Ken (not his real name, of course) is a GP.

I had just given a presentation on Type 1 management to a group of GPs. Ken was the person hosting the session. His job was to introduce the speakers and ensure everything ran on time. After I had finished, he was naturally keen to get the microphone off me and get me out of the auditorium. He was there for that reason.

“That was an interesting talk. I have had Type 1 for 20 years. I might give low carb a go.”

It was a nice closing pleasantry and a goodbye. I wished him well, and we parted company. I thought no more of it.

Ken was in his late middle age and had had adult-onset Type 1 diabetes for 25 years. His management plan had not served him particularly well. He was portly and using large amounts of insulin to deal with the carbohydrate in his diet.

We tend to think of insulin as the hormone that lowers blood glucose. It does, of course. But that is only part of the story.
Insulin is also a storage hormone and a fuel-management hormone.
When we eat carbohydrate, it is digested largely into glucose. Glucose enters the bloodstream and insulin rises.

Insulin then helps move glucose out of the bloodstream and into tissues where it can be used or stored. Some can be stored as glycogen in the liver and muscles. When energy is abundant, the body can also convert carbohydrate into fat. But insulin does something else that is crucial to this story.
It tells the fat cells to hold on to their fat.

Insulin suppresses lipolysis – the process by which stored triglyceride is broken down and fatty acids are released from our fat cells. Put simply, when insulin is high, getting stored fat out of the fat cells becomes more difficult.

This makes perfect evolutionary sense. If a meal has just arrived and glucose is plentiful, why would the body simultaneously need to empty its stored-energy cupboards? It doesn’t. Use the incoming fuel. Store the surplus. Leave the reserves alone. That is the high-insulin state.
Now reverse the situation.

Carbohydrate availability falls. Insulin falls. The brake on the fat cells starts to come off.
Fatty acids are released and can be transported around the body and burnt for energy. If carbohydrate availability remains sufficiently low, the liver can also turn some of those fatty acids into ketones. The body has changed fuel.

This is an important distinction. High insulin doesn’t mean that absolutely no fat can ever be burnt, and low insulin doesn’t magically guarantee weight loss. We burn mixtures of fuels throughout the day, and overall energy intake still matters. But insulin has a powerful influence over which fuels are available and which are being prioritised.

This is one of the most extraordinary things about human metabolism. We aren’t designed to run on glucose alone. Nor are we designed to run permanently on fat.

We are multi-fuelled animals.

We can burn glucose. We can burn fatty acids. We can burn ketones.

And our metabolism can continually alter the mixture according to the prevailing conditions. Eat carbohydrate and insulin rises. Glucose becomes readily available and we move towards greater glucose use. Stop eating for a while and insulin falls. Stored fat becomes increasingly available. Restrict carbohydrate further and ketone production can rise. Exercise hard and the fuel mixture changes again.

The healthy human metabolism isn’t defined by one particular fuel. It is defined by its ability to change fuels.

That ability is sometimes called metabolic flexibility. I prefer to think of it as changing gears. Ken had spent years supplying his body with carbohydrate and then injecting enough insulin to deal with it.

Lots of carbohydrate. Lots of insulin. Day after day.

His metabolic environment was therefore very different from the one he was about to create. Change the environment and the body changes with it.

So, it came as a total surprise when I received this email three weeks to the day after meeting him.

That was indeed genuinely staggering. This man was medically trained, on high-dose antacids, had undergone three endoscopies to investigate his reflux over two and a half years and was heading for surgery.

He told me that he had cancelled his operation.

The metabolic changes were less surprising to me. What was remarkable was the speed at which they had happened. Ken had dramatically changed the prevailing conditions.

He had reduced the carbohydrate coming in.

His requirement for injected insulin had fallen dramatically.

With lower circulating insulin for much of the time, the brake on his fat stores was reduced. His body had greater access to the enormous amount of energy already stored in his adipose tissue.

Instead of continually supplying one fuel and injecting insulin to manage it, he was increasingly able to call upon another fuel he already carried around with him.

His own fat.

He hadn’t suddenly acquired a new metabolism. He had changed the conditions, and his metabolism had adapted to them.