Got diabetes? Need advice? Of course you do! And you came to the right place: Ask D'Mine, our weekly Q&A column hosted by veteran type 1 and diabetes author Wil Dubois in New Mexico.

Today, Wil takes on a universal question about why (oh why) those of us on insulin can experience low blood sugars even when it seems we've done everything right?! Seriously, Wil... we all want to know the answer to that one so please share your wisdom!

{Have diabetes questions of your own? Email us at}


Mike, type 1 from Ohio, writes: I love the D’Mine column and I hope I’m not duplicating a question here. My question is more sophisticated than it might seem: Why do we (T1’s on insulin) get lows from a reasonably close to correct dose of insulin? I’m not talking about a dose that is way off or an activity level that ramps up the metabolism a lot. Just a slight miscalculation, or a little more walking than usual, or a little too much basal, or waiting too long to eat: Why can’t the body’s own system with the liver protect against these cases? Or am I wrong and it does protect more than I think? And maybe it’s just that it can’t handle as much as I think? I’m just comparing to a sugar normals BG after eating: They don’t go low, but even with really precise dosing and watching the CGM like a hawk, I’ll still drift down sometimes. Happy to snack and prop it back up, but I’m just curious why my body doesn’t or can’t. 

Wil@Ask D’Mine answers: Thank you for your kind words. Your question is a great one, and I don’t recall answering it before. Of course, over time, repeated lows cause brain damage. And as you point out, most of us T1s have lows no matter how hard we try to do our “jobs” right, grrr… 

But moving on, I think I have enough brainpower left to tackle your question, and to do that we must first talk about homeostasis. Homeomeans “the same,” and stasis means “staying,” so in the purest sense, homeostasis means staying the same.


In biology, homeostasis is usually defined as a stable state, or a state of equilibrium. Examples include the fact that warm-blooded critters keep their body temps in a narrow range. Red-blooded critters maintain healthy blood oxygen levels and blood pressure. The various minerals that course through human bodies—calcium, sodium, copper, iron, potassium—are carefully kept at the optimum levels, as are hormones. Steady. Unchanging.

All of which is a big fat lie.

Because there’s actually nothing stable about the act of homeostasis. It’s more of a walk along a tight rope than a walk down the sidewalk. The “stable state” is maintained by constant adjustments and counter adjustments. Did you ever have one of those cars where the thermostat settings were just not quite right? One click up was too hot, but one click down was too cold? So what did you do? You constantly fiddled with it, didn’t you? As you got uncomfortably warm, you’d lower the temp, which of course made you uncomfortably cool, making you raise it again.

This dance of too damn cool and too damn warm is an exercise in manual homeostasis. You are trying to maintain a target temp by controlling the input variables of hot and cold.

And that’s the key to homeostasis. This steady, “unchanging” biological state is created by nearly constant change, a hyper flurry of adjustment and counter adjustment on a tiny scale. One of the biggest “Ah-ha!” moments of my life came when I was in college, reading one of those too-frickin’-heavy-to-actually-carry textbooks on human anatomy and physiology. The author described homeostasis not as a stable state, but as a dynamic state of equilibrium.

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That blew me away. In my mind’s eye I could see dozens of clockwork gears spinning, clicking, ticking. A thousand moving parts dancing together to create, well, nothing. Well, nothing changing, anyway.

So how does this affect us? Welcome to glucose homeostasis. That’s right, as you pointed out, sugar-normals don’t have lows. Or highs for that matter. The Dance of 1,000 Veils inside their bodies keeps their blood sugar in a normal range with constant input and counter input.

How does that work? The simple answer is that insulin from the pancreas and glucose from the liver dance a Tango late into the night. But the real answer is far more complex and involves not only glucose and insulin but glucagon, epinephrine, cortisol, incretins, zinc, neurotransmitters, peptides, neuropeptides, nitric oxide, leptin, chloride, and probably a host more players yet to be discovered. It’s a body-wide process, involving the brain, the pancreas, the adrenal glands, the liver, the kidneys, fat and muscle.

The human body ain’t simple.

Now, we all understand that as type 1s, our bodies don’t produce insulin. But as you point out, shouldn’t the rest of that complex glucose homeostasis system still be working and protecting us? 

Actually, no. Sorry. And there are two reasons for that. First, let’s start with another breakdown you didn’t know you had. A key part of glucose homeostasis is an alert system for detecting changing blood sugar in the body in the form of specialized neurons that react to fluctuations in glucose. These detectors are on the front lines of the body’s glucose homeostasis regulation system. They give the alert that starts the entire homeostasis process for glucose. They live in your brain, its periphery, and in the ventromedial hypothalamus, which is the primitive fear and feeding “animal brain” encased in your smarter grey matter. 

But, apparently, these neurons are somewhat delicate little flowers. After about five years of type 1 diabetes, with its wild sugar rides, the receptors cease to function. I guess they have a limited shelf life, sorta like the batteries in an emergency flashlight that get used up by turning on flashlight too many times. The point being that once they are fried, they no longer detect the opening stages of a drop in glucose.

Diabetes just dropped a crowbar into that finely running Swiss watch.

So with the first phase of the counter regulatory response out of action, is it any wonder that our bodies can’t maintain glucose homeostasis? Sure, some of the system still works. Those shaking hands you get when a low hits? That’s epinephrine trying to raise your blood sugar level. It’s too little, too late, but the body still tries to do its thing.

But even if all the pathways were intact, there’s a fundamental flaw in our approach that doesn’t give our bodies a fighting chance, and that’s our insulin. In a sugar normal, insulin is main-lined into the blood stream, where it works quickly, and can be shut down just as quickly. In maintaining glucose homeostasis, the body can signal the pancreas to stop production and delivery of insulin, and quickly soak up any excess with some sugar from the liver. 

Problem solved.

But you aren’t injecting insulin into the blood. You are injecting it into fat, where it sits like a giant reservoir. The scientific types call this hyperinsulinemia, or too damn much insulin. It’s as if the pancreas blew off its instructions and just kept on pumping out insulin. The liver isn’t equipped to deal with this kind of over abundance and the available sugar supplies are overwhelmed. Remember the Swiss watch? Little parts. Small movements. The equilibrium is maintained be the smallest of adjustments. It isn’t designed for floods.

I like the way one researcher put it: “Insulin delivered exogenously is not subject to normal physiological feedback regulation, so it may induce hypoglycemia even in the presence of an intact counter regulatory response.”  The same guy (his name is Rory J. McCrimmon) points out that the average type 1 has two hypos a week, and that this average, despite changes in technology, hasn’t budged in two decades.

So I think everyone can see how things go south on us quickly when the apple cart gets tipped over. But why do things so often go south on us following your “reasonably close to correct dose?” Shouldn’t the injected insulin and the carbs equal out in some reasonable approximation of homeostasis?

Sadly, we can never hope to have a “reasonably correct dose.” Why? Well, we aren’t just covering carbs. Instead, we are making major changes to a delicate system. With every shot, we are not just skipping a stone across the calm pond of homeostasis, we are lugging a boulder to the edge and dropping it in with a giant splash. 

Using our earlier analogy of a finely made Swiss watch with its jewels, gears, springs, and rotors as the body’s natural system of glucose homeostasis, you, my friend, are using stone tools and bear skins to try to do the same. And you are using one element, insulin, to try to artificially control a process that uses dozens of elements in nature. Plus, rather than dripping constantly into the system, frequently turning the insulin on and off, we just pour a giant pail of stuff into the body. Is it any wonder that we fail?

Sure, with wonder drugs that don’t yet exist to properly mimic all the myriad chemicals that dance this dance, and with 27 networked Cray Super Computers, maybe—just maybe—we could come close to artificial glucose homeostasis.

But with a Flex Pen and a bag of Skittles? We haven’t got a prayer.

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. But we are not MDs, RNs, NPs, PAs, CDEs, or partridges in pear trees. Bottom line: we are only a small part of your total prescription. You still need the professional advice, treatment, and care of a licensed medical professional.