The carbohydrate-insulin model of obesity

There is likely more than one reason for gaining weight across a population. This post is directed at those who follow western dietary guidelines (high-carbohydrate; low-fat) and who are nevertheless overweight, obese or diabetic. This is a significant (and increasing) proportion of the population. In particular, those who have not had success with ‘dieting’, but still want to reduce weight. I will start by outlining the problems with a well-known and mostly ineffective approach to weight-loss.

1. ‘Eat less. Move more’

This is the energy-balance (calories in, calories out) model of obesity, and it is the most popular model by far. In general, it can work in the short-term but usually not over the longer-term.

The model falls down because it is not based on our biology. It is based on two concepts in physics: a unit of heat energy (the calorie) and the law of conservation of energy (hence calories-in vs. calories-out). The failure to be biologically-relevant is why this model is unsuccessful in the longer-term. For example, it does not account for metabolic adaptations that occur with a change in energy supply and demand, such as lowering resting metabolic rate to match calories-in.

We should not even be using physics to explain a complex biological phenomenon. It’s like using the law of gravity to explain why people die if they fall out of a tall building. Of course the law of gravity is in action, but we would look foolish if we used it as our explanation. Likewise, the law of conservation of energy.

2. It’s not your fault

When a dieter following ‘Eat less. Move more’ advice is unable to lose weight sustainably, s/he might be thought of as lacking willpower. The dieter might even blame themselves and try again with another calorie-based diet. The onus is put on the dieter, not the energy-balance model. However, it is not the dieter’s fault, it is the fault of the model.

Let’s have a look at our biology instead. I’m going to start by defining obesity.

3. A definition of obesity

It may seem unnecessary to define obesity (surely it’s obvious) but this is how science advances – define the terms as unambiguously as possible. This is rarely done in the health sciences. For example, what is the definition of: health, fitness, exercise or wellbeing? We sort of know what we mean by them, but they are undefined. This means that terms such as: healthy food, healthy living, healthy diet, etc mean different things to different people because ‘healthy’ is undefined. So, with that in mind, lets define obesity:

Obesity (noun): A disorder of fat accumulation

This is a biological definition of obesity. It doesn’t have anything to say about weight, body-mass index, waist circumference, calories or energy balance. It defines obesity by what is happening in the body. Now we can see the power of a definition, because it automatically tells us the next question to ask – what regulates fat accumulation in the body?

4. The biological regulation of fat

All of our biological functions are regulated so, of course, we regulate fat accumulation. Energy-balance enthusiasts would claim that our biology is not that sophisticated – fat accumulation is just calories-in vs. calories-out.

We have multiple signalling pathways (usually hormonal) that do the regulating. The critical hormonal signal for fat accumulation is the level of insulin – more insulin means more accumulation. We also have hormones to signal fat release, appetite, satiety and energy-signalling pathways to name a few. However, to understand fat accumulation we need to understand insulin.

5. Insulin and fat

The primary function of insulin is to manage the level of blood glucose (often referred to as blood sugar). Circulating blood glucose is highly damaging to us and it must be burned for energy or stored safely for later. Insulin normally manages this by enabling glucose to enter cells in the body that burn it as fuel for their metabolism.

However, if there is too much glucose in the blood, or if insulin cannot get glucose into cells because they have become resistant (insulin resistance), insulin changes tactics and signals the liver to use the glucose to make fats. Insulin then prioritises storing these new fats in our liver and in adipose (fat) tissue. Furthermore, insulin blocks the release of these stored fats – they will not be released for energy even if they are needed. It is a one-way street for fat when there is insulin around. Insulin drives fat accumulation and opposes fat utilisation. This is the “carbohydrate-insulin model” of obesity.

6. Why gaining weight means eating more and exercising less

The problem with excessive fat accumulation is that too much dietary energy is being stored as inaccessible fat, leaving the body with insufficient energy to fuel its metabolism. The brain starts to get energy-deficit messages, and instructs the person putting on weight to eat some more. It will also reduce non-essential functions to conserve energy. Exercise is opposed as a wasteful use of calories (the brain can easily discourage exercise).

You can now see how dietary authorities can get confused. What they see from the outside is an overweight person eating more than a lean person and minimising unnecessary activity such as exercise. However, what is happening on the inside makes perfect sense: Too many dietary calories are being shunted into fat stores and locked away, leaving the person with insufficient calories for normal function. The body responds by eating more calories and expending fewer. An overweight person eats more and moves less for a perfectly sound biological reason. This way of thinking makes the term ‘eating too much’ a meaningless concept. An overweight person eats what they need, just as a lean person does.

7. Cause and effect

With this model, eating more and exercising less are effects, not causes, of fat accumulation.

However, with time, cause-and-effect get blurred. The more fat that is stored, the more the need to eat. The more that is eaten, the more fat is stored. In parallel, the more that energy is conserved. The more that is conserved, the more is available to store as fat. At this chronic stage, health authorities can easily mistake the effect for the cause.

8. What chronically elevates insulin?

There are two main factors, insulin resistance and high dietary carbohydrate.

Insulin resistance occurs when cells oppose insulin’s signal to take up glucose. This might be a consequence of a lifetime of high carbohydrate (especially sugar) consumption. Or, there may be a genetic predisposition. As cells start to oppose insulin, the pancreas responds by releasing more insulin, which signals fat accumulation.

Insulin resistance is not all-or-nothing, everyone falls somewhere on a spectrum. There are indications that insulin resistance increases slowly with age in many people. In the presence of even mild insulin resistance and high carbohydrate consumption, chronic fat accumulation would be expected.

9. Type 2 diabetes

The role of insulin resistance in obesity explains why people with type 2 diabetes are often obese. Obesity doesn’t cause diabetes (although it may contribute to symptoms in later stages). Obesity and diabetes occur together because they share a common mechanism – insulin resistance. It only looks like obesity causes diabetes, because obesity is apparent before the threshold for a diagnosis of diabetes has been crossed. Obesity can increase alarmingly when diabetics start taking insulin – raised insulin is driving fat accumulation. Telling such people to lose weight is particularly disingenuous (or ignorant).

10. How to fix it

Obesity and type 2 diabetes are dietary disorders, and both can be reversed with dietary changes. For anyone familiar with my writing, you know that I am suggesting a low-carbohydrate high-fat ketogenic diet.

With a ketogenic diet, low circulating glucose reduces demand for insulin, and insulin loses its hold over fat stores. Consequently, another hormone (glucagon, also secreted by the pancreas) can release fat from adipose tissue that can be used for energy, either directly (fatty acids) or indirectly (ketones). Burning body fat for energy will reduce the demand for calories-in, and the brain will get satiety signals. There should be no feeling of hunger as weight reduces. Activity levels will increase naturally.

Notice that something important has happened here – people who follow this strategy are now eating less and moving more.  ‘Eat less. Move more’ has become a result, not a method.


We don’t get fat because we eat, we eat because we are accumulating fat. We are accumulating fat because of an hormonal imbalance (raised insulin). Insulin is raised because of high dietary glucose and insulin resistance. High dietary glucose and insulin resistance can be reversed by a change in dietary macronutrient composition that lowers carbohydrate consumption.

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Note: The content of this post is intended to be educational and informative. It should not be taken as medical advice.

Further information: I recommend the writings and presentations of Professor Tim Noakes, Dr Jason Fung, Dr Zoe Harcombe, Dr Eric Westman, Gary Taubes, Nina Teicholz and the website

I have expanded on Type 2 Diabetes here.

This is a nice (1 min 41 sec) explanation by Eric Westman of the basic principles:

How to Do an LCHF Diet