So after a couple of weeks of nothing, it’s time to continue this series, which will invariably run to 4 parts because that’s just how I do things (tediously and in an overwritten fashion).
As an overview of last time, I described how the Glycemic Index (GI) is measured along with the implications that it had for diabetes treatment, potentially weight loss and for athletes. The main take home is that, the development of the GI had an impact on diabetes treatment but was a huge hassle to use.
For weight loss, studies were about half and half on whether or not low GI foods (typically higher in protein and fiber) were more filling or not. So far as athletes, the benefit of high and low GI are context specific while the physique athletes were the ones who really got hung up on the GI based on what would turn out to be an incorrect assumption about insulin dynamics (discussed today).
Problems with the GI
While the GI concept made a lot of sense in that carbohydrates would digest and impact on blood glucose differently, there were a lot of problems with the method. Perhaps the largest was the most obvious: feeding someone 50 grams of digestible carbohydrate after an overnight fast isn’t really that relevant to how people eat in the real world in a number of ways.
Problem 1: Only One Meal is Eaten After Fasting
Yes, fine, breakfast by definition occurs after an overnight fast but are measurements made at that single time point indicative of the rest of the day? It turns out that the answer is no.And it was found early on that there was a second meal effect, that how the body responded to the next meal of the day could be profoundly different. In one study, a low glycemic dinner changed the glycemic response to breakfast on the next day.
Things like insulin sensitivity may change during the day, a previous meal may still be digesting and there were clearly residual hormonal effects from the first meal that impacted how the body responded at the second meal (I’m not getting into this but there are a huge number of hormones, incretins, etc. released when people eat that impact on all of this).
I mentioned training last time (and how the more aerobically trained the lower the GI response) and I’d mention in passing that the idea that insulin sensitivity is always highest or lowest at some point is always measured in diabetics. If you train at night, your insulin sensitivity is high no matter what a non-training diabetic with god knows what else is going on may be.
Problem 2: Few Eat a Single Carbohydrate Source
A second major issue is that GI is invariably tested with a single source of carbohydrates, either the reference food or the test food. And people don’t eat like that in the real world generally. As soon as you start mixing carbohydrates things change. As I sort of mentioned last time (when I talked about sucrose being an average of glucose and fructose), the net GI of a meal is the weighted average of the grams of each type of carbohydrate times it’s GI.
So if someone eats 25 grams of digestible carbohydrate with a GI of 25 and 25 grams of digestible carbohydrate with a GI of 75, the net GI ends up being ((25 grams * 25 GI) + (25 grams * 75 GI)) / 50 grams = 50 GI. At this point you need a freaking spreadsheet to track your meals, hence the researchers comment that GI was deceptively complex.
Problem 3: People Don’t Eat Carbohydrates in Isolation
Ignoring the sheer stupidity of food combining, the fact is that people rarely eat carbohydrates in complete isolation (well, some do but they shouldn’t). Rather, they eat meals that may contain carbohydrates, protein, fat and fiber and this changes the picture for a number of reasons ranging from hormonal responses to altering how quickly a meal digets.
One interesting early observation was that higher fat foods often had a lower GI (ice cream is about 51 and full fat milk about 31 due to the fat content). This was primarily due to fat slowing digestion which slowed the blood glucose response. This led to the truly moronic idea in the late 80’s or early 90’s that the way to decrease the problems with high GI foods was to add a bunch of fat to them. Which is about as intelligent as adding a stick of butter into your diet to lose weight. You don’t decrease the problem with fat gain or a lack of weight loss or diabetes or anything else from eating something by ADDING a ton of fat to it.
As noted above, fat slows digestion. So does fiber which may has it’s own separate health benefits. And then there is protein. One early observation is that protein invariably lowered the GI (and one super old book I have on controlling blood glucose for diabetics talks about adding protein to carbohydrates specifically for that reason.
Certainly both fat and fiber slow down digestion but that simple fact starts to bring the issue of how relevant the GI is into question. Protein is a little bit interesting. It was observed early on that adding protein to carbohydrate would lower the GI of the meal. That’s in addition to all of the other potential benefits
GI and the Insulin Response: Part 1
As much as I imagine that readers know what insulin in and what it does, here’s a primer. Insulin is a hormone released from the pancreas (trust me, click that link) that is involved in overall nutrient storage. It pushes glucose into skeletal muscle, turns off glucose release from the liver, pushes glucose into fat cells, impairs fatty acid release from fat cells, decreases protein breakdown and a host of other stuff. Random note: if you’re still hung up on the bs “Insulin Hypothesis of Obesity” I entreat you to read James Krieger’s series on it.
Insulin responds to food intake (in some cases, the smell of food can cause what’s called a cephalic insulin response, a small increase that occurs in preparation for food intake). When blood glucose goes up, insulin goes up to try to bring it down. When blood glucose goes down, insulin goes down and glucagon goes up stimulating the liver to release glucose. Fat has no direct impact on insulin and I’ll talk about protein in a second.
I’d also mention that a number of other hormones increase when food is eaten (and this is distinctly different from when insulin is injected). Amylin is a critically important one and it’s interesting to note that a synthetic form has been trialed with injectable leptin for weight loss.
While diabetes is really an issue of blood glucose response, there is also the issue of insulin since either insulin deficiency (Type I and the extreme end situations of type II when the pancreas craps out) or insulin resistance are a big part of why blood glucose levels become uncontrolled.
Insulin deficiency means that insufficient insulin can be released to control blood glucose whereas insulin resistance is a situation where insulin can’t do it’s job to push glucose into cells, leaving it to hang out in the bloodstream. Treatment of Type I diabetes revolves around insulin injections of one sort of another while Type II treatment is usually drugged in many different ways that I won’t get into (it includes drugs that increase insulin response or increase fat cell numbers, etc). Of course, this is where the idea of modulating carbohydrate intake came from in the first place; by reducing blood glucose changes in the first place, the decreased role of insulin is less of an issue.
GI and the Insulin Response: Part 2
Now one assumption that was always present was that a lower GI food automatically meant a lower insulin response. As above, insulin goes up when blood glucose goes up so this seemed to be fairly logical. Lower the GI and you lower the insulin response and this was always the basis of the physique athlete’s focus on low GI foods while dieting. To avoid inhibiting fat loss, the idea was to keep insulin low although, as I talked about last time, this may not matter since even small increases in insulin (from eating anything) basically shut down fatty acid release.
But this is where the assumption turns out to be wrong. A long while back, I described a study where a low GI food actually caused a larger EARLIER insulin response than a high GI food. If this seems confusing remember what insulin does which is to push glucose into tissues such as muscle. The blood glucose response is ultimately related to how much glucose is exiting the bloodstream as well as how much is entering. If you push glucose out of the bloodstream faster than it is coming in, you get a lower measured GI response. But it’s because insulin is going more quickly to a higher level.
Similarly, I noted that adding protein to carbohydrate invariably lowered the measured GI response. And it turns out that it was because adding protein to carbohydrate INCREASES the insulin response. This means that blood glucose is pushed out of the bloodstream more quickly. The measured GI response is lower but it’s because insulin is going up MORE. Even in the bran cereal study linked above, the researchers thought that the increased insulin response was due to the higher protein content of the bran.
In one study, in diabetics, mind you, it was shown that the addition of either whey or casein to the same amount of carbohydrate increases the insulin response by 190-270%. However, insulin action was decreased so the overall effect was the same. But this is also in diabetics. In the brain study, healthy males were studied. It’s also been known for a while that, at least when carbohydrate intake is too low, adding protein to the carbohydrate increases the insulin response and glycogen storage after exercise.
The point being that one of the huge primary assumptions about either low GI foods having a lower insulin response or how adding protein to carbohydrate lowered insulin since it lowered GI as was assumed in the physique community turn out to be wrong. And being snarky again, given the insane obsession with insulin in that community and given that nobody would argue that increasing protein or adding it to carbohydrates somehow INHIBITS fat loss, maybe it’s time to rethink this whole insulin thing.
And that’s where I’ll wrap up. Next time, next week if I get my head out of my rear end, Part 4th and the final.