In need of help navigating life with diabetes? You can always Ask D’Mine! Yep, our weekly Q&A column by veteran type 1 and diabetes author Wil Dubois is here for you.

High blood sugars (aka hyperglycemia) bring on not-so-pleasant feelings and can be a dangerous when they tiptoe toward possible diabetes ketoacidosis (DKA). Today, Wil dives into a question pool on why even short-lived after-meal spikes can be a bigger deal than you might think. 

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Jeremy, type 2 from Arkansas, asks: Why is it so bad if your blood sugar spikes two hours after eating if you get it back down to where it’s supposed to be in 3-4 hours? What’s the big deal? I thought what counted the most was not how high it went, but how much time it spent up in the stratosphere. Am I wrong? 

Wil@Ask D’Mine answers: The truth is, you could be right that it’s no big deal at all. Or, you might be playing Russian Roulette with only one empty chamber, instead of only one bullet. 

Here’s the deal: You, me, and everybody else in the D-family are caught in challenging, changing times. The current methods of treating diabetes are being questioned by some very smart people, while at the same time, some other very smart people are questioning those doing the questioning. Everything may be about to change. Or maybe not. But if it does, it wouldn’t be the first time. Consider this: Everyone knows that too high blood sugar is bad. But it wasn’t all that long ago that no one knew that. The connection between high sugar and diabetes complications was discovered only 26 years ago. I mean, obviously, many folks suspected there might be a connection before that, but the science just wasn’t there to back it up. 

That all changed with the Diabetes Control and Complications Trial, the famous DCCT. What the DCCT looked at was the effects of, essentially, trying harder. At the time, the gold standard for diabetes treatment — and this was for type 1s — was not to die. Well, not to die too early, anyway. Standard treatment at the time was a couple of intermediate-range insulin shots a day, and using a urine glucose test kit as a proxy for understanding what the overall blood sugar levels might be. DCCT compared that to what is now today’s gold standard: Basal/Bolus multiple daily injection with a newfangled device called a fingerstick meter to attempt to keep blood sugar at “normal” levels.

The results of this new alternate therapy were so profound that the study was stopped early, and the volunteers in the control group—those using the standard treatment of the day—were shifted to the new more intensive treatment, because it was judged as unethical to keep anyone in the control group.

Science had come a long way since the infamous Tuskegee experiment. 

The rest, as they say, is history. The study changed diabetes treatment worldwide. That was great. Many lives were greatly improved and others, frankly, were saved by the research and the shift to more intensive treatment. The DCCT also created our current treat-to-A1C culture: Using whatever combination of meds—for both type 1 and type 2 diabetes patients—to drag average blood sugar below a zone consider “safe.”

And where would that be? Well, for perspective, folks without the Big D typically have A1C levels below 5.7, and complications seem to be a larger issue above 9, so it stands to reason that people with diabetes (PWDs) should be somewhere in between. This number — usually between 6 and 7 — has been a moving target over the years, but that’s beside the point for today’s discussion. What’s not beside the point is that as intensive treatment took hold, clinicians started noticing something odd: PWDs with identical A1Cs were not faring the same. Some folks with, say, A1Cs of 6.8 where thriving; while other folks with A1Cs of 6.8 were falling apart at the seams.


Clearly, there was more to the picture than just average glucose measured by the A1C. But what was it? Well, just as the fingerstick meter in the 1990s helped shed new light on blood glucose, a new technology would reveal yet more new secrets hiding below our skins.

The advent of continuous glucose monitoring (CGM) gave researchers the next level of understanding: Equal A1Cs are created by widely different inputs. Actually, we all know this instinctively: You can get 100 by averaging 75 and 125; or you can get 100 by averaging 50 and 150. The results are the same, but how you got there couldn’t be more different. No one had thought much about that before, when it came to blood sugar, until CGM came along and made it obvious.

Once CGM became a tool in the workshop of clinical research, it was clear that some people’s blood sugar took some pretty wild rides compared to other people’s. So how did these wild rides, these excursions, fit into the picture of diabetes complications? Could that be the explanation as to why some PWDs were doing worse than others?

Some clinical researches thought so. Others didn’t

As you might expect, there’s been no shortage of disagreement on this subject over the last few years; with the largest issue not being so much if glucose variably is the smoking gun in increased complication risk, but what kind of variability increases that risk. Some eminent scientists support the any-excursion-is-a-bad thing belief. Others, that the daily ups and downs are harmless, but that yo-yo A1Cs are the demon.

If our best eggheads can’t figure it out, I doubt that I can, either. In keeping an open mind, of course, both could be true. 

When was I first diagnosed with diabetes, I was told it was a game of averages: Keep your A1C in a good space, and you get to keep your eyes, kidneys, and toes. Spikes were no big deal. But then, I started noticing something: Excursions made me feel like crap. If I made the (common and easy) mistake of partaking in excess carbs, I paid for it. As my Dexcom CGM squawked at me and flashed two arrows up, my muscles ached, my energy plummeted, I was irritable. Likewise, if I hammered the high down with a rage bolus and found myself in free-fall, I paid a physical price once again.

To me, it was clear that if I could feel rapid swings physically — like the punches of a prize fighter pummeling me—it just couldn’t be a good thing for my body. And it didn’t take much imagination for me to think that getting the shit kicked out of me by a prize fighter on a regular basis could lead to some lasting damage. I remember that the first time I read about the excursion theory, I was nodding my head as I plowed through the words, Yeah, that sounds about right.

But that’s not to diss the yo-yo theory, either. The human body doesn’t like change much, and I can see where trying to force it to adjust, re-adjust, and re-re-adjust to changing average sugar environments could be corrosive as well.

Time and science will bring the answer. I have faith in that. But what are we to do in the meantime while we wait for diabetes’ latest secrets to be revealed? If you want to look at this as a war, we need both a strategic vision and tactics to win. As a strategy, get your A1C into the current best-guess target zone, and do what you can to keep it there. Then, tactically, take one day at a time and do what you can to minimize those nasty little excursions.

And if you don’t like military analogies, think of this approach as hedging your bets.


This is not a medical advice column. We are PWDs freely and openly sharing the wisdom of our collected experiences — our been-there-done-that knowledge from the trenches. Bottom Line: You still need the guidance and care of a licensed medical professional.