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  • Writer's pictureRyan Allen

The backwards logic of a common treatment

Arguably the most well-known drug out there is insulin. A hormone typically produced inside the body itself, additional exogenous (produced outside the body) insulin may be beneficial or necessary under certain conditions. Many often hear about insulin in the news because of the price gouging of pharmaceutical companies who produce it, depriving diabetic patients of the critical medicine they need. While this is undoubtedly a moral issue that must be resolved immediately, it actually should only apply to type 1 diabetics. This is because, in my view, it could be counterproductive for a type 2 diabetic to take insulin.

The underlying pathology that type 1 diabetics face with managing their blood sugar is a lack of insulin as a result of the failure to produce it. For these patients, it’s clear to see that they desperately need that insulin to prevent severe, unregulated high blood sugar. Type 2 diabetics, however, suffer from an entirely distinct mechanism of hyperglycemia. As we’ve previously described, these patients experience a phenomenon known as insulin resistance. Their cells struggle to respond to the signal of insulin to uptake and store sugar from the blood. Consequently, sugar molecules are refused entry into cells, blood sugar levels rise, and the pancreas produces more insulin to try and force the blood sugar down. One problem with this is, because of the cells’ insulin resistance, it requires far more insulin to dispose of glucose compared to an insulin-sensitive person. The body will keep making more and more insulin to try and shove all of that glucose into the cell, and insulin levels are so high that type 2 diabetics are considered hyperinsulinemic (high insulin) in addition to hyperglycemic (high glucose). This is the critical distinction: whereas type 1 diabetics have no insulin, type 2 diabetics have too much insulin.

With this in mind, you start to realize that it doesn’t make much sense for a type 2 diabetic to take exogenous insulin. Not only does it fail to fundamentally address the actual problem (there’s no “lack of insulin” in type 2 diabetics; they just can’t respond to it), but it actually appears to further exacerbate the issue. High levels of insulin in the bloodstream are the first sign of insulin resistance pathology, and it’s believed that increasing levels of insulin can make cells even more resistant to its signaling, similar to drug tolerance safety mechanisms. In addition, there is evidence that high levels of blood insulin can lead to decreased production of insulin by the pancreas, causing the patient (previously with severe hyperinsulinemia) to adopt a phenotype that resembles type 1 diabetes in addition to their type 2 diabetes. This concerning situation, a phenomenon known as double diabetes, implies both impaired insulin secretion and cellular resistance to that insulin. Unfortunately, it is becoming ever-more present in our society as a result of diabetes mismanagement, for both type 1 and type 2 patients. With diabetes, we want to move two needles in the right direction: our insulin production (healthy, moderate-to-low but non-zero levels), and our insulin sensitivity. So far, it appears that increasing insulin moves both of those metrics in the wrong direction.

The other key issue with exogenous insulin for type 2 diabetics is that it remains unclear if high blood sugar is even the real culprit behind further disease pathology. Maybe it’s the blood sugar, but maybe it’s insulin itself. Maybe it’s both. Type 2 diabetes has been linked with several chronic diseases, although there is some debate as to whether these links are mediated through the hyperglycemia or the compensatory hyperinsulinemia. The truth is likely that both of these factors contribute to increased disease risk. There is clear evidence that reducing the metric of blood sugar alone, approximated by hemoglobin A1C (which has its own issues we won’t discuss now), lowers risk of microvascular complications. However, as it turns out, resolving these issues by lowering blood sugar does not have a major impact on patient deaths. Many go on to develop large-vessel cardiovascular issues, cancer (more on this soon), neurodegenerative disease, etc. due to their hyperinsulinemia. This demonstrates that treating type 2 diabetes cannot simply mean lowering the blood sugar, but instead addressing the underlying problem.

To do so, the patient must be insulin-sensitive. The solution is not to throw enough insulin into their system to cram every last bit of sugar into their cells despite how hard it gets. It seems this disease can often be reversed solely by improving diet, and in this case that typically appears to mean carbohydrate restriction. There are many different ideas on the molecular process by which this dietary intervention increases insulin sensitivity, but clinically the observation cannot be ignored. In the meantime, there are numerous blood sugar-lowering medications available that do not act through insulin. Metformin, for example, is believed to decrease blood sugar by downregulating gluconeogenesis, the body’s process of making sugar anew.

Shockingly, the vast majority of patients on insulin in the United States are type 2 diabetics, not type 1. Of course, the fact that an estimated 90-95% of all diabetes cases are type 2 will skew this. Nevertheless, the number of type 2 diabetics on insulin should arguably be much closer to zero. If you or someone you know has been diagnosed with type 2 diabetes and takes either insulin or an insulin secretagogue (drug that lowers blood sugar by raising insulin), I would strongly recommend inquiring with your doctor about an alternative method of blood sugar management.


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