An additional factor, also discussed in the book is that there is often an increase…
Carbohydrates Part 2: Glycemic Index
Ok, so I’ve clearly been delaying this article which continues from part 1 and talks about the Glycemic Index and I’ll apologize up front if it kind of sucks. As usual, it wasn’t planned and the best structure flow has kind of eluded me. So I’m just going to hammer it out and hope for the best. But it will probably blow overall.
So two weeks ago I looked semi-briefly at carbohydrate structure and classification and will summarize that even more briefly here. There are three primary single sugars (glucose, fructose, galactose) which combine with each other to produce double sugars (sucrose, lactose, and maltose). There is also High-Fructose Corn Syrup (HFCS) which for all practical purposes is identical to sucrose. I should have also mentioned that glucose is sometimes called dextrose which explains the naming of maltodextrins, longish chains of glucose that are often found in sports and other food products.
Extremely long chains of glucose are called starch in food and glycogen in the body. Very generally the above can be divided into simple (the sugars) and complex (starches) carbohydrates with maltodextrins being in a weird middle place (probably best to consider them as complex carbs I guess). There is also fiber which, while a carbohydrate, is treated very differently in the body in terms of how it is metabolized and it’s effects.
Diabetes Treatment: Part 1
In the early days of nutrition, here I am talking about the first half and maybe a little bit later in the 20th century, it was generally thought that sugars were more or less ‘bad’ and starches/complex carbohydrates were ‘good’.
At least some of this was based on nothing more than the foods that each were found in were generally thought to be ‘healthy’ or ‘unhealthy’. Sugar bad, complex carbohydrates good, ook ook. It’s worth noting that fruits contain simple sugars and, especially at the time, few would have considered those unhealthy. That type of extremist stance would come later (thanks, Parillo).
But of more relevance to this piece was interest in treating diabetes. There are two kinds of diabetes which are Type I and Type II. Type I diabetes is a genetic condition where the pancreas doesn’t produce insulin. Until insulin was synthesized in the early 20th century, it was untreatable. Now it is but requires regular insulin injections.
Type II diabetes certainly has a genetic aspect but is mostly lifestyle related. Obesity, inactivity and a bad diet all contribute and the basic gist of it is that the body becomes insulin resistant which simply means that the hormone insulin can’t do it’s job in terms of storing nutrients in tissue like skeletal muscle and fat cells. A lot happens here but a common effect is increased blood glucose levels; since insulin can’t push glucose into muscle or fat cells, it hangs around in the bloodstream and this eventually causes damage to the body.
Note: Type II diabetes used to be called Adult Onset Diabetes since it was almost exclusively seen in adults (Type I, as a genetic condition shows up very early in life). This is no longer the case as more and more children are developing the condition due to increasing levels of obesity and inactivity. So now it’s just Type II. There is also the Metabolic Syndrome (formerly Syndrome X) which consists of a whole bunch of different metabolic dysregulations that tend to occur together.
The Glycemic Index: Part 1
For a lot of years, like most of the 20th century, the basic advice for diabetics was to limit simple sugars and consume primarily complex carbohydrates as it was assumed that simpler sugars, since they digested faster, would impact on blood sugar worse than more complex carbs. But as is commonly the case, the assumption wasn’t quite correct although it would be a while until it was formally tested and this was determined.
So far as I can tell, the first study to look at this more systematically was in 1981 when the first paper on the Glycemic Index (GI) was published. Originally, subjects were fed 50 grams of pure glucose on an empty stomach after an overnight fast and the blood glucose response was measured. More specifically the Area Under the Curve or AUC of blood glucose over 2 hours was measured. So imagine that the food is eaten and blood glucose is measured. It will go up over some time frame, maybe stay high and then come back to normal. This forms a curve. The total area under that curve is the AUC. Here’s kind of what it looks like and if you took high school calculus, you may remember how some of this works.
This value of AUC is arbitrarily defined as 100 and I need to make it very clear that the 100 doesn’t actually mean anything. It’s not the actual area under the curve or anything to do with blood glucose. It’s just an arbitrary reference value. You could define it as 1, 473 or Bob and means just as much. And that’s because GI is just a relative/comparative scale where the AUC of a given food is compared to the test food.
So after feeding them the 50 grams of pure glucose, at some later point, you feed them the equivalent of 50 grams of digestible carbohydrate of some other food and measure that AUC as well. Then you compare the two. If the second food has an AUC that is 70% of the reference food, the GI is 70. If that second food has an AUC that is 110% of the reference food, the GI is 110. Beating a dead horse (what is the GI on horse meat), it’s just a relative value.
The methodology of the GI changed a bit later (I honestly don’t know when). It was felt that 50 grams of glucose didn’t represent a real world situation and the reference food was changed to 50 grams of digestible carbohydrate from white bread (tho I think some studies still use glucose as a test food).
Everything else was the same, subjects were fed white bread and AUC was measured. Then they were fed another food, AUC was determined and the values were compared. There are charts online that show the two different sets of values and the relative positions of the foods don’t change although the actual numbers change. It’s just that glucose is now higher then 100 since white bread is the standard.
The Glycemic Index: Part 2
And even after the first study/studies were done, some interesting observations were made. One, that has recently become a big deal for some reason is that there was pretty large variability between people and that might point out that it’s fairly unreliable (it might also explain some of the divergent study results that I’ll mention). Clearly you can’t define a diet by GI if two different people have completely different blood glucose responses. But that’s neither here nor there. Of more importance was that the old assumptions about simple and complex carbohydrates didn’t turn out to be completely correct.
Some complex carbohydrates generated a pretty large blood glucose response while some simple sugars didn’t. Fructose was a good example and had a very low GI which made it attractive as a sweetener (pure fructose was super popular in the health freak community for a while but most people can’t handle a large amount of it in pure form without stomach upset). This is because fructose first has to be metabolized in the liver, converted to glucose/glycogen and then released which slows down how quickly it gets to the bloodstream.
Glucose was high of course since it gets right into the bloodstream and was the original test value. Sucrose (which recall is a glucose bound to a fructose) was halfway between fructose and glucose as you might expect. This is an important point I’ll come back to: when you add carbs together, the resulting GI ends up being the weighted average (more or less) of the two.
But it was even weirder than that as frequently complex carbohydrates had higher GI’s than sucrose. For example, white potatoes turn out to have a HIGHER GI than table sugar while sweet potatoes are about the same. Let that roll around in your head for a second, a baked potato (which most would assume is healthier due to it’s complex nature) generates a higher blood sugar response than straight up table sugar. All three are much higher than fructose. On at least one scale, potatoes come in with a GI of about 80 depending on how it is cooked, sweet potatoes are about 63 with table sugar at 65 and fructose at 15. Even brown rice has a GI of 68. I think you get the idea.
There were at least some generalities. Generally more complex carbs, especially if they were high in fiber tended to have a lower GI than more refined and/or low fiber carbs. Beans are all pretty low but they contain fiber and protein. So is fruit, probably due to the small amount of fiber and the fructose content. Ice cream actually had a very low GI due to the fat content (see below). Clearly, looking only at the GI, ice cream is an excellent food for diabetics (hmm….)
The above would lead to a complete shift in diabetic meal planning from complex and simple carbs to diets based around GI. Since the largest issue with diabetics is keeping blood glucose stable and controlled, using GI was deemed to be more effective. By eating low GI foods you lowered blood glucose and certainly some studies showed improved values (note that actual weight/fat loss always improves diabetic issues almost regardless of how you do it). The problem was that GI is not easy to use (one researcher described it as deceptively complex). There are also a significant number of issues with it beyond that I’ll discuss in the next part of the series.
Glycemic Index for Weight Loss
As you might imagine, the development of the GI was examined for other populations. One was weight loss and at least some studies showed that low GI foods were more filling than higher GI foods and generated better fat loss. This was questionable and the study results were about half and half. Not everyone agrees. I think that part of the problem is invariably that other nutrients are being impacted by high and low GI diets. Fiber intake usually varies and we know that fiber is filling. So does protein and protein is the most filling nutrient of all.
If a low GI diet causes someone to eat more protein, it will work better to keep them full due to the higher protein. It’s hard to do exact comparisons of low and high GI without other stuff changing. To take this into account, exactly one paper tried to determine a Satiety Index (how filling a given food is) all the way back in 1995 but for whatever reason, nobody ever bothered to follow up on it.
I think it was due to enormous individual variability but I wouldn’t swear to that. And, of course, GI has the same issues here as elsewhere in terms of being difficult to use. Certainly a diet telling someone to eat more beans, fruits and whatever amounts to low GI carbs is not a bad thing but that’s just focusing on things like fiber, slower digestion, etc. Trying to use GI in the real world is just a pain.
Glycemic Index and Athletes
And then of course there were athletes. Certainly for some performance sports, variations in GI can matter under certain circumstances. There has been some interest for example in low vs. high GI foods before competition (usually endurance type events) where it’s often recommended to consume low GI foods. Some very early work suggested that blood sugar might drop with carbs right before competition but this is individual and fairly irrelevant. Low GI foods to give a more even blood sugar response.
In one sense this is good in that it pushes carbohydrate oxidation during exercise (carbs are more efficient than fat). But it also inhibits fat mobilization and this could be problematic for long-events due to the benefit of using fat for fuel to spare muscle glycogen. So it’s a mixed bag and depends on the type of competition.
For a time-trial (a fixed distance event raced at maximum effort) using carbs is superior. For a 4 hour cycling race that will do a lot of time at lower intensities, sparing glycogen is paramount. There is also the issue of low GI foods potentially causing stomach upset because they digest more slowly. This tends to be of more relevance for running due to the movement in the stomach (it’s actually called “joggling”) and less so for other sports.
During workout has the same basic set of issues although it’s more common to consume more rapidly digesting carbohydrates under these conditions to avoid stomach upset.
For glycogen resynthesis following training or competition, GI may matter. This is especially true when rapid glycogen resynthesis is needed. Here higher GI foods consumed in small amounts frequently for the first 3-4 hours work better than lower GI foods. But even this is only important when an athlete has two intensive training bouts within 6-8 hours of one another. So long as an athlete either a) does not fully deplete glycogen and b) has 20-24 hours between workouts for the same muscle groups, the rate of glycogen resynthesis is irrelevant (at the slowest rates you can hit 100% in about 20 hours) and low and high GI both work identically.
And then there are physique athletes. I don’t know if they were the first to get hung up on the GI but certainly they got very hung up on it and certain foods (such as carrots, often high GI) were flat out put on the never eat list (I’ll discuss why this is nonsensical in the next part). First it’s important to realize that training status modulates GI, the more well (at least aerobically) trained you are, the lower the GI for any food. Training improves insulin sensitivity across the board (as does being lean generally) and since insulin response to food is part of this, GI goes down.
Certainly lower GI foods can be more filling (again, fiber, protein, etc.) which is nice but the assumption here usually had to do with GI and the insulin response to foods (insulin was bad since it inhibited fat mobilization and/or increased fat storage). The assumption was that lower GI meant a lower insulin response; as I’ll discuss in the next part that’s actually not always (or possibly even generally true). But there are issues with this.
Even basal levels of insulin after an overnight fast inhibit lipolysis by about 50% (Type I diabetics who let insulin fall too low get enormous fatty acid release) and this is a safety valve to keep the body from flooding the bloodstream with fatty acids which can cause problems. Raising insulin above basal fasting (basically when you eat anything) inhibit lipolysis pretty extremely/almost completely and it doesn’t look like GI really impacts on fuel partitioning, fat gain, or fat loss to any significant degree.
Make no mistake work here is usually done on overweight people and it’s entirely possible that a very lean individual dieting to the extremes is in a different situation. One adaptation to dieting is a huge improvement in insulin sensitivity and this is clearly to limit further fat mobilization so keeping insulin lower during extreme diets does make some logical sense. But even correlating that with the GI per se is problematic and I’ll come back to why this is next time.
And that’s where I’ll wrap this up. I’m still not happy with the flow of the article but this will have to do.