Testing hypotheses for high morning Blood Glucose

I've focused more on measurements of Hemoglobin A1c than blood sugar, as that gives a time average indication. Even so, my A1c numbers, while good for a diabetic at between 5% and 5.4%, are not great by Steve's targets. A value of 5.4% corresponds to an average BG of 108 mg/dL. Going the other way, having an average BG less than 100 mg/dL means an A1c of 5.1. The fact that my averages are much higher than my fasting levels during the day suggests that my post-meal levels, and early morning levels, are very much higher than I'd like. I've got a series of experiments underway looking at BG after eating, but what about overnight highs in Blood Glucose?

So I think this is a perfect setup for adaptive management.

There are two hypotheses for high morning blood glucose in a Type 2 diabetic. The "hormone hypothesis" posits that an increase in growth hormone production in the middle of the night triggers a cascade of events leading to the release of glucose from the liver. Presumably this is to set one up for a vigorous start to the day. In a healthy person this extra glucose triggers an insulin response, and blood glucose remains steady. In a person with insulin resistance (like me), the insulin response is not effective, and blood glucose rises. The second hypothesis is "The Somogyi effect", where low blood glucose values overnight trigger the the release of glucose from the liver to avoid too low blood sugar values. That also involves hormones, but they are activated for different reasons.

Which of these hypotheses is true does matter; under the 2nd hypothesis I should be able to avoid high morning sugar by making sure my overnight sugar levels don't drop too low. I could eat a snack before going to bed, for example. Under the hormone hypothesis there's not much I can do except to try harder to ameliorate the insulin resistance. I could start taking Metformin, which acts in two ways, first by suppressing liver production of glucose and second by reducing insulin resistance. Both of those actions should act directly on the dawn phenomenon.

I can also learn which of these hypotheses is true by monitoring my blood sugar. Ideally, I'd measure my blood sugar every hour or so all night ... hmm. That sounds like a sucky experiment. According to this article, I can get away with just measuring at bedtime, 3 a.m., and the morning.

So I tried it for 2 nights, and I think I've discovered a 3rd hypothesis, the "Drew Tyre Effect"! On the first night, 9pm 101, 3am 116, and 6am 122! OK, that's consistent with the hormone hypothesis, but maybe I missed a drop in BG between 9pm and 3am. So last night I took the middle measurement earlier, and 9:20pm 112, 12:25am 110, and 6:40am 116. My BG is high all night. 

So, a bit of reading on what stimulates Cortisol levels is warranted. As it happens, sleep deprivation stimulates cortisol production, so this could be an instance in which the observation of a process affects the process itself. I need one of those continuous glucose monitors!

Here's another hypothesis: I've been taking a fish oil supplement for the past 3 months after learning that I was low in tissue levels of EPA and DHA. However, it turns out that fish oil supplements can blunt insulin response and increase resting glucose levels. So looks like I have to wait 18 weeks and then try this experiment again.

And another hypothesis! I'm swimming in the damn things ... It turns out that taking a statin can interfere with blood glucose control. I starting taking 10 mg of Crestor every evening about the same time I started taking fish oil. Well, the results of my latest bloodwork will be very interesting.