One basic nutritional tenet I subscribe to is the idea that the diet should be based on foods that give relatively slow sustained release of sugar into the blood stream. Some of the reason for this thinking comes from the fact that fast sugar-releasing (high glycaemic index) foods will tend to cause surges in the hormone insulin that can predispose individuals to weight gain, cardiovascular disease and type 2 diabetes. Better stability in blood sugar and insulin is one important way, I believe, to reduce the risk of these major ills.
I was interested to read a study which tested the effects of low and high GI diets in mice. Two groups of mice were fed diets that were the same in macronutrient content (68% carbohydrate, 13% fat and 19% protein). One group of mice ate a diet rich in a form of starch which releases sugar quickly into the blood stream known as amylopectin. The other group of mice ate a diet in which the majority of the starch they ate came from a slower sugar-releasing form of starch known as amylose. The mice were allowed to eat as much food as they wished for a period of up to 40 weeks.
At the end of the study, the weight of the mice in each group was not significantly different.
However, the mice who had eaten the high GI diet had, overall, 40 per cent more body fat.
They also had a greater tendency to ‘insulin resistance’ (a state where the body is somewhat ‘numb’ to the effects of insulin, which in time can lead to type 2 diabetes).
Seeing as insulin is the chief fat-storage hormone in the bodies of both mice and men, it is perhaps not a major surprise that a high GI diet (which will tend to cause considerable insulin secretion) turns out to lead to more in the way of fatty accumulation. However, could a high GI diet have other adverse effects on the body which might lead to the build up of fat?
One possibility here, of course, is that a high GI diet might somehow inhibit the breakdown and metabolism of fat. One way to gauge this is to measure what is known as the ‘respiratory quotient’, which is calculated by analysing the amount of oxygen an individual or animal uses and comparing that with the amount of carbon dioxide released.
Respiratory quotients vary between 0.7 and 1.0. In theory, if an animal or individual were to burn nothing but sugar, their respiratory quotient would be 1.0. Metabolism of nothing but fat would be registered as a respiratory quotient of 0.7. Basically the higher the respiratory quotient, the more sugar and the less fat is being burned metabolically in the body.
The mice in this study being discussed here were subjected to assessment of their respiratory quotients. This revealed that the mice eating the high GI diet had higher respiratory quotients and were therefore burning, relative to the lower GI diet eaters, less fat.
One other interest finding from this study was that, at the end of the study, the mice eating the high GI diet moved less (actually, about half as much) as the mice eating the lower GI diet. The authors speculate that this might reflect better availability of fuel (leading to higher energy) and greater lean body mass (e.g. muscle). Whatever the explanation, the idea that lower GI diet might lead to more in the way of spontaneous activity has obviously important implications if the same were to apply to humans.
We need to be cautious, I think, about over-interpreting the results of this study, primarily because it was performed in mice and not humans. However, what is clear from this study is that higher GI diets, compared to lower GI ones, have the capacity to induce physiological and metabolic changes that predispose towards accumulation of fat in the body. It provides support for the notion that for optimal health, the diet should be based on foods that tend not to disrupt blood sugar levels. Suitable foods from this perspective include meat, fish, eggs, green vegetables, some fruits including apples and berries, nuts and seeds.
References:
Scribner KB, et al. Long-term effects of dietary glycemic index on adiposity, energy metabolism and physical activity in mice. Am J Physiol Endocrinol Metab. Sept 9, 2008 [Epub ahead of print]