Glycemic index in early type 2 diabetes

In this issue of the Journal, Wolever et al (1) report the results of the Canadian Trial of Carbohydrates in Diabetes. This is an interesting report comparing the effects of highand lowglycemic-index (GI) diets with those of a low-carbohydrate diet on various metabolic markers of disease. The bottom line is that following these 3 diets for 1 y produced essentially no difference in the subject groups with respect to glycated hemoglobin (HbA1c), lipids, or insulin. As reported in a recent Cochrane review (2), few to no high-quality long-term data are available on the dietary treatment of type 2 diabetes mellitus. Therefore, a well-carried-out, extended study such as that of Wolever et al is very welcome, and, from it, several interesting observations emerge. First, the report by Wolever et al shows the difficulty of accurately measuring food intake in overweight persons. The average body mass index (BMI; in kg/m) of the group was 31, and the range was 24–40. The average caloric intake reported with the 3 diets at baseline ranged from 1810 to 1930 with an average weight of 84 kg and at the end of the study ranged from 1800 to 2020 with a slightly higher average weight. Patients did not lose weight; they actually gained. But, even if he or she is very sedentary, a person weighing 84 kg requires more calories than are reported in the study to maintain weight. Thus, the reporting of caloric intake by diaries is shown clearly to be inaccurate, and there is significant underestimation of energy intake. Such underestimation has been reported previously from this laboratory (3) and by many others. The tools for measuring food intake in humans are very imprecise, as documented here. Yet investigators (and journals) persist in publishing such data as if they were accurate and persist in presenting percentages of macronutrients to one decimal place (see Table 3 in reference 1) as if there were any confidence in such decimals. Second, compared with baseline data, these mildly diabetic type 2 patients actually did worse with regard to HbA1c and weight while following each of the 3 experimental diets (1). This finding suggests that we must be careful about disrupting subjects’ or patients’ diets with radical, doctrinaire changes that may actually be counterproductive. Furthermore, the diets had carbohydrate contents that varied from 39% to 52% of energy intake, and yet this variability had no effect on the subjects’ HbA1c. This finding confirms previous reports that the proportion of carbohydrate in the diet is not very important in determining the concentration of fasting blood glucose and that variations of 10% to 15% of total calories make little difference to overall control in patients with early type 2 diabetes. This report is unique in having followed subjects for 1 y and in using careful monitoring of the subjects’ diet and providing continued professional nutritional advice. It is interesting that the long-term results show that the 3 diets had little ultimate effect on either triacylglycerol or HDL-cholesterol concentrations. Thus, the arguments of the champions of a low-GI or a lowcarbohydrate diet—that these 2 types of diets will result in lower triacylglycerol and higher HDL concentrations—have not been upheld in this careful, year-long dietary study. One of the few statistically significant results of the study by Wolever et al was that the cohort following the low-GI diet had a higher fasting glucose and a lower glucose concentration 2 h after an oral glucose challenge than did the subjects following the other 2 diets (1). The difference, however, is small, and its effect on HbA1c is clearly nil. A lower 2-h post-glucose challenge glucose concentration would be expected, but a higher fasting glucose is not. The cause of a higher fasting glucose is not immediately evident, because insulin did not change in these patients. The authors state that the concentrations of free fatty acids (FFAs) were 8% higher than at baseline but not significantly different (data not given), and they suggest that this may be the cause. If the FFA concentrations did not differ significantly between baseline and year 1, FFAs cannot be considered a cause of the higher fasting glucose concentration. In addition, when the results of the breakfast meal from the patients’ initial “regular diet” and those of the breakfast meal from their subsequent “test diet” (see Figure 6 in reference 1) were compared, no significant difference in postprandial glucose excursions was found between the high-GI and low-carbohydrate diets. A slight decrease in postprandial glucose was found in subjects in the low-GI diet group, but, to this observer, it seems biologically insignificant. Wolever et al (1) also observed a drop of 20% from baseline in C-reactive protein (CRP) concentrations with the low-GI diet, but the diet time interaction was not significant. Nevertheless, Wolever et al make much of this result. A few comments seem indicated with regard to this outcome. First, the CRP was significantly different at baseline in the 3 treatment groups (3.34, 2.64,