Treating type 2 diabetes with insulin leads to weight gain and worsens risk factors for heart disease. Should we still be doing it?
Next year will mark the 100th anniversary of a critical moment in modern medicine. In 1920, the Canadian surgeon Frederick Banting lay down in bed to read a research article on diabetes and was inspired to enter the field. Three years later, Banting shared the Nobel Prize for the discovery of the hormone insulin.
If the body can be thought of as a warehouse and the foods we eat as the incoming goods, then insulin is the warehouse manager. It directs cells in different parts of the body to take up nutrients, which can then be stored or burned for energy. When someone’s pancreas cannot produce insulin, glucose, or blood sugar, will rise to dangerously high levels, just as a warehouse cannot function if goods are piling up everywhere. This is the condition known as type 1 diabetes.
Prior to the discovery of insulin, a diagnosis of type 1 diabetes was a death sentence—patients typically survived for less than a year. After Banting’s discovery, type 1 diabetes remained a difficult condition to manage, but patients could live normal lifespans. It was a world-changing medical breakthrough that has saved millions of lives. But now, nearly a century later, diabetes specialists like me are facing a painful reckoning: The vast majority of people with diabetes have a different type of disease, known as type 2 diabetes. For these many millions, the insulin treatments we’ve been prescribing may not be the best way of controlling a patient’s blood sugar.
By the time I finished my training in endocrinology in 2004, differences between type 1 and type 2 diabetes were long understood. Type 1 diabetes is a disease of too little insulin and type 2 is too much. People with type 2 diabetes can still produce insulin. The problem is that they are insulin resistant: their cells are no longer paying attention to insulin’s instructions. The pancreas sends out more and more insulin to clear away the glucose. For years this extra insulin might be enough to keep blood levels under control, but as type 2 diabetes sets in, even the extra insulin from the pancreas is not enough.
A good solution for this problem, I learned in my medical training, was to prescribe insulin to such patients. These were people who already had higher than normal insulin levels, or hyperinsulinemia, but I was telling them they needed to supplement with still more insulin.
I was convinced I was doing the right thing. At the hospital in New York where I began my career, my patients had great short-term outcomes. I met the medical establishments’ markers of success: my patients had lower blood sugar and LDL cholesterol. Back then I was fighting for patients to receive a new insulin called Lantus instead of the old NPH so often that my residents called me the “Lantus Queen.”
Over time, though, I read study after study showing the correlation between heart disease and high insulin levels. Elevated insulin is also associated with a wide range of other chronic diseases. The hormone I was giving my patients might be keeping their blood sugar down, but, I realized, it might also be damaging their bodies in ways that were not yet fully understood. Insulin, among other effects, causes people type 2 diabetes to gain weight by signaling the fat cells to accumulate fat. As Dr. Ralph DeFronzo, Professor of Medicine and Chief of the Diabetes Division at the University of Texas Health Science Center, put it to Science in 2008, “When you’re treating and trying to control type 2 diabetes, you have to understand that the basic defect is insulin resistance. You have to give enormous amounts of insulin to overcome the resistance, and when you do that, you activate growth-promoting inflammatory pathways.”
The more I thought about insulin therapy, the clearer it was that I needed a different approach for my type 2 diabetes patients. What I needed, specifically, was a way for them to achieve normal blood sugar levels, while requiring less insulin rather than more. And, though I had learned nothing about it in medical school, there is, in fact, a way to do exactly that: eating fewer of the foods that cause the pancreas to release insulin in the first place.
When we eat mostly protein and fat, both of which are essential to life, we require small amounts of insulin. When we eat carbohydrates, which break down into glucose, we require a lot of insulin. Prior to the discovery of insulin, people with diabetes were instructed to avoid carbohydrates for the simple reason that they raise glucose levels most and require more insulin.
Over the last four years since I began prescribing a low carb diet with plenty of fat and protein to hundreds of my patients, I have seen one after another lose weight. On a low carb diet, my patients’ triglycerides go down, HDL cholesterol goes up, and blood pressure and glucose levels normalize. Some people with type 2 diabetes do need insulin therapy, but many can avoid insulin by minimizing or eliminating carbohydrates from their diets.
A century ago, diabetes doctors looked on in awe as type 1 patients responded to insulin therapy. Today, I feel the same awe watching type 2 patients get off it.
Jessica Apple is coauthor of this article.