Why Do People with Type 1 Diabetes Develop Insulin Resistance?

Trump To Slash Insulin Costs for Medicare Patients

Why do people with Type 1 diabetes develop insulin resistance despite seemingly good health overall? It’s an important question. Insulin resistance is associated with a host of negative health outcomes, including heart attack and stroke. If you have Type 1 diabetes, you cannot assume that staying fit and trim – or even maintaining excellent blood sugars – will eliminate the risks.

It has already been established that people with Type 1 diabetes tend to exhibit much higher levels of insulin resistance than expected from typical risk factors (such as age, body fat percentage, blood pressure, exercise rate, etc). There is something about Type 1 diabetes itself, or the way that it is treated, that itself causes insulin resistance independent of all of the usual factors that the general population is asked to look out for. This may be disheartening for those of us with T1D that seem conventionally healthy: we share a major risk factor for heart disease that “cannot be easily identified using standard clinical predictors (including poor glycemic control).”

A recent study published by the American Diabetes Association represents an attempt to understand why this occurs. The authors isolated two proposed contributors to the phenomenon: hyperglycemia and iatrogenic hyperinsulinemia.

Hyperglycemia should be familiar to us all: high blood sugars. What is iatrogenic hyperinsulinemia? “Hyperinsulinemia” is the condition of having too much insulin circulating throughout the blood. “Iatrogenic” refers to an illness that is caused by medical treatment. Iatrogenic hyperinsulinemia is when a patient has an excess of insulin due to a medical regimen, in this case, routine and necessary injections of exogenous insulin.

To study the issue, the researchers matched groups of people with and without T1D with a third group afflicted with MODY2, a non-auto-immune variant of Type 1 diabetes that is typically mild and devoid of serious complications. The MODY2 group experience chronic mild hyperglycemia but retain all beta cell function and usually require no insulin injections, which allowed the researchers to isolate the effect of hyperglycemia on insulin resistance in a population that does not experience hyperinsulinemia. All three groups were hooked up to hyperinsulinemic-euglycemicclamps, in which patients are injected continuously with both glucose and insulin until their blood sugar stabilizes. It’s the gold standard for measuring insulin sensitivity.

The results seem fairly definitive. The Type 1’s experienced significant insulin resistance, but the MODY2 group exhibited no more insulin resistance than did the control group.  With no correlation at all between hyperglycemia and insulin resistance, the researchers were able to attribute the increased insulin resistance of the T1’s to iatrogenic hyperinsulinemia. (Caveats: the study was fairly small, and the authors could not rule out some other, unknown factor.)

In short: injecting insulin makes your tissues insulin resistant.

A careful person with diabetes might reasonably object: ‘but I manage my blood sugars well, and rarely experience hypoglycemia, so I know that I don’t use excess insulin.’ Unfortunately, that’s not quite the way it works. In a healthy body, insulin secreted by the pancreas is transported to the liver. But subcutaneously injected insulin bypasses the liver and goes straight into peripheral circulation. As a result, insulin users have abnormally high concentrations of insulin outside the liver, and abnormally low concentrations within it, an arrangement that only partially mimics the natural action of insulin in the healthy body. This has been called “suboptimal” by researchers, and it has a variety of complex consequences for the insulin-user’s metabolism.

One such consequence: your insulin injections may also promote inflammation. An earlier article concludes that the heightened levels of insulin associated with “optimal insulin therapy” can be the cause of dangerous inflammation: “The tight glycemic control in type 1 diabetes may thus increase the risk for atherogenesis [clogged arteries] via inflammation.”

Scientists have proposed several fixes for this, and work continues on improved insulins. The startup Diosome, to take one notable example, is testing an additive that will allow injected insulin to travel directly into the liver. But until new insulins are available, we’re stuck with today’s options.

Blood sugar control remains the critical focus for people with Type 1 diabetes, and it would be extremely dangerous to purposely take less insulin in order to avoid the risk factors discussed in this article. We know conclusively that a lower A1C dramatically decreases the frequency of cardiovascular events and stroke. Insulin resistance is a minor concern for an otherwise healthy person with Type 1 diabetes in comparison to the ravages of chronic hyperglycemia.

That doesn’t mean that there’s nothing to be done. The conventional advice given to non-diabetics that want to reduce their insulin levels – lose fat, exercise more frequently, put on muscle, and avoid carbohydrates (especially refined carbs) – should also work to decrease the insulin needs of people with Type 1 diabetes. The Pediatrics article analyzing the TypeOneGrit Facebook community confirmed that a very low carbohydrate diet can decrease daily insulin requirements, and to us that seems like a good place to start.

Ross Wollen
Ross Wollen

Ross Wollen is a chef and writer based in Maine's Midcoast region. Before moving East, Ross was a veteran of the Bay Area restaurant and artisanal food scenes; he has also worked as a food safety consultant. As executive chef of Belcampo Meat Co., Ross helped launch the bone broth craze. Since his diagnosis with Type 1 diabetes in 2017, he has focused on exploring the potential of naturally low-carb cooking. Follow Ross on Twitter: @RossWollen

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Elizabeth Ariza
Elizabeth Ariza
4 years ago

I read this original study that this article is based on a few months back. I think N=10, if I recall correctly. an incredibly small number from which to make any general assumptions. I’d rather see it replicated with at least ten times that N.

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