Let’s talk the following misconception:
“Diabetes is a state of carbohydrate toxicity and insulin resistance is a state of carbohydrate intolerance”
Probably the single most debated topic around type 2 diabetes (T2D) is whether carbs or fat is the cause. This confusion is a consequence of how to measure diabetic state and interpreting test results. The argument that carbs are a cause comes from two observations: 1) When eating a carb-rich food, a spike in blood sugar is observed and 2) the increase in insulin production that must occur for the resulting glucose to be absorbed by muscle cells and the liver. The argument is that since carbs increase the production of insulin, if you continue to stress your body with excess carbs over time, eventually you will compromise the pancreas’ ability to produce insulin. This, in turn, results in high blood glucose, and over time, an elevated A1C value that leads to a clinical diagnosis of T2D.
As further evidence of this model, those who blame carbs as a cause show what happens when someone that is either borderline T2D or actually T2D restricts carbs (perhaps to 10% or less of calories). It has been shown that in a low carb diet, blood glucose values will drop. Furthermore, A1C values, which are a measure of how well blood glucose is controlled over a period of time (about 3 months), also drops. Slam dunk, carbs are to blame, right?
The problem with this way of thinking is conflating a symptom with a cause. First, let’s look at how fat, carbs, and insulin interact. When you eat a high fat diet, fat is stored in the liver and in the muscle cells (intramyocellular lipids) as well as other places. This fat in the liver and muscle cells form the foundation to the symptoms talked about earlier. With this fat in place, if you eat a carb rich food, insulin naturally is produced to deal with this. As we know, the primary job of insulin is to admit glucose into cells, however, in this scenario, the insulin receptors essentially say, “there is no way I am letting that glucose energy in. I already have energy in my cell (in the form of fat), and only after I burn this energy, will I let in your glucose.” This, of course, traps the glucose in the blood and eventually leads to high A1C numbers.
In this scenario, is it any surprise that dramatically reducing carbs would result in lower blood glucose and A1C numbers? Of course not, because you aren’t truly testing your body’s ability process carby foods. Here’s an analogy: We have often heard T2D is like having the locks of a door gummed up so a key won’t work (where insulin receptors are gummed up by intra-cellular fat, so the insulin hormone doesn’t work effectively). Let’s say your front door is gummed up and your key doesn’t work easily. Let’s also say, for the last three months, you decide to get in your house you should just go through a back window. In this scenario, let’s take a measure during those three months of how many times you struggled to open the front door. Zero, right? Are we able to conclude, therefore, that you don’t have a problem with the front door? This is analogous to what A1C is measuring. If you never attempt to use the front door, you won’t have enough information to conclude there is a problem. The only way to measure insulin sensitivity is via a glucose challenge, sometimes called an oral glucose tolerance test.
This is how the test works:
Drink a solution of 75 - 100 grams of glucose dissolved in water
Sample the blood at 0, 60, 120, and 180 minutes
The blood samples are analyzed for glucose and insulin
The results of this analysis are measured against a known standard
Don’t be fooled by those who say when they measured their fasting blood glucose numbers on a low carb diet who think a low value means they have increased insulin sensitivity. Only a glucose challenge can make this conclusion.
Based on what we have discussed, this is a far more accurate formulation of the original statement:
“Insulin resistance is a state of carbohydrate intolerance first created by the consumption of excess dietary fat.”