…according to a recent report in Nutrition, Metabolism & Cardiovascular Disease. LDL cholesterol is the type we think contributes to coronary artery disease and other forms of atherosclerosis.
Learn about glycemic index at NutritionData.
…according to a recent report in Nutrition, Metabolism & Cardiovascular Disease. LDL cholesterol is the type we think contributes to coronary artery disease and other forms of atherosclerosis.
Learn about glycemic index at NutritionData.
The American Diabetes Association has published a list of Top 10 Diabetes Superfoods. They share a low glycemic index and provide key nutrients, according to the ADA. Click the link for details. Here they are in no particular order:
Regular readers here know I have no problem generally with regular or high-fat versions of dairy products. An exception would be for people trying to lose weight while still eating lots of carbohydrates; the low- and no-fat versions could have lower calorie counts, which might help with weight management.
But compare non-fat and whole milk versions of yogurt in the USDA nutrient database. One cup of non-fat fruit variety yogurt has 233 calories, compared to 149 calories in plain whole milk yogurt. The “non-fat” version reduced the fat from 8 to 2.6 g (not zero g) and replaced it with sugars (47 g versus 11 g).
Unfortunately, your typical supermarket yogurts are low-fat yet loaded with sugar or high fructose corn syrup that impede weight loss.
Nevertheless, this superfoods list may give us some guidance in design of a Diabetic Mediterranean Diet. Except for “fat-free,” everything else on the list is a component of the traditional healthy Mediterranean diet. “Fat-free” is a modern invention and not necessarily an improvement.
Beans and peas improve control of blood sugar in diabetics and others, according to a recent report from Canadian researchers. The effect is modest.
Dietary pulses are dried leguminous seeds, including beans, chickpeas, lentils, and peas. Pulses fed to healthy volunteers have a very low glycemic index, meaning they don’t cause much of a rise in blood sugar compared to other carbohydrates. They are loaded with fiber and are more slowly digested than foods such as cereals.
Investigators examined 41 clinical trials (1,674 participants) on the effects of beans and peas on blood glucose control, whether used alone or as part of low-glycemic-index or high-fiber diets. Eleven trials looked at the effect of beans and peas alone, with the experimental “dose” averging 1oo g per day (about half a cup). The article doesn’t specify whether the weight of the pulse was the dry weight or the prepared weight. I will assume prepared.
Pulse given alone or as part of a high-fiber or low-glycemic index diet improved markers of glucose control, such as fasting blood sugar and hemoglobin A1c. The absolute improvement in HgbA1c was around 0.5%. Effects in healthy non-diabetics were less dramatic or non-existent.
This study was very difficult for me to digest. The researchers lumped together studies on diabetics and non-diabetics, using various doses and types of pulses. No wonder they found “significant interstudy heterogeneity.”
Cardiovascular disease is common in diabetics. I’m aware of at least one study linking legume consumption with lower rates of cardiovascular disease. I was hoping this study would answer for me whether I should recommend legumes such as peas and beans for my type 2 diabetics. Beans and peas do represent a low glycemic load, which is good. But I think I’ll have to keep looking for better-designed studies.
Reference: Sievenpiper, J.L., et al. Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetes. Diabetologia, 52 (2009): 1,479-1,495. doi: 10.1007/s00125-009-1395-7
Duke University (U.S.) researchers demonstrated better improvement and reversal of type 2 diabetes with an Atkins-style diet, compared to a low-glycemic index reduced-calorie diet.
Ninety-seven overweight and obese adults, 78% women and 40% black, were randomly assigned to either:
Thirty-eight were in the Atkins group; 46 in the low-glycemic index (low-GI) group. Seventeen dropped out of each group before the end of the 24-week study. Average weight was 234.3 pounds (106.5 kg); average body mass index was 37. The Atkins group averaged 13% of total calories from carbohydrate; the low-GI cohort averaged 44%.
Both groups lost weight and had improvements in hemoglobin A1c, fasting insulin, and fasting glucose.
The Atkins group lowered their hemoglobin A1c by 1.5% (absolute drop, not relative) versus 0.5% in the other group.
The Atkins group lost 11.1 kg versus 6.9 kg in the other group.
The Atkins group increased HDL cholesterol by5.6 mg/dl versus no change in the other group.
All the aforementioned comparisons were statistically significant.
Diabetes medications were stopped or reduced in 95% of the Atkins group versus 62% of the low-GI group.
Total and LDL cholesterol levels were unchanged in both groups.
Triglycerides fell significantly only in the Atkins group.
You may be interested to know that this study was funded by the Robert C. Atkins Foundation.
One strength of this study is that it lasted for 24 months. Many similar studies last only eight to 12 weeks. A drawback is that, with all the drop-outs, the number of participants is low.
The GI Diet performed pretty well, too, all things considered. Sixty-two percent reduction or elimination of diabetes drugs—not bad. For a six-year-old book, it’s still selling fairly well at Amazon.com. That may be why they chose it as the comparison diet.
The diet with fewer carbohydrates—Atkins induction—was most effective for improving control of blood sugars. So effective, in fact, that the researchers sound a note of warning:
For example, participants taking from 40 to 90 units of insulin before the study were able to eliminate their insulin use, while also improving glycemic control. Because this effect occurs immediately upon implementing the dietary changes, individuals with type 2 diabetes who are unable to adjust their own medication or self-monitor their blood glucose should not make these dietary changes unless under close medical supervision.
[Not all insulin users were able to stop it.]
Overall, lipids were improved or unchanged in the Atkins group, despite the lack of limits on saturated fat intake. A common criticism of the Atkins diet is that it has too much saturated fat, leading to higher total and LDL cholesterol levels, which might raise long-term cardiovascular risks. Not so, here.
When you reduce carbohydrate intake, the percentages of fat and protein in the diet also change. In this Atkins diet, protein provided 28% of daily calories, and fat 59%. In the low-GI diet, protein provided 20% of daily calories, fat 36%. The beneficial effects of the Atkins diet probably reflect the low carbohydrate consumption rather than high protein and fat.
The Atkins induction-phase diet was clearly superior to the low-glycemic index diet in this overweight diabetic sample, without restricting calories.
Reference: Westman, Eric, et al. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutrition & Metabolism 2008, 5:36 doi:10.1186/1743-7075-5-36
Samaha, F., et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. New England Journal of Medicine, 348 (2003): 2,074-2,081.
Boden, G., et al. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Annals of Internal Medicine, 142 (2005): 403-411.
Vernon, M., et al. Clinical experience of a carbohydrate-restricted diet: Effect on diabetes mellitus. Metabolic Syndrome and Related Disorders, 1 (2003): 233-238.
Yancy, W., et al. A pilot trial of a low-carbohydrate ketogenic diet in patients with type 2 diabetes. Metabolic Syndrome and Related Disorders, 1 (2003): 239-244.
Dentists are considering a return to an old theory that dietary carbohydrates first cause dental diseases, then certain systemic chronic diseases, according to a review in the June 1, 2009, Journal of Dental Research.
We’ve known for years that some dental and systemic diseases are associated with each other, both for individuals and populations. For example, gingivitis and periodontal disease are associated with type 2 diabetes and coronary heart disease. The exact nature of that association is not clear. In the 1990s it seemed that infections – chlamydia, for example – might be the unifying link, but this has not been supported by subsequent research.
The article is written by Dr. Philippe P. Hujoel, who has been active in dental research for decades and is affiliated with the University of Washington (Seattle). He is no bomb-throwing, crazed, radical.
The “old theory” to which I referred is the Cleave-Yudkin idea from the 1960s and ’70s that excessive intake of fermentable carbohydrates, in the absence of good dental care, leads both to certain dental diseases – caries (cavities), periodontal disease, certain oral cancers, and leukoplakia – and to some common systemic chronic non-communicable diseases such as coronary heart disease, type 2 diabetes, some cancers, and dementia. In other words, dietary carbohydrates cause both dental and systemic diseases – not all cases of those diseases, of course, but some.
Dr. Hujoel does not define “fermentable” carbohydrates in the article. My American Heritage Dictionary defines fermentation as:
As reported in David Mendosa’s blog at MyDiabetesCentral.com, Dr. Hujoel said, “Non-fermentable carbohydrates are fibers.” Dr. Hujoel also shared some personal tidbits there.
In the context of excessive carbohydrate intake, the article frequently mentions sugar, refined carbs, and high-glycemic-index carbs. Dental effects of excessive carb intake can appear within weeks or months, whereas the sysemtic effects may take decades.
Hujoel compares and contrasts Ancel Keys’ Diet-Heart/Lipid Hypothesis with the Cleave-Yudkin Carbohydrate Theory. In Dr. Hujoel’s view, the latest research data favor the Carbohydrate Theory as an explanation of many cases of the aforementioned dental and systemic chronic diseases. If correct, the theory has important implications for prevention of dental and systemic diseases: namely, dietary carbohydrate restriction.
Adherents of the paleo diet and low-carb diets will love this article; it supports their choices.
I agree with Dr. Hujoel that we need a long-term prospective trial of serious low-carb eating versus the standard American high-carb diet. Take 20,000 people, randomize them to one of the two diets, follow their dental and systemic health over 15-30 years, then compare the two groups. Problem is, I’m not sure it can be done. It’s hard enough for most people to follow a low-carb diet for four months. And I’m asking for 30 years?!
Dr. Hujoel writes:
Possibly, when it comes to fermentable carbohydrates, teeth would then become to the medical and dental professionals what they have always been for paleoanthropologists: “extremely informative about age, sex, diet, health.”
Dr. Hujoel mentioned a review of six studies that showed a 30% reduction in gingivitis score by following a diet moderately reduced in carbs. He mentions the aphorism: “no carbohydrates, no caries.” Anyone prone to dental caries or ongoing periodontal disease should do further research to see if switching to low-carb eating might improve the situation.
Don’t be surprised if your dentist isn’t very familiar with the concept. Has he ever mentioned it to you?
Steve Parker, M.D.,
Author of The Advanced Mediterranean Diet
Reference: Hujoel, P. Dietary carbohydrates and dental-systemic diseases. Journal of Dental Research, 88 (2009): 490-502.
Mendosa, David. Our dental alarm bell. MyDiabetesCentral.com, July 12, 2009.
A Canadian study last year found no overall effect on type 2 diabetes control by using a low-glycemic-index diet and lower-carbohydrate diet, although the low-glycemic-index diet did reduce post-meal glucose levels and C-reactive protein.
For many years, a high-fat, low-carbohydrate diet was recommended for type 2 diabetics. Then in 1979 the American Diabetes Association recommended a high-carb, low-fat diet. Later, the ADA allowed more fat, mostly monounsaturated.
The experts are still debating how much and what kind of carbohydrate people with diabetes should eat. Recent years have seen a trend towards lower carbohydrate intake and lower-glycemic-index eating. Much of the supportive evidence we have is based on short-term studies – six to 12 weeks.
A Cochrane review in 2004 concluded that there was no high-quality data on the effectiveness of dietary treatment of diabetes.
The authors of the Canadian study at hand wrote:
Although almost everyone would agree that diet is the cornerstone of diabetes therapy, there is marked disagreement about what kind of dietary advice is best, particularly with respect to dietary carbohydrate.
We can put a man on the moon, but still aren’t sure what’s the best diet for people with diabetes despite years of experience and experimentation.
The Canadian researchers aimed to compare the effects of altered glycemic index and amount of carbohydrate on hemoglobin A1c, blood glucose, lipids, and C-reactive protein in men and women with type 2 diabetes.
162 subjects with mild diabetes, 35-75 years old, managed by diet alone, were randomly assigned to one of three diet groups:
Average body mass index was 31 (mildly obese); average weight 83 kg (183 lb). The study lasted one year, a major strength of the study.
Results One Year Later
Hemoglobin A1c rose from 6.1% to 6.3%, with no difference between the various diet groups. There were no differences in insulin levels, whether fasting or two hours after an oral glucose tolerance test. Blood sugar levels after a glucose tolerance test were 7% lower with the low-GI diet compared to the other diet groups. No difference in LDL cholesterol levels. Little effect on triglycerides and HDL cholesterol. No differences in weight. C-reactive protein in the high-GI group fell from3.34 mg/L to 2.75. C-reactive protein in the low-GI group fell from 2.64 to 1.95. [All these C-reactive protein readings are in the normal range.]
Nearly all the people with diabetes I encounter are very different from this study cohort: they are on drug therapy for diabetes. So the results here don’t necessarily apply to the more typical cases of moderate or severe diabetes that require one or more glucose-control drugs.
Low-carb diet advocates can justifiably argue that the carb intake was still too high, and that’s why their numbers weren’t better. Vernon and Eberstein in their book, Atkins Diabetes Revolution, note that many people with type 2 diabetes will have to limit carboydrates (“net carbs”) to 40-60 grams a day. In the study at hand, the low-carb diet aimed for 39% of calories from carbohydrates. On a 2000-calorie diet, that’s 195 grams – a far cry from 60 grams.
Low-Gi advocates also can justifiably argue that the glycemic index was not low enough to make a difference. The researchers admit that the test diet reductions in carb intake and glycemic index were “modest.” Perhaps they thought that more drastic reductions were unsustainable.
Attempts to control diabetes with low-carb or low-glycemic-index eating should make more dramatic changes.
The low-glycemic-index diet lowered two-hour glucose levels on the glucose tolerance tests. The authors state that this parameter is a better indicator of heart disease risk – lower in this case – than are fasting glucose levels. Findings suggests improvements in insulin resistance and/or pancreas beta cell function. This finding may have no real-world clinical significance: remember that hemoglobin A1c levels were the same across all groups.
The changes in C-reactive protein just don’t seem clinically significant to me (nor to an editorialist in the same journal issue).
The aforementioned editorialist, Dr. Xavier Pi-Sunyer, had an interesting comment:
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.
I would emphasize “. . . in patients with early type 2 diabetes.”
A Mediterranean-style diet, then, could be just as effective as, if not better than, all the other “diabetic diets” out there.
Steve Parker, M.D.
References: Wolever, Thomas, et al. The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein. American Journal of Clinical Nutrition, 87 (2008); 114-125.
Additional Resource: Michael R. Eades, M.D. Making worthless data confess. The Blog of Michael R. Eades, December 13, 2008. Accessed July 10, 2009. [Highly critical analysis from a leading low-carb, high-protein advocate.]
The concept of glycemic index was introduced by Jenkins et al in 1981 at the University of Toronto.
Studies investigating the association between disease risk and GI/GL have been inconsistent. By “inconsistent,” I mean some studies have made an association in one direction or the other, and other studies have not. Diseases possibly associated with high-glycemic diets have included diabetes, cardiovascular disease, cancer, gallbladder disease, and eye disease.
“Diet” in this post refers to a habitual way of eating, not a weight loss program.
Researchers with the University of Sydney (Sydney, Australia) identified the best-designed published research reports investigating the relationship between certain chronic diseases and glycemic index and load. The studied diseases were type 2 diabetes, coronary heart disease, stroke, breast cancer, colorectal cancer, pancreatic cancer, endometrial cancer, ovarian cancer, gallbladder disease, and eye disease.
Literature databases were searched for articles published between 1981 and March, 2007. The researchers found 37 studies that enrolled 1,950,198 participants ranging in age from 24 to 76, with BMI’s averaging 23.5 to 29. These were human prospective cohort studies with a final outcome being occurrence of a chronic disease (not its risk factors). Twenty-five of the studies were conducted in the U.S., five in Canada, five Europe, and two in Australia. Ninety percent of participants were women [for reasons not discussed]. Food frequency questionnaires were used in nearly all the studies. Individual studies generated between 4 to 20 years of follow-up, and 40,129 new cases of target diseases were identified.
Associations between GI, GL, and risk of developing a chronic disease were measured as rate ratios comparing the highest with the lowest quantiles. For example, GI and GL were measured in the study population. The population was then divided into four groups (quartiles), reflecting lowest GI/GL to medium to highest GI/GL diets. The lowest GI/GL quartile was compared with the highest quartile to see if disease occurrence was different between the groups. Some studies broke the populations into tertiles, quintiles, deciles, etc.
Comparing the highest with the lowest quantiles, studies with a high GI or GL independently
Overall, high GI was more strongly associated with chronic disease than was high GL
So low-GI diets may offer greater protection against disease than low-GL diets.
Comments from the Researchers
They speculate that low-GI diets may be more protective than low-GL because the latter can include low-carb foods such as cheese and meat, and low-GI, high-carb foods. Both eating styles will reduce glucose levels after meals while having very different effects in other areas such as pancreas beta cell function, free fatty acid levels, triglyceride levels, and effects on satiety.
High GI and high GL diets, independently of known confounders, modestly increase the risk of chronic lifestyle-related diseases, with more pronounced effects for type 2 diabetes, coronary heart disease, and gallbladder disease.
. . . 90% of participants were female; therefore, the findings may not be generalizable to men.
There are plausible mechanism linking the development of certain chronic diseases with high-GI diets. Specifically, 2 major pathways have been proposed to explain the association with type 2 diabetes risk. First the same amount of carbohydrate from high-GI food produces higher blood glucose concentrations and a greater demand for insulin. The chronically increased insulin demand may eventually result in pancreatic beta cell failure, and, as a consequence, impaired glucose tolerance. Second, there is evidence that high-GI diets may directly increase insulin resistance through their effect on glycemia, free fatty acids, and counter-regulatory hormone secretion. High glucose and insulin concentrations are associated with increased risk profiles for cardiovascular disease, including decreased concentrations of HDL cholesterol, increased glycosylated protein, oxidative status, hemostatic variables, and poor endothelial function
Low-GI and/or low-GL diets are independently associated with a reduced risk of certain chronic diseases. In diabetes and heart disease, the protection is comparable with that seen for whole grain and high fiber intakes. The findings support the hypothesis that higher postprandial glycemia is a universal mechanism for disease progression.
Studies like this tend to accentuate the differences in eating styles since they compare the highest with the lowest post-prandial (after meal) glucose levels. Most people are closer to the middle of the pack, so a person there has potentially less to gain by moving to a low-GI diet. But still some to gain, on average, particularly in regards to avoiding type 2 diabetes and coronary heart disease.
[To be fair, many population-based studies use this same quantile technique. It increases the odds of finding a statistically significant difference.]
Only two of the 37 studies examined coronary heart disease, the cause of heart attacks. One study was the massive Nurses’ Health Study database with 75,521 women. The other was the Zutphen (Netherlands) Elderly Study which examined men 64 and older. Here’s the primary conclusion of the Zutphen authors verbatim:
Our findings do not support the hypothesis that a high-glycemic index diet unfavorably affects metabolic risk factors or increases risk for CHD [coronary heart disease] in elderly men without a history of diabetes or CHD.
So there’s nothing in the meta-analysis at hand to suggest that high-GI/GL diets promote heart disease in males in the general population.
However, the recent Canadian study in Archives of Internal Medicine found strong evidence linking CHD with high-glycemic index diets. Although not mentioned in the text of that article, Table 3 on page 664 shows that the association is much stonger in women than in men. Relative risk for women on a high-glycemic index/load diet was 1.5 (95% confidence interval = 1.29-1.71), and for men the relative risk was 1.06 (95% confidence interval = 0.91-1.20). See reference below.
Nine of the 37 studies examined the occurrence of type 2 diabetes. Only one of these studied men only – 42,759 men: the abstract is not available online and the Sydney group does not mention if high-GI or high-GL was positively associated with onset of diabetes in this cohort. Two of the diabetes studies included both men and women, but the abstracts don’t break down the findings by sex. [I’m trying to deduce if the major overall findings of this meta-analysis apply to men or not.]
I don’t know anybody willing to change their diet just to avoid the risk of gallstones. It’s only after they develop symptomatic gallstones that they ask me what they can do about them. The usual answer is surgery.
The report is well-done and seems free of commercial bias, even though several of the researchers are authors or co-authors of popular books on low-GI eating.
Barclay, Alan W.; Petocz, Peter; McMillan-Price, Joanna; Flood, Victoria M.; Prvan, Tania; Mitchell, Paul; and Brand-Miller, Jennie C. Glycemic index, glycemic load, and chronic disease risk – a meta-analysis of observational studies [of mostly women]. American Journal of Clinical Nutrition, 87 (2008): 627-637.
Brand-Miller, Jennie, et al. “The New Glucose Revolution: The Authoritative Guide to the Glycemic Index – The Dietary Solution for Lifelong Health.” Da Capo Press, 2006.
Mente, Andrew, et al. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine, 169 (2009): 659-669.