What gets measured, gets managed… this is what I measure to determine a patient’s blood sugar regulation and insulin resistance.
Video Transcript
Today we’re talking about labs, and specifically, three relatively new patients and their blood sugar labs.
These patients all went to their primary care physicians and had their general chemistry panel done. The only thing that was done on all three of the clients from a blood sugar perspective was their fasting blood sugar. And they were all about the same: 89.
But I ran a more comprehensive panel on the patients, and I want to explain why all three of these clients were told that they didn’t have a blood sugar problem and that their blood sugar looked great, yet they all had some blood sugar-related symptomatology.
(01:21)
So when we ran the more comprehensive panel… Patient 1: fasting blood sugar of 89. Patient 2: fasting blood sugar of 89. Patient 3: fasting blood sugar of 89.
Now what’s optimal is the 82 to 88 range, but remember the value is what it is; our job is to interpret it. The lab reference range may be something like 65 to 99, which is really too broad of a range, but the lab value is not the problem. In this situation, we might say that this person’s a little bit outside the optimal range. Why is that a problem? I don’t know. And I can’t tell you that by just looking at fasting blood sugar.
(01:58)
Now all of these clients have some symptoms of high and low blood sugar symptoms. So they all have some challenges with their blood sugar regulation. But we need to take a different look at the numbers. I’m not really worried that worried the values were 89 and everything else is normal because just the stress of going and getting a blood draw done for some people is gonna raise their fasting blood sugar. And you know, you have a cortisol awakening response that can result in some rise in glucose.
So I’m never concerned just about the fasting glucose per se. I always wanna see the context and since all of these people have some signs and symptoms of blood sugar regulation issues, we need to take a deeper look at what’s going on. I typically never run a fasting glucose by itself, I always run it with other values. So you have some context along with their signs and symptoms.
(02:58)
So we ran a hemoglobin a1C (HbA1C) and a fasting insulin on all three patients.
So patient one, fasting glucose is 89, HbA1C is 5.3. Now what’s optimal might be 5.0 to 5.3, the lab reference range is 4.8 to 5.6 or 5.7 depending on the lab. So this person’s doing pretty good with their hemoglobin. A one C sec
Person two, HbA1C is 5.4. It’s a little bit out of the reference range.
And person three: 5.6. Now, depending on the lab, they might be considered in a pre-diabetic state.
(03:40)
So hemoglobin a1C (HbA1C) is a marker of how much glucose is actually sticking to the red blood cells. The longer you have more glucose in the bloodstream, the more likely it is to stick to stuff. So that’s what we’re measuring.
And so HbA1C, even though they all have the same fasting blood sugar, the HbA1Cs are all a little bit different. So just looking at those numbers, even though glucose is the same, we would start to say person number three has more glucose staying in the blood sugar for a longer period of time.
(04:21)
Now there’s another caveat. We have to look at the HbA1C in relationship to the red blood cell physiology, but we’re not going do that in this explanation. So we’re just gonna take a look at these values.
Now the next number is really the kind of telltale sign that there are more significant problems going on and it’s a test that’s rarely run, it’s the insulin levels.
Insulin is the hormone that’s released when we eat to help get glucose into the cells. It should be relatively low in a fasted state ’cause you shouldn’t have a lot of blood sugar and glucose in circulation. But if you have some glucose resistance, then the body’s gonna continue to pump out insulin to try and get the glucose out of the bloodstream and into the tissues.
(5:00)
So now we look at person one to maintain a fasting glucose of 89, it takes 4.2 – we’ll call it units – of insulin in their bloodstream.
For person two, it takes a lot more, it takes almost three times the amount of insulin to force the glucose into the cells.
And person three, it takes a little bit more than four times the amount of insulin to get the glucose into the cells and maintain that fasting glucose of 89.
So what’s going on? Patient two is more glucose-resistant and therefore more insulin-resistant than patient one. Patient three is actually even more glucose and insulin-resistant.
And I don’t really like the term “insulin resistance” as much as I like the term “glucose resistance” because even in a fasted state you’re not eating. So something’s resisting the glucose from coming into the cell. It’s probably less about insulin and more about glucose.
(5:59)
Anyway, we can run a calculation here. It’s called the Homa-IR. And if we look at the Homa scoring system, there’s a little calculator you can get online.
The Homa IR score for patient one is 0.55. That’s within the optimal range. So this person really doesn’t have any insulin resistance going on.
Patient two they’re at 1.69, which means they are in that kind of developing insulin resistance stage.
And patient three is in full-blown insulin resistance.
So even though their doctor said, “Hey, you don’t have any problems with your blood sugar, everything looks great,” – it isn’t great for either one of these patients, they’re already in a state of glucose and insulin resistance.
The medical physician is waiting to see if they have pre-diabetes or diabetes. In functional medicine, we wanna see when this glucose and insulin resistance starts, so we can address why somebody’s starting to develop it.
(07:02)
The next calculation we can take a look at is their beta cell sensitivity. How hard are their beta cells working? These are the cells in the pancreas that produce insulin to keep that blood sugar stable.
The beta cells in patient one are working at about 65%. They’re not having to work too hard to pump out insulin.
Patient number two, their beta cells are at 140% to try and make the insulin to get the glucose to stay at that level. That’s more difficult and more work on the pancreas that says, “Hey, I gotta make even more insulin to try and force this stuff into the tissue” And if you have glucose and insulin resistance, the tissues that are gonna become glucose and insulin resistance first are probably gonna be the liver, the muscle tissue. And then where does all of the excess glucose have to go? When you have this glucose and insulin resistance, it’s going to your adipose tissue.
And then patient three, they’re at 168%. So their pancreas is working even harder to try and make more insulin to get this glucose out of the bloodstream and get it into the tissues. And the tissues that are gonna get the most of it are the fat cells.
(8:18)
And then you can look at cellular sensitivity.
Patient one, they’re at 82%. So their cells are super sensitive to glucose.
Patient two, they’re at 59.1% sensitive to insulin and glucose. And then patient three is 45%. So these two, their cells are resisting the glucose and the insulin.
Okay, so why does that occur?
Some people say you’re eating more glucose than your body can use and that’s why you become glucose resistant – the cells are “full” because you eat too much and you don’t exercise enough. I’d take a look at it a little bit differently. I think there’s some type of cell stress going on. The cells are adapting to stress and they aren’t pulling glucose into the cell.
(8:55)
Just of note… Patient one, their blood sugar symptoms are the result of something that’s going on in their GI tract. That’s for another day.
Patient two, they have cellular hypothyroidism going on, meaning that their cells are favoring the deactivation of T4 to reverse T3, versus the conversion to T3. So their free T3 to free T4 ratio is low, but their thyroid gland is producing enough T4.
(09:17)
Patient three: this is a person who’s already been diagnosed as primary hypothyroid. They’re already on thyroid medication and their free T3 to free T4 is very low. That means the cells are not wanting to bring glucose in. The cells are insulin-resistant and glucose resistant.
The cells are also resisting the increased T4. They’re not converting it to T3 – not because the cells are broken, but because the cells are adaptively downregulating the metabolism and downgrading glucose transport into the cell. So this person, despite having a “normal” fasting glucose level, is extremely insulin resistant!
