There are 2 kinds of insulin resistance in a sense. In diabetes, we see pathological (meaning bad) insulin resistance. On a ketogenic diet, we see physiological (meaning normal) insulin resistance.

The ketogenic diet diverts blood sugar preferentially towards your brain and less towards your muscle by making your muscles insulin resistant. So your brain is kept happy with its 30-50% glucose requirements and your muscle can do without the glucose by happily burning away fatty acids. This is normal metabolic flexibility.

In diabetes, you’ve got generalized insulin resistance that is metabolically inflexible, making you a poor fat burner and hyper-reliant on glucose. This is damaging to your cells and organs. It results in glycated tissues and peroxidized fats that essentially age you, increasing your risk of heart disease, cancer and even losing a limb!

Insulin resistance is caused by several mechanisms, one of which is chronically elevated insulin levels. So what increases insulin levels? Mainly sugar. A poor nights sleep can do it too, but sugar is a big one. This can be sugar that is part of our diet or carbohydrates that are broken down to glucose or other simple carbs. Proteins put together with fats can also be converted into sugar, a process called gluconeogenesis. However, it is really the effect of dietary refined sugars and starches (flour) causing blood sugar and insulin spikes (not protein). These insulin spikes from added sugars and flour are then often followed by a blood sugar crash, leading to a sense of discomfort, even sweating, and usually a craving for more high-carb foods.

When we eat this carby kind of food multiple times per day with little time in-between meals, insulin levels are consistently high throughout the day. Over the years, cells react to this constant overflow of glucose and fat by shutting down their insulin receptors. With fewer insulin receptors, cells become less sensitive to the action of insulin. For the same amount of glucose to be taken up, the pancreas has to produce more insulin.

Not only cells that use glucose as fuel become insulin resistant but also chronically inflamed fat cells. When they become insulin resistant, they take up fewer circulating lipids despite high insulin levels. Insulin resistance also increases the release of free fatty acids from fat storage. Free fatty acids in the blood reduce the glucose uptake into muscle cells and further contribute to insulin resistance.

Insulin resistance is often characterized by high triglycerides, as well as a high ratio of triglycerides to HDL-cholesterol.

Another organ that plays an essential role in blood sugar regulation is the liver. It stores excess glucose as glycogen, and when glucose levels are low, glycogen is broken down to provide glucose [6]. This process is regulated by two hormones: insulin and glucagon. Insulin normally promotes glycogen synthesis and interferes with glucose release from the liver.

With increasing insulin resistance, the liver may release glucose despite the presence of insulin. Another mechanism how insulin resistance leads to an increase in blood sugar.

Insulin resistance becomes worse over time, so more and more insulin has to be produced.

At some point, the pancreas is literally burned out and can’t produce enough insulin to keep even basic blood sugar under control, let alone after a high-carb meal. This state is end-stage of type 2 diabetes where insulin injections become necessary [7]. Type 2 diabetics do not produce less insulin than normal, but the insulin resistance increases the need for insulin. A diabetic pancreas is eventually unable to supply this increased demand.

This sounds like a vicious cycle, and it is! More and more insulin is needed, and increased amounts of insulin further exaggerate insulin resistance. Is there a way to escape this cycle?

Good news: yes, there is a way!