The application of the glycemic index and glycemic load in weight loss: A review of the clinical evidence
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 prevention 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. © 2011 IUBMB IUBMB Life, 63(1): 7–13, 2011
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 constitutes 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 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 glycemic 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 consumes 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 carbohydrate in that food or diet divided by 100 (14). For a meal, GL is calculated by multiplying the mean GI weighted according 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 metabolic 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 children 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 comparison with reduced fat diets (17, 19). Ebbeling et al. (17) in a 12 month (6 months intervention + 6 months follow-up) clinical trial showed that a low GL diet prescribed ad libitum is more effective in promoting weight loss than a calorie-restricted, traditional reduced fat diet (25–30% of total energy from fat). The study demonstrated statistically significant reductions in fat mass (−3.0 ± 1.6 vs. 1.8 ± 1.0 kg; P = 0.01) and BMI (−1.3 ± 0.7 vs. 0.7 ± 0.5 kg/m2; P = 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 approximately 4.3 months in length, demonstrated statistically significant reductions in weight (−2.03 ± 0.59 vs. 1.31 ± 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 not only verify these findings but also determine if low GI/GL diets are more effective than other dietary alternatives.
Table 1. Summary of clinical trials that assess the effect of low GI/GL diets on weight loss in children and adults
|Abete et al. (24)||32 (14f ; 18m)||8 weeks||36 ± 1.2||32.5 ± 0.8||Low GI (40-45) vs. High GI (60-65)||−5.3 ± 0.65%||−7.5 ± 0.73%c|
|Aston et al. (25)d||26 Females (19 completers)||12 weeks||51.9 ± 1.7||33.1 ± 1.1||Low GI (55.5) vs. High GI (63.9)||1.7 ± 5.0 kg||1.6 ± 4.9 kg|
|Bahadori et al. (26)||120 (66f ; 54m) (109 (61f ; 48m) completers)||24 weeks||44||33.4 ± 4.4||Low GI||No Control||−8.9 kg|
|Bellisle et al. (39)||96 females (65 completers)||12 weeks||45.7 ± 1.6||30.3 ± 0.5||Low GI Weight Watchers vs. Standard Weight Watchers||−4.5 ± 3.4 kg||−4.0 ± 3.1 kg|
|Bouche et al. (27)§||11 males||5 weeks||46 ± 3||28 ± 1.0||Low GI (41) vs. High GI (71)||0.5 ± 3.3 kg||−0.3 ± 3.3 kg|
|Das et al. (28)||34 (26f ; 8m) (29 completers)||6 months + 6 months follow-up||34.5 ± 0.9||27.6 ± 0.2||Low GI (52) vs. High GI (85)||−9.1 ± 1.1%||−10.4 ± 1.1%|
|De Rougemont et al. (29)||38 (18f ; 20m)||5 weeks||38.4 ± 1.5||27.4 ± 0.2||Low GI (46.5) vs. High GI (66.3)||−0.2 ± 0.2 kg||−1.1 ± 0.3 kgc|
|Ebbeling et al. (17)||16 (11f ; 5m) (14 completers)||6 months + 6 monthsfollow-up||16.1 ± 0.8||36.0 ± 0.8||Low GL (GL: 68) vs. Low Fat (GL: 77)||BMI: +0.02 ± 0.46 kg/m2||BMI: −0.96 ± 0.75 kg/m2c|
|Ebbeling et al. (30)||34 (30f : 4m) (23 completers)||6 months + 6 monthsfollow-up||28.4 ± 1.0||32.5 ± 1.2||Low GL (GL: 54) vs. Low Fat (GL: 78)||−7.8 ± 1.5%||−8.4 ± 1.5%|
|Ebbeling et al. (31)||73 (58f : 15m)||6 months+ 12 months follow-up||27.5 ± 0.5||36.9 ± 0.7||Low GL (GL: 35-40) vs. Low Fat (GL: 65-70)||−3.5 ± 1.0 kge||−4.5 ± 1.0 kge|
|Fajcsak et al. (18)f||9 (3f ; 6m) (8 completers)||6 weeks||11.0 ± 0.4||24.7 ± 1.3||Low GL||No Control||Body fat: −3.9 ± 2.4%|
|Maki et al. (32)||86 (58f ; 28m) (84 completers)||12 weeks + 24 weeks follow-up||49.7 ± 1.18||31.9 ± 0.4||Low GL (46) vs. Low Fat (51)||−2.5 ± 0.5 kg||−4.9 ± 0.5 kgc|
|McMillan-Price et al. (33)||129 (98f : 31m)||12 weeks||31.8 ± 0.8||31.2 ± 0.4||High-Carb/High GI (HCHGI; 70) vs. High-Carb/Low GI HCLGI; 45) vs. High-Protein/High GI (HPHGI; 59) vs. High-Protein/Low GI (HPLGI; 44)||HCHGI: −3.7 ± 0.5 kg; HPHGI: −5.3 ± 0.5 kg||HCLGI: −4.8 ± 0.5 kg; HPLGI: −4.4 ± 0.5 kg|
|Pereira et al. (23)||39 (30f : 9m)||Variedg||30.5 ± 0.9||91.5 ± 2.3 kg||Low GL (50) vs. Low Fat (82)||−9.5 ± 0.3 of body weight in 69.4 ± 3.8 d||−9.6 ± 0.3 of bodyweight in 65.2 ± 3.3 d|
|Pittas et al. (34)||32 (25f ; 7m)||6 months||34.7 ± 0.9||27.6 ± 0.3||Low GL (53) vs. High GL (86)||−7.2 kg||−7.7 kg|
|Raatz et al. (35)||29 (24f ; 5m)||12 weeks + 24 weeks follow-up||18-70||36.3 ± 1.0||Low GI (33) vs. High GI (63) vs. High Fat (59)||High GI: −9.3 ± 1.3 kg; High Fat: −8.4 ± 1.5 kg||−9.95 ± 1.4 kg|
|Retterstol et al. (22)h||16 males||4 weeks||36-66||30.4 (26.6-34.9) Median (range)||Lipid Lowering vs. Low GI vs. High GI||HGI: 0 kg Lipid Lowering: −1.4 kg (range: −3.6 to 0.2)||−2.4 kg [Range: −3.9 to −1.4]|
|Sichieri et al. (21)||203 females (123 completers)||18 months||37.3 ± 0.3||26.8 ± 0.1||Low GI (40) vs. High GI (79)||−0.26 ± 0.46 kg||−0.41 ± 0.37 kg|
|Slabber et al. (36)||30 females||12 weeks||35.2 ± 1.1||34.8 ± 0.8||Low GI vs. Standard Energy Restricted Diet||−7.41 ± 1.09 kg||−9.34 ± 0.64 kg|
|Slabber et al. (36)h||16 females||12 weeks||N/A||N/A||Low GI vs. Standard Energy Restricted Diet||−4.48 kg||−7.42 kgc|
|Sloth et al. (37)||45 females||10 weeks||29.8 ± 0.9||27.6 ± 0.2||Low GI vs. High GI||−1.3 ± 0.3 kg||−1.9 ± 0.5 kg|
|Spieth et al. (19)i||107 (58f: 49m)||4.3 months||10.4 ± 0.3||33.3 ± 0.7||Low GI vs. Low Fat||1.31 ± 0.72 kg||−2.03 ± 0.59 kgc|
|Thompson et al. (38)||90 (77f ; 13m) (72 completers)||48 weeks||41.4 ± 0.9||34.8 ± 0.3||High Calcium/Low GI (LGI) vs. High Calcium (HC) vs. Moderate Calcium/Moderate Fiber (MCMF)||HC: −8.8 ± 1.37 kg; MCMF: −9.1 ± 1.30 kg||−8.8 ± 1.42 kg|
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 primary 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. Conversely, 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 (−4.5 ± 3.4 kg vs. −4.0 ± 3.1 kg; P = 0.68).
A study by Aston et al. (25) showed a nonsignificant weight gain in both the groups (P = 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 = 0.17 between treatments). 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 = 0.88 between treatments).
The majority of studies in adults also reported on other outcomes 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 percentage body fat or fat mass, only two (27, 29) reported statistically 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 populations. 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 (−5.8 kg vs. −1.2 kg; P = 0.004 and −2.6% vs. 0.9%; P = 0.03, respectively). 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-carbohydrate/low GI diet induces a statistically significant drop in fat mass when compared with a high-carbohydrate/high GI diet in women (n = 98).
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-analysis 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 potentially 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 participants. 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 reduction 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.
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 current findings, the majority of studies found a trend that favored 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 clinical 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 favorable effects on obesity-related risk factors such as heart disease and diabetes by mechanisms that are independent of weight loss (4).