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Category Archives: Glycemic Index
Julianne Taylor has a fine post with the sciencey details. She talks about insulin, glycogen, digestion, glycemic index, and the benefits of vegetable and fruit carbohydrates over grains.
High blood insulin levels and insulin resistance promote age-related degeneration of the brain, leading to memory loss and dementia according to Robert Krikorian, Ph.D. He’s a professor in the Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati Academic Health Center. He has an article in a recent issue of Current Psychiatry – Online.
Proper insulin signaling in the brain is important for healthy functioning of our brains’ memory centers. This signaling breaks down in the setting of insulin resistance and the associated high insulin levels. Dr. Krikorian makes much of the fact that high insulin levels and insulin resistance are closely tied to obesity. He writes that:
Waist circumference of ≥100 cm (39 inches) is a sensitive, specific, and independent predictor of hyperinsulinemia for men and women and a stronger predictor than body mass index, waist-to-hip ratio, and other measures of body fat.
Dr. Krikorian thinks that dietary approaches to the prevention of dementia are effective yet underutilized. He mentions reduction of insulin levels by restricting calories or a ketogenic diet: they’ve been linked with improved memory in middle-aged and older adults.
Dr. K suggests the following measures to prevent dementia and memory loss:
- eliminate high-glycemic foods like processed carbohydrates and sweets
- replace high-glycemic foods with fruits and vegetables (the higher polyphenol intake may help by itself)
- certain polyphenols, such as those found in berries, may be particularly helpful in improving brain metabolic function
- keep your waist size under 39 inches, or aim for that if you’re overweight
I must mention that many, perhaps most, dementia experts are not as confident as Dr. Krikorian that these dietary changes are effective. I think they are, to a degree.
I’ve written before about how blood sugars in the upper normal range are linked to brain degeneration. Dr. Krikorian’s recommendations would tend to keep blood sugar levels in the lower end of the normal range.
And why should you care?
Because these concepts are related to some common chronic diseases. Diets – i.e., habitual ways of eating – with a high glycemic index or glycemic load increase the risk of type 2 diabetes, coronary heart disease, gallbladder disease, and breast cancer. At least in women.
Glycemic index is a measure of how much a specific food is likely to influence blood sugar (glucose) levels. Carbohydrates we eat, except for fiber, are usually converted by the process of digestion into glucose which we use as fuel. Any glucose not needed immediately for energy is converted into a storage form called glycogen, for use later. We have the capacity to store only a half days’ worth of energy in the form of glycogen. Carbohydrates are converted to fat when eaten in excess of what we can use immediately or store as glycogen.
The standard for glycemic index is set by eating 50 grams of pure glucose, a type of sugar. The pattern of bloodstream glucose levels over the next two hours is given a rank of 100. Oral glucose leads to a more rapid and higher peak in blood sugar compared to nearly all other carbohydrates. All other foods containing carbs (carbohydrates) can be ranked in relation to glucose, on a scale of 0 to 100. Test subjects are given specific foods in whatever serving size contains 50 grams of available carbohydrate, and eaten without other foods. Blood glucose levels are measured repeatedly over the next two hours, and compared to the pattern observed for ingested glucose. The comparison yields a number, the gylcemic index.
Even when they have the same grams of carbohydrate, some foods cause a higher rise in blood sugar. That is, they have a higher glycemic index.
Cashews have a glycemic index (GI) of 22, which means they don’t raise blood sugar nearly as quickly or as much as glucose. An overripe banana has a GI of 52, so it would tend to raise your blood glucose more than cashews. Watermelon’s GI is 72. Doesn’t eating watermelon remind you of drinking flavored sugar water?
With higher GI foods, your body digests and absorbs the foods’ carbs faster, leading to greater release of insulin by the pancreas to reduce the blood sugar levels back to normal.
Some of you have already figured out the the actual rise in blood sugar will depend on other factors, such as how much of the food you eat! To account for the amount of food eaten, the Glycemic Load concept was devised (at Harvard?). You calculate the glycemic load by taking the grams of carbohydrate in the serving size, multiply by the food’s glycemic index, then divide by 100. For example, a cup of white rice has a glycemic load of 33 points; a cup of brown rice has a glycemic load of 23 points.
Remember, the glycemic index is based on the observed blood sugar rise after eating the serving of a food that contains 50 grams of carbohydrate. For example, corn’s glycemic index is 53. One half cup of canned yellow corn has 15.2 grams of carbohydrate. So to get the full glycemic effect, you’d have to eat over one and a half cups of corn. Most people just eat a half cup as a serving. The glycemic load of a half cup of corn is 8 points (15.2 x 53, then divide by 100). Carrots are a classic example of a healthy food with a high glycemic index, but a good/low glycemic load of 2.8 points per half cup (slices, frozen, boiled).
(I’m ignoring for now the grams of nondigestible carbohydrate (fiber) in the corn and carrots.)
Doesn’t this sound just like something you’d like to do at every meal?
Let not your hearts be troubled. You can get most of the pertinent GI’s and GL’s free on the Internet or in various books or pamphlets. If you’re interested.
(Blood sugar and blood glucose are identical. Glucose is also a simple sugar you can eat. I’ve eschewed the term “blood glucose” today to prevent confusion.)
For additional information, see Laura Dolson’s good work at About.com.
WebMD.com has an article on factors that affect glycemic index and glycemic load.
Jenkins, D.J., et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. American Journal of Clinical Nutrition, 34 (1981): 362-366. This paper from the University of Toronto introduced the concept of glycemic index to the world.
Any diet that contains carbohydrates can be ranked as being either low-, medium-, or high-glycemic, referring to the glycemic index or load. This ranking system would apply to both weight-loss diets and habitual ways of eating.
Specific foods with significant amounts of carbohydrate have been tested for their ability to rapidly raise blood sugar levels as compared to eating pure glucose, a type of sugar. The number generated by the test is the glycemic index (GI) and ranges between 0 and 100.
Here are some GI values from Wikipedia’s entry on glycemic index:
Low GI (55 or less)
- most fruit and vegetables (except potatoes, watermelon), grainy breads [made of or resembling grain?], pasta, legumes/pulses, milk, products extremely low in carbohydrates (fish, eggs, meat, nuts, oils), brown rice
Medium GI (56 – 69)
- whole wheat products, basmati rice, orange, sweet potato, table sugar, most white rices (eg, jasmine),
High GI (70 and above)
- corn flakes, baked potato, watermelon, croissant, white bread, extruded cereals (eg, Rice Krispies), straight glucose (100)
Low-GI diets encourage the low-GI foods. High-GI diets favor the high-GI foods. Well, duh!
The Human Nutrition Unit at the University of Sydney (Australia) maintains a free online database of glycemic index values of various foods. For example, the GI of Doritos is 42 (corn chips, plain, salted, 1998).
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
- increased the risk of type 2 diabetes by 27 (GL) or 40% (GI)
- increased the risk of coronary heart disease by 25% (GI)
- increased the risk of gallbladder disease by 26% (GI) or 41% (GL) (gallstones and biliary colic, I assume, but the authors don’t specify)
- increased the risk of breast cancer by 8% (GI)
- increased risk of all studied diseases (11) combined by 14% (GI) or 9% (GL)
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.
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:
- the anaerobic conversion of sugar to carbon dioxide and alcohol by yeast
- any of a group of chemical reactions induced by living or nonliving ferments that split complex organic compunds into relatively simple substances
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?
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.