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Unsugarcoated: The high glycemic path to metabolic disease
When people hear mention of the glycemic index, they often think about measuring carbs.
But in my last post, I hope I made it clear that the glycemic index is also about measuring disease risk.
That’s because insulin, produced and excreted from your pancreas, is the all-important hormone for each cell of your body; it is the “key” that opens the gate (on the cell membrane) for glucose to enter.
In addition to causing sugar to enter the cell for energy production, it also stimulates your liver to store glucose (as glycogen).
We know that consuming high glycemic foods spikes your blood sugar, which in turn stimulates insulin secretion.
What’s so bad about these repeated insulin surges?
The repeated insulin surges lead to insulin resistance (insulin stops being effective). What happens to blood sugar in this case? It remains elevated in the bloodstream — a condition known as diabetes.
Insulin resistance, therefore, is the main problem behind metabolic syndrome — a cluster of conditions that increase your risk for many other diseases.
Metabolic syndrome
In 1998 the World Health Organization defined “metabolic syndrome” as the combination of hypertension, low HDL, high triglycerides, insulin resistance, glucose intolerance or type 2 diabetes, high waist-to-hip ratio, and albumin protein in the urine (microalbuminuria).
Remember that high-glycemic food consumption causes:
- Increased production of free fatty acids and fat storage (obesity). It is thought that your body changes sugar into 2 to 5 times more fat in the bloodstream than it does starch (starch is a complex carbohydrate that does not surge insulin nor cause obesity)
- Decreased fat oxidation (i.e. fat does not get used as an energy source)
- 2 hours after consuming high glycemic foods (e.g. a glazed donut) the nutrients are gone but the insulin surge remains… so you get a drop in your blood sugar, which then triggers hunger even more
- It is known that high glycemic foods increase the amount of food that you eat
Therefore, high-glycemic food consumption directly promotes metabolic syndrome, obesity and disease.
The high-glycemic foods
The Glycemic Index (GI) gives a number value to foods relative to glucose itself, which is 100 on the GI scale. It ranks food as to how quickly they get absorbed across your intestinal wall and into your blood. As a general rule:
- Low-GI foods are below 55
- Moderate-GI foods are 56-70
- High-GI foods are above 70.
Here are some examples of foods and their GI score:
- Glucose 100
- Mashed potato 87
- Rice milk 86
- Baked potato 85
- Cornflakes 81
- Watermelon 76
- White bread 71
- Sucrose 65
- White rice 64
- Honey 61
- Pineapple 59
- Muesli cereal 57
- Sweet corn 54
- Banana 51
- Spaghetti 42
- All-bran cereal 42
- Boiled carrots 39
- Raw apple 36
- Soy milk 34
- Kidney beans 28
- Peanuts 16
- Fructose 15
You will find it interesting to see the GI of many other foods listed on the Harvard Health website.
Note that foods high on the glycemic index (GI) not only produce more sugar in your bloodstream, but they are low in fiber and micronutrients.
Advantages of a low-glycemic diet
People dieting on a Low-GI diet had many advantages over those on a high-GI diet even though both groups lost the same amount of weight:
- Low-GI dieters lost more body fat
- Low-GI dieters lost less muscle
- Low-GI dieters’ decline in calorie burning was half that of high-GI dieters
- Low-GI people kept weight off better after calorie restriction was lifted
- Low GI diet people had better satiety
Furthermore, in a crossover study of two groups of men who spent equal time on a low-glycemic diet as they did a high-glycemic diet, there was equal weight loss, but the low-GI diet period resulted in greater fat loss and lower waist circumference compared to their high-GI diet period.
Now when you add in a high fiber component to the diet, you have even more benefits — and we’ll talk about that in my next article.
Michael Cutler, M.D.
Sources:
- Beck, Nielsen H, Pedersen O, Schwartz S. Effects of Diet on the Cellular Insulin Binding and the Insulin Sensitivity in Young Healthy Subjects — Diabetologia. 1978;15:289-296.
- Nutrition Health Review. Fall 85. “Sugar Changes into Fat Faster than Fat”
- Allen S. Levine, Catherine M. Kotz, and Blake A. Gosnell. Sugars and Fats: The Neurobiology of Preference — J. Nutr.2003 133:831S-834S.
- Yoo, Sunmi, et al. Comparison of Dietary Intakes Associated with Metabolic Syndrome Risk Factors in Young Adults: the Bogalusa Heart Study — Am J Clin Nutr. 2004 Oct;80(4):841-848.
- “Bupropion SR in obesity: A randomized double-blind placebo-controlled study.” Gadde KM, et al. — Duke University Medical Center. Presented at the American Psychiatric Association annual meeting, May 18, 1999.
- Munro, JF, et al. Comparison of Continuous and Intermittent Anorectic Therapy in Obesity — British Medical Journal 1:352-354,1968.
- Munro JF. “Clinical aspects of the treatment of obesity by drugs: a review” — Int J Obes. 1979;3(2):171?180.