When I was a medical student at McGill in the late 1970s, we learned a straightforward explanation for the cause of Type 2 diabetes, the most common form of diabetes in adults, accounting for about 90 per cent of all diabetes cases. We were told the insulin resistance responsible for Type 2 diabetes was caused by high levels of insulin. Hyperinsulinemia–increased insulin levels in the blood–was said to “downregulate” insulin receptors, making cells with those receptors less responsive to the insulin message. From a physiology point of view, this makes perfect sense. It’s analogous to the development of tolerance that can happen with regular heroin use when a person no longer responds to the drug in the way they did initially.
Sometime in the 1980s this explanation for the cause of insulin resistance was abandoned. Instead, the medical community adopted a new theory that insulin resistance comes first, and is behind high insulin levels in Type 2 diabetes. To overcome insulin resistance, the pancreas secretes larger-than-normal amounts of insulin, resulting in so-called “reactive hyperinsulinemia.” The cause of this insulin resistance is never clearly explained, although obesity, chronic inflammation, and genes are all said to contribute.
When I ask prominent endocrinologists about how insulin resistance comes about in this new paradigm, they say, sometimes condescendingly: “It’s too complicated for a psychiatrist to understand.” That may be. But I’m also an engineer, and when I studied at the University of Waterloo the saying was “BBB”, short for “Bulls**t Baffles Brains.” I consider myself to be a critical thinker, so if the new explanation for what causes insulin resistance is incomprehensible to me, that’s probably because it’s nonsense.
Why did the medical community make a 180-degree reversal of its theory for the cause of Type 2 diabetes? Why discard a nice, coherent, easy-to-test explanation and replace it with a theory no one seems able to describe in terms that an engineer and physician can understand? Time to apply another useful saying: “Follow the money.”
Who profits from this paradigm shift? To answer this question, let’s compare the consequences of diabetes management approaches under the old paradigm and the new one. If we follow the old theory that high insulin levels cause insulin resistance, then treatment involves lowering insulin levels, assuming that insulin resistance is reversible. Since the main stimulus to insulin secretion is the level of glucose in the blood, we can get the pancreas to release less insulin by decreasing the amount of glucose going into the bloodstream. For people who eat regularly, that main source of blood glucose is carbohydrates in the diet, i.e., sugars and starches.
Treatment options for lowering blood glucose include medications such as acarbose, which reduces the absorption of dietary carbohydrates in the small bowel. Metformin, the first-line treatment of choice for Type 2 diabetes, is believed to have a similar effect and may also contribute to weight loss. Traditional and folk remedies for obesity and Type 2 diabetes, including yerba maté tea and the gourd bitter melon, may act in the same way. An easier route for some would be to lower the amount of carbohydrates in the diet, and/or pick foods with a low glycemic index. Research demonstrates a low-carb diet can reduce or even eliminate the need for medication to control blood sugar, in effect, curing diabetes in some patients, and, more importantly, showing that Type 2 diabetes is likely caused by diet for people with susceptible genes.
If we follow the new paradigm and believe obesity, inflammation and genes cause insulin resistance, what can we do? Lose weight? Many find this impossible. Reduce inflammation? Difficult if we don’t know its cause. Change our genes? Maybe in the future. Typically the victim is blamed for overeating and not exercising enough. In the absence of effective ways to reduce insulin resistance in this paradigm, the usual solution is medication to control blood sugar levels.
Some commonly prescribed anti-diabetic medications stimulate the pancreas to produce more insulin, while others act at the level of the insulin receptor to decrease insulin resistance. And of course, insulin itself, typically given in amounts way larger than what the pancreas secretes in normal individuals, can help people overcome insulin resistance. Yes, blood sugar levels will decrease. But there are side effects: insulin itself, and many of the medications that increase insulin or increase its effectiveness, may cause weight gain. And if obesity is a cause of insulin resistance, there is no way these treatments can stop a patient’s diabetes. Instead, for many victims, the diabetes just gets worse.
So let’s follow the money. If today’s treatment approaches don’t cure diabetes and may even make it worse, who benefits? Drug companies, who gain customers for life due to diabetes and its many complications, including vascular disease, dementia, kidney and eye problems, even cancer. Medical device manufacturers profit when diabetic patients need cardiac pacemakers, artificial valves, and prosthetic limbs. Kidney failure requires expensive machines, products and dialysis facilities. Many professions, including physicians, pharmacists, dietitians, physiotherapists, social workers, occupational therapists, and others are called upon to provide care and diabetics need hospitals, clinics, blood test labs, MRI machines, offices, exercise machines, and more. Simply put, the new paradigm is good for the economy. It’s too bad that patients must suffer.
If the theory that high insulin levels cause insulin resistance has no scientific basis, where is the research disproving this hypothesis? And why aren’t the current treatment approaches truly helping Type 2 diabetics fight a disease that has huge health consequences? I don’t mind being wrong. Show me the evidence!
- The role of diet in gout
- A new federal political party for us nerds