by 100/70 to arrive at the
bread scale value. Generally, based on the bread scale, low GI
foods are those that have a value lower than 70 and high GI
foods are those with values greater than 100 (13).
GL examines the total impact of the dietary carbohydrate on
postprandial glycemia. The GL is the product of the GI of the
food or diet under study and the grams of available carbo-
hydrate in that food or diet divided by 100 (14). For a meal,
GL is calculated by multiplying the mean GI weighted accord-
ing to the grams of total available carbohydrate by the grams in
the meal or diet.
In general, low GI diets are thought to be metabolically
advantageous because of their potential in improving glycemic
control (4). The potential link between GI and obesity relates to
the lipogenic effects of hyperinsulenmia (15). Therefore, it has
been proposed that diets that elicit a low insulin response (i.e.,
low GI/GL diets) may play a significant role in weight loss.
One possible mechanism suggests that the higher postprandial
insulin response following a high GI/GL meal may lead to a
quicker hunger response and overeating by depleting the meta-
bolic fuels in the body (16). Another mechanism of action may
be through increased satiety and decreased voluntary food
intake (4). This is especially important in subjects who are
overweight or obese. However, more studies are required to
substantiate these and other potential mechanisms of action.
GI, GL, AND WEIGHT LOSS IN CHILDREN
AND ADOLESCENTS
Our search yielded three trials that were conducted in chil-
dren and adolescents (17–19) (Table 1). The evidence from
these trials suggests that low GI and GL diets are effective in
promoting weight loss in children and adolescents by compari-
son with reduced fat diets (17, 19). Ebbeling et al. (17) in a
12 month (6 months intervention 1 6 months follow-up) clini-
cal trial showed that a low GL diet prescribed ad libitum is
more effective in promoting weight loss than a calorie-re-
stricted, traditional reduced fat diet (25–30% of total energy
from fat). The study demonstrated statistically significant reduc-
tions in fat mass (23.0 6 1.6 vs. 1.8 6 1.0 kg; P 5 0.01) and
BMI (21.3 6 0.7 vs. 0.7 6 0.5 kg/m2; P 5 0.02) in the low
GL group by comparison to the reduced fat control group (17).
Spieth et al. (19), in a similarly designed study of approxi-
mately 4.3 months in length, demonstrated statistically signifi-
cant reductions in weight (22.03 6 0.59 vs. 1.31 6 0.72 kg;
P \ 0.05) and BMI in the low GL group by comparison to the
control (19). An uncontrolled, 6-week trial in nine children
showed significant reductions in the percentage of body fat,
waist-to-hip ratio, and improvements in self-reported hunger
level with a low GL diet despite no reductions in weight (18).
Similarly, a study in children that focused on energy intake
rather than weight loss also showed that low GI diets tend to
favor lower energy intake in comparison to high GI diets (20).
Overall, the limited evidence from studies in children and
adolescents tend to favor low GI/GL diets by comparison to
conventionally recommended reduced fat diets in terms of
weight loss and related markers such as fat mass and body fat
percentage. However, more long-term studies are required to
 Table 1
Summary of clinical trials that assess the effect of low GI/GL diets on weight loss in children and adults
Number of Weight/BMI Control diet/
Reference subjects Length Age (y) (kg/m2) Treatmentsa other interventionsb Low GI/GL dietb
Abete et al. (24) 32 (14f ; 18m) 8 weeks 36 6 1.2 32.5 6 0.8 Low GI (40-45) vs. 25.3 6 0.65% 27.5 6 0.73%c
High GI (60-65)
Aston et al. (25)d 26 Females (19 12 weeks 51.9 6 1.7 33.1 6 1.1 Low GI (55.5) vs. 1.7 6 5.0 kg 1.6 6 4.9 kg
completers) High GI (63.9)
Bahadori et al. (26) 120 (66f ; 54m) 24 weeks 44 33.4 6 4.4 Low GI No Control 28.9 kg
(109 (61f ; 48m)
completers)
Bellisle et al. (39) 96 females (65 12 weeks 45.7 6 1.6 30.3 6 0.5 Low GI Weight 24.5 6 3.4 kg 24.0 6 3.1 kg
completers) Watchers vs.
Standard Weight
Watchers
Bouche et al. (27)§ 11 males 5 weeks 46 6 3 28 6 1.0 Low GI (41) vs. 0.5 6 3.3 kg 20.3 6 3.3 kg
High GI (71)
Das et al. (28) 34 (26f ; 8m) (29 6 months 1 34.5 6 0.9 27.6 6 0.2 Low GI (52) vs. 29.1 6 1.1% 210.4 6 1.1%
completers) 6 months High GI (85)
follow-up
De Rougemont et al. 38 (18f ; 20m) 5 weeks 38.4 6 1.5 27.4 6 0.2 Low GI (46.5) vs. 20.2 6 0.2 kg 21.1 6 0.3 kgc
(29) High GI (66.3)
Ebbeling et al. (17) 16 (11f ; 5m) (14 6 months 1 16.1 6 0.8 36.0 6 0.8 Low GL (GL: 68) vs. BMI: 10.02 6 BMI: 20.96 6 0.75 kg/m2c
completers) 6 months Low Fat (GL: 77) 0.46 kg/m2
follow-up
Ebbeling et al. (30) 34 (30f : 4m) (23 6 months 1 28.4 6 1.0 32.5 6 1.2 Low GL (GL: 54) vs. 27.8 6 1.5% 28.4 6 1.5%
completers) 6 months Low Fat (GL: 78)
follow-up
e e
Ebbeling et al. (31) 73 (58f : 15m) 6 months1 27.5 6 0.5 36.9 6 0.7 Low GL (GL: 35-40) 23.5 6 1.0 kg 24.5 6 1.0 kg
12 months vs. Low Fat (GL:
follow-up 65-70)
Fajcsak et al. (18)f 9 (3f ; 6m) (8 6 weeks 11.0 6 0.4 24.7 6 1.3 Low GL No Control Body fat: 23.9 6 2.4%
completers)
Maki et al. (32) 86 (58f ; 28m) (84 12 weeks 1 49.7 6 1.18 31.9 6 0.4 Low GL (46) vs. 22.5 6 0.5 kg 24.9 6 0.5 kgc
completers) 24 weeks Low Fat (51)
follow-up
McMillan-Price et al. 129 (98f : 31m) 12 weeks 31.8 6 0.8 31.2 6 0.4 High-Carb/High GI HCHGI: 23.7 6 0.5 kg; HCLGI: 24.8 6 0.5 kg;
(33) (HCHGI; 70) vs. HPHGI: 25.3 6 0.5 kg HPLGI: 24.4 6 0.5 kg
High-Carb/Low GI
HCLGI; 45) vs.
High-Protein/High
GI (HPHGI; 59) vs.
High-Protein/Low GI
(HPLGI; 44)
Pereira et al. (23) 39 (30f : 9m) Variedg 30.5 6 0.9 91.5 6 2.3 kg Low GL (50) vs. Low 29.5 6 0.3 of body 29.6 6 0.3 of body
Fat (82) weight in 69.4 6 3.8 d weight in 65.2 6 3.3 d
 Table 1
(Continued)
Number of Weight/BMI Control diet/ Low GI/GL
Reference subjects Length Age (y) (kg/m2) Treatmentsa other interventionsb dietb

Pittas et al. (34) 32 (25f ; 7m) 6 months 34.7 6 0.9 27.6 6 0.3 Low GL (53) vs. High 27.2 kg 27.7 kg
GL (86)
Raatz et al. (35) 29 (24f ; 5m) 12 weeks 1 18-70 36.3 6 1.0 Low GI (33) vs. High High GI: 29.3 6 1.3 kg; 29.95 6 1.4 kg
24 weeks GI (63) vs. High Fat High Fat: 28.4 6 1.5 kg
follow-up (59)
Retterstol et al. (22)h 16 males 4 weeks 36-66 30.4 (26.6-34.9) Lipid Lowering vs. HGI: 0 kg Lipid Lowering: 22.4 kg [Range: 23.9
Median (range) Low GI vs. High GI 21.4 kg (range: 23.6 to 0.2) to 21.4]
Sichieri et al. (21) 203 females 18 months 37.3 6 0.3 26.8 6 0.1 Low GI (40) vs. High 20.26 6 0.46 kg 20.41 6 0.37 kg
(123 completers) GI (79)
Slabber et al. (36) 30 females 12 weeks 35.2 6 1.1 34.8 6 0.8 Low GI vs. Standard 27.41 6 1.09 kg 29.34 6 0.64 kg
Energy Restricted
Diet
Slabber et al. (36)h 16 females 12 weeks N/A N/A Low GI vs. Standard 24.48 kg 27.42 kgc
Energy Restricted
Diet
Sloth et al. (37) 45 females 10 weeks 29.8 6 0.9 27.6 6 0.2 Low GI vs. High GI 21.3 6 0.3 kg 21.9 6 0.5 kg
c
Spieth et al. (19)i 107 (58f: 49m) 4.3 months 10.4 6 0.3 33.3 6 0.7 Low GI vs. Low Fat 1.31 6 0.72 kg 22.03 6 0.59 kg
Thompson et al. (38) 90 (77f ; 13m) 48 weeks 41.4 6 0.9 34.8 6 0.3 High Calcium/Low GI HC: 28.8 6 1.37 kg; 28.8 6 1.42 kg
(72 completers) (LGI) vs. High MCMF:
Calcium (HC) vs. 29.1 6 1.30 kg
Moderate Calcium/
Moderate Fiber
(MCMF)
a
Numbers inside the brackets indicate the reported GI values, unless stated otherwise.
b
Reduction in either absolute or % body weight from baseline, unless otherwise states.
c
P \ 0.05 between treatments.
d
Crossover design with no washout.
e
Approximated based on values on a graph.
f
Not controlled.
g
Depended on the amount of time it took to lose 10% of body weight.
h
Crossover design.
i
Nonrandomized trial.
 GLYCEMIC INDEX AND GLYCEMIC LOAD IN WEIGHT LOSS
not only verify these findings but also determine if low GI/GL
diets are more effective than other dietary alternatives.
GI, GL, AND WEIGHT LOSS IN ADULTS
A total of 20 trials (19 reports) were found to have
assessed the effect of low GI/GL diets in weight loss as a pri-
mary outcome (Table 1) (21–39). All but one (26) of these
studies were controlled. The majority of the controlled trials
used a parallel design and compared a low GI/GL diet to
either low fat or high GI/GL controls. Four trials reported
statistically significant differences in weight loss between the
treatments. All four of these studies favored low GI/GL diets
over the control or other interventions (24, 29, 32, 36). In
10 of the other studies, low GI/GL diets enhanced weight loss
by comparison to the control (21–23, 27, 28, 30, 31, 34–37),
though the differences were not statistically significantly. Con-
versely, a study by Bellisle et al. (39) showed better, albeit
nonsignificant, weight reduction with a standard Weight
Watchers diet by comparison to a Weight Watchers diet
supplemented with low GI foods (24.5 6 3.4 kg vs. 24.0 6
3.1 kg; P 5 0.68).
A study by Aston et al. (25) showed a nonsignificant weight
gain in both the groups (P 5 0.8). The remaining two studies
consisted of multiple interventions (33, 38). In the study by
McMillan-Price et al. (33), four different diets (high protein/
high GI or low GI and high carbohydrate/high GI and low GI)
led to similar reductions in weight (P 5 0.17 between treat-
ments). In another study (38), three different diets (high
calcium, high calcium/low GI and moderate calcium/moderate
fiber diet) resulted in similar reductions in weight (P 5 0.88
between treatments).
The majority of studies in adults also reported on other out-
comes including changes in fat mass, body fat percentage, lean
muscle, energy intake, weight regain, and satiety. Of the 13
controlled trials (23–25, 27–33, 35, 37, 38) reporting on per-
centage body fat or fat mass, only two (27, 29) reported statisti-
cally significant improvements with a low GI/GL diet by
comparison to the control. The others showed no significant
differences between the groups.
Limited evidence from the aforementioned studies suggests
that low GI/GL diets may be more effective in certain popula-
tions. For instance, Ebbeling et al. (31) in a subgroup analysis,
showed that a low GL diet resulted in significant reductions in
weight and body fat percentage by comparison to a low-fat diet
in subjects with high postprandial insulin levels (25.8 kg vs.
21.2 kg; P 5 0.004 and 22.6% vs. 0.9%; P 5 0.03, respec-
tively). Another study in subjects with hyperinsulinemia showed
statistically significant reductions in weight in the low GI group
by comparison to the control (36). In another subgroup analysis,
McMillan-Price et al. (33), demonstrated that a high-carbohy-
drate/low GI diet induces a statistically significant drop in fat
mass when compared with a high-carbohydrate/high GI diet in
women (n 5 98).
11
Overall, the results indicate that low GI/GL diets, if not
more, are as effective as other dietary alternatives in inducing
weight loss. None of the studies suggested that low GI/GL diets
are an inferior regimen and in fact, even though not statistically
significant, low GI/GL diets induced more weight loss by
comparison to the control in the majority of the studies. This
conclusion is supported by a 2007 meta-analysis (40) that
included six of the aforementioned studies (17, 27, 30, 33, 36,
37), which concluded that low GI/GL diets result in statistically
significant reductions of approximately 1 kg in weight, 1 kg in
total fat mass, and 1.3 units of BMI by comparison to the
control diets in adolescents and adults (P \ 0.05 for all three
outcomes) (40). Moreover, a more inclusive recent meta-analy-
sis by Livesey et al. (41), which included results from 23
studies that measured weight loss in low GI/GL diets showed
that body weight fell with reduction in dietary GL and vice
versa in studies where; (a) subjects are under ‘‘free-living’’
conditions and (b) food intake control is limited (41). Weight
loss, however, was not a primary outcome measure in a number
of the studies included in this meta-analysis. Despite the poten-
tially beneficial role for low GI/GL diets in weight loss there
are a number of limitations that need to be addressed.
First, several studies in this review were not designed to
induce weight loss by restricting the caloric intake of the parti-
cipants. Even though low GI diets have been shown to increase
satiety, this is not a proven mechanism of action. Therefore, in
cases where caloric intake was not restricted, it would have
been helpful if the effect of the diet on satiety were assessed.
Second, evidence suggests that weight maintenance is crucial
for sustaining the physiological benefits associated with a reduc-
tion in weight (42). However, none of these studies were
designed specifically to compare weight regain between the
groups. Therefore, future interventions should focus on weight
maintenance following a significant reduction in weight.
Third, in several studies the GI/GL values were not reported.
Furthermore, even in the studies where the GI and GL values
were reported it was not necessarily indicated whether the
reported GI values were based on the glucose or bread scales.
To further complicate matters, there was significant variability
in what was considered low GI or high GI diets. For instance,
in one study (25) the GI units were 55.5 and 63.9 (difference of
8.4 units) while in another 78.6 and 102.8 (difference of 24.2)
for low- and high-GI diets, respectively (37). Even though these
differences in GI were statistically significant in both studies,
the clinical significance of these differences should be assessed.
In addition, more research has to be conducted to determine
how GI/GL values and ranges relate to study findings.
CONCLUSION
Over the past decade, the body of research that links low GI/
GL diets to weight loss has grown rapidly and significantly.
While there is a significant amount of inconsistency in the cur-
rent findings, the majority of studies found a trend that favored
12 ESFAHANI ET AL.
low GI/GL diets in weight loss. A pooled analysis of the current
data may therefore be useful for placing the topic of low GI/GL
diets and weight loss in a better perspective. However, more
importantly, more long-term, large randomized controlled clini-
cal trials, designed for weight loss, with large differences in
dietary GI/GL between test and control groups are required.
Furthermore, more ‘‘real world’’ effectiveness studies that assess
long-term weight maintenance need to be conducted, in addition
to studies that aim to determine the possible mechanisms of
action. However, even if ‘‘a calorie is a calorie,’’ the benefits of
low GI and GL diets extend beyond weight loss and have favor-
able effects on obesity-related risk factors such as heart disease
and diabetes by mechanisms that are independent of weight
loss (4).
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