US Pharm. 2012;37(5)(Diabetes suppl):11-14.

Diabetes mellitus is a metabolic disorder that takes two forms. In type 1 diabetes, the body’s immune system destroys the insulin-producing pancreatic cells. In type 2 diabetes, insulin is produced, but either the pancreas generates insufficient insulin or the body cannot properly utilize it (i.e., reduced insulin receptor sensitivity). Diabetes impairs the body’s ability to transport glucose into fat and muscle tissue.1 Blood glucose (BG) remains elevated, and protein and fat are metabolized to meet the body’s energy needs.1,2 Higher postprandial glucose and insulin levels are thought to contribute to the complications associated with diabetes.3 Sequelae of diabetes are microvascular (neuropathy, retinopathy, and nephropathy) and macrovascular (cardiovascular disease).1,2

The goals of diabetes management are to reduce BMI, prevent complications (hypoglycemia and chronic disease states), and keep BG levels as close to normal as possible. These objectives are accomplished via medication and dietary management.1,3 Conventional dietary recommendations have focused on the amount of carbohydrates (CHO) consumed. The total amount of CHO consumed is important; however, the quality of CHO may have an added benefit.3

The Importance of CHO

The most important source of energy in the human diet is CHO. CHO traditionally have been classified according to their molecular size as sugars, oligosaccharides, polysaccharides, or polyols.1 CHO are broken down into monosaccharides before being absorbed. The digestion of CHO starts in the mouth, but the majority of the process occurs in the small intestine.1 The monosaccharides are glucose, fructose, and galactose. Maltose (from starch) comprises two glucose molecules. Lactose (in dairy products) is composed of one glucose molecule and one galactose molecule, whereas sucrose (table sugar) consists of one glucose molecule and one fructose molecule. These sugars are digested to their constituent monosaccharides and transported through the intestinal wall to the liver via the hepatic portal vein. Fructose and galactose must be converted to glucose by the liver before they can be used as energy. Glucose undergoes one of three possible actions: It may be catabolized to produce adenosine triphosphate (which is used for energy), stored as glycogen (if a sufficient energy supply already exists), or converted into fatty acids (once the glycogen stores of the liver and muscles are saturated).1

The Glycemic Index (GI)

Following dietary guidelines in diabetes management is a universally accepted concept; however, there is no consensus on what constitutes the ideal diet. In 1981, Jenkins and colleagues developed the concept of GI to classify CHO.4 The GI classifies food based on the postprandial glycemic response (GR) following consumption of that food.1

The GI is calculated by measuring the GR of 10 healthy subjects to a test food compared with their GR to pure glucose. First, a subject ingests 50 g of pure glucose (after an overnight fast), and glucose levels are measured every 30 minutes over 2 hours. BG levels are graphed, and the AUC is assigned a value of 100. The same subject ingests 50 g of CHO in the test food (after an overnight fast), and again glucose levels are measured over 2 hours and the AUC is calculated. The GI, which is the percentage of the AUC of the test food compared with that of pure glucose, is calculated by dividing the AUC of the test food by the AUC of pure glucose.4,5

The rates of food digestion and stomach emptying influence the rate of increase in BG and, consequently, the secretion of insulin in response to glucose levels.6 Low-GI foods are digested and absorbed slowly, causing a gradual increase in postprandial BG levels. High-GI foods are digested and absorbed quickly, resulting in large spikes in postprandial BG levels.1 Generally, foods with a high fiber or fat content have a lower GI; however, this is not always the case. For instance, a baked potato with the skin has a high GI despite being a good source of fiber.5

A low GI is considered 55 or less, medium GI is 56 to 69, and high GI is 70 or greater.7 To calculate the GI of a meal, the GI of each food is averaged in proportion to the amount of CHO each contributes.7,8 For instance, the GI of a meal of peaches and low-fat ice cream would be calculated as follows: Total CHO are 60 g (peaches, 20 g; ice cream, 40 g). The GI of peaches is 42, and that of low-fat ice cream is 46. The total GI for the meal is calculated as follows: 42 (GI of peaches) × 20 (CHO in peaches) ÷ 60 (total CHO) = 14; 46 (GI of ice cream) × 40 (CHO in ice cream) ÷ 60 (total CHO) = 31; 14 + 31 = 45 (total GI of meal).7 This example demonstrates that consuming a higher-GI food is not necessarily bad if a low-GI food is eaten in the same meal.

There is no consensus regarding whether the GR is affected by the quantity of CHO in the food. Some experts believe that the quantity of CHO consumed has no effect on the GR, while others think that quantity affects the GR.1 To address this concern, researchers at Harvard University developed the concept of glycemic load (GL) in the 1990s.1 The GL, which accounts for both the quantity and the quality of CHO in a food, is calculated by multiplying the GI by the total amount of CHO divided by 100 (GI/100 × amount of available CHO).1 This is a measure of the total increase of BG following ingestion of a food. A GL of 10 or below is low, 11 to 19 is medium, and 20 or more is high.5 The total GL of a meal is the sum of the GL of each food item.8

The GL can be altered by changing either the overall GI of the meal or the amount of CHO in the meal. Some experts believe that focusing on the overall GI of a meal (by substituting low-GI foods for high-GI foods) is more valuable than focusing on the amount of CHO in a meal.1 This is because CHO are a necessary source of energy and very-low-CHO diets are high in fat. Additionally, many important nutrients (i.e., vitamins, minerals, and fiber) are found in CHO-containing foods.1

Physiologic Responses

After a high-GI food is consumed, a high spike in BG stimulates the pancreatic beta cells to secrete an excessive amount of insulin, and glucagon release is inhibited. Fat oxidation is inhibited by this hyperglycemia, and the level of free fatty acids in the blood remains low. At approximately the midway point of the postprandial stage (2-4 hours), the high insulin spike causes BG to drop rapidly, sometimes to below fasting levels. The oxidation of fat continues to be inhibited, and fatty acid levels remain low. At the late postprandial stage (4-6 hours), the resulting hypoglycemia stimulates counterregulatory hormones (e.g., epinephrine, cortisol, and growth hormone) to restore euglycemia, and fat oxidation is stimulated in order to meet the body’s energy needs. This results in a sizable increase of free fatty acids in the blood, resembling a state of fasting normally seen several hours after food consumption.1,6

The consumption of a low-GI food is followed by a lower but prolonged level of BG. The pancreas secretes less insulin in response to the lower glucose level. Free fatty acids in the blood do not increase dramatically at the late postprandial stage.1

Elevated BG, insulin levels, and free fatty acids can induce insulin resistance. In both nondiabetic and diabetic individuals, regular consumption of high-glycemic foods has a negative impact on the body’s metabolic factors, such as higher 24-hour BG levels, insulin levels, C-reactive protein (CRP) excretion, and glycosylated hemoglobin (A1C) concentrations.6

Adiponectin, a cytokine secreted by adipose tissue, also is affected by BG levels in diabetic patients. Plasma levels of adiponectin are low in patients with insulin-resistant diabetes, and there is evidence that adiponectin improves insulin sensitivity (IS) and glucose metabolism. Plasma adiponectin levels are inversely associated with plasma glucose levels in diabetic patients. In a study of diabetic men, subjects with high-GI and high-GL diets had lower adiponectin levels than those with low-GI and low-GL diets. The difference was dose dependent and independent of dietary fiber intake.9

The GI and Diabetes

Glycemic control is improved with the consumption of a low-GI diet. Low-GI foods result in steadier postprandial glucose levels with lower peaks and less fluctuation.1 Does this mean that the GI has a role in diabetes management? While most international diabetes organizations endorse use of the GI in the prevention and management of diabetes, the American Diabetes Association does not fully advocate it for diabetes prevention because of insufficient evidence of any benefit.10 Data are inconsistent regarding the advantages of maintaining a low-GI diet. Many studies have been done comparing low-GI and high-GI diets and the resultant effects on A1C, lipids, CRP, insulin levels, and BG levels.

There is evidence that the A1C of diabetic patients consuming a low-GI diet is lower than that of patients following a high GI-diet. Although in one study of type 1 diabetic patients LDL and triglycerides (TG) were not affected by the GI of the diet, HDL was higher in patients consuming a low-GI diet. This was independent of dietary fiber intake.11

The Canadian Trial of Carbohydrates in Diabetes assessed the effects of low-GI, high-GI, and low-CHO diets on A1C, plasma glucose, lipids, and CRP in subjects with type 2 diabetes. (CRP is an inflammatory marker associated with a higher risk of cardiovascular disease in diabetes patients.) After 12 months, fasting glucose was higher with the low-GI diet versus the low-CHO diet, but 2-hour postload glucose was lower (consistent with findings from other studies demonstrating greater IS with low-GI diets). There were no significant differences between the low-GI and low-CHO diets in fasting and 2-hour postload insulin concentrations. Compared with the low-CHO diet, the low-GI diet yielded 12% higher TG and 4% lower HDL. There was no difference in total cholesterol:HDL ratio between the low-GI and low-CHO diets. CRP was lowest with the low-GI diet and highest with the high-GI diet. With the low-GI diet, CRP fell throughout the study period to below baseline; CRP continued to rise with the high-GI diet, and with the low-CHO diet CRP was in between. The study failed to demonstrate a significant difference in A1C with any of the diets, perhaps because of the longer study duration or the subjects’ optimal baseline A1C (6.1%).12

In a small crossover study, LDL declined after 4 weeks on a low-GI diet. TG remained unchanged, but free fatty acids declined with the low-GI diet. Lower A1C levels were found with a low-GI diet versus a high-GI diet.3

In a 6-year prospective trial examining the effects of GI on lipids, results varied by gender. In men, a low-GI diet reduced total cholesterol, whereas a low-GL diet reduced LDL. These effects were more pronounced in younger men. In women, there were no overall associations between GI or GL and changes in lipid profile. In younger women and obese women, GI modified LDL levels modestly.13

The Women’s Health Study demonstrated an association between GI and GL diets and LDL, HDL, LDL:HDL ratio, and CRP. Compared with the GI, GL was more strongly associated with HDL and LDL:HDL ratio, and the GI (not GL) was associated with lower LDL and CRP. It was concluded that lower-GI and lower-GL diets resulted in a more favorable lipid profile and lower CRP.14 In a study of Asian Indians (a high-risk diabetes population), high-GL diets were associated with lower HDL levels and higher triglyceride levels.15

A meta-analysis performed in 2008 investigated the effects of low-GI and low-GL diets in patients with diabetes. A low-GI diet resulted in a 0.5% reduction in A1C and a significant reduction in hypoglycemic episodes.16

The GI and Diabetes Prevention

Certain lifestyle choices and medical conditions (e.g., lack of exercise, obesity) have been linked to the development of diabetes. What has been the subject of speculation is whether the amount and characteristics of CHO consumption affect the risk of developing type 2 diabetes.10

In the Whitehall II study, there was no evidence of an increased risk of diabetes with a high-GI diet.8 Likewise, a different study found no protective effects from low-GI or low-GL diets in adults aged 70 to 79 years.10 A third study found no association between the GI or GL and diabetes risk in a cohort of nearly 26,000 men aged 50 to 69 years.17 These studies are consistent with results of other studies. The Atherosclerosis Risk in Communities Study and the Iowa Women’s Health Study found no evidence of a protective effect of a low-GI diet on risk of diabetes.18,19

Other studies noted a direct association between high-GI or high-GL diets and incidence of type 2 diabetes. In two studies, a high-GL, low-cereal-fiber diet increased the incidence of diabetes in women aged 40 to 65 years and men aged 40 to 75 years.20,21 The Nurses’ Health Study II noted a positive correlation between high-GI and low-fiber diets and increased risk of diabetes in women aged 24 to 44 years.22

The conflicting results of these studies were addressed in a meta-analysis examining the relationship between high-GI and high-GL diets and the risk of developing diabetes, as well as other diseases. High-GI and high-GL diets were found to increase the risk of diabetes independent of any other factors. The GI had more of an impact than GL on the risk of chronic disease. In addition, the risks of heart disease, gallbladder disease, and breast cancer were positively associated with the GI. The protective effect of a low-GI diet is comparable to the protective effect of a high-fiber diet.23

The GI of Foods

Jenkins and colleagues calculated the GIs of various foods and then categorized the foods into groups. There was variation between different foods within a group (except dairy products). The average GI for each group was: legumes, 31 ± 3; dairy products, 35 ± 1; fruit, 50 ± 5; biscuits, 60 ± 3; breakfast cereals, 65 ± 5; vegetables, 65 ± 14; sugars, 71 ± 20; and root vegetables, 72 ± 6.4 See TABLE 1 for the GI of some common foods.7


Some of the leading researchers on the GI are at the University of Sydney in Australia. Their Web site, www.glycemicindex.com, lists the GI of many foods, as well as useful resources and additional information.

Ways to Lower the GI

Factors that affect the GI of a food include 1) fructose content; 2) high fiber content (slows gastric emptying and enzymatic hydrolysis); 3) consumption of fat in the meal (slows gastric emptying); and 4) high protein content (stimulates insulin secretion).8 The physical form of the food affects the GI, as does how and whether the food is cooked.1

The GI of a high-GI (but not low-GI) meal may be lowered with the addition of vinegar.24 In healthy subjects, it was found that the consumption of peanuts and vinegar (individually) both lowered the GR to high-GL meals by more than 50% (56% and 54%, respectively). Only vinegar significantly reduced the 60-minute insulin response (IR).25

Potatoes, a staple of the Western diet, have an extremely high GI. In one study, the GIs of and insulinemic responses to freshly boiled potatoes, cold refrigerated potatoes, and cold potatoes with a vinaigrette dressing (vinegar and olive oil) were determined. The GI (but not IR) was lower after the potatoes were refrigerated. Both the GI and IR were lower with the cold potatoes with vinegar (43% and 31%, respectively).26 The GI of a meal is lowered with the addition of low-GI foods.7

Conclusion

There is controversy regarding the beneficial effects of a low-GI diet. Some experts argue that the benefits of a low-GI diet are too small and may not outweigh the benefits of a reduced-CHO diet. There is also concern that the practicality of a low-GI diet is overshadowed by the complexity of implementing it; however, there are simple ways to reduce the overall GI of a meal. Another point to consider is that the low-GI diet has no adverse effects, unlike the low-fat diet, which adversely affects serum HDL and TG.6 Overall, the implementation of low-GI practices into daily meals does no harm and may improve health and the risk of chronic illness.

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