Insulin resistance is exactly what the name suggests – the cells of the body become resistant and do not respond to insulin as they would do when the body is in a state of optimal function.

Insulin is the hormone produced by the pancreas in response to any food that is ingested and absorbed by the gut. The magnitude of this response is very much determined by the type of food and we refer to the glycaemic index which is an objective measure of this response. So, each individual type of food can be classified according to its glycaemic index or GI. Therefore, high GI foods produce a pronounced insulin response where as low GI foods produce an attenuated response. And this is very much related to the actual amount of glucose that an individual food releases when it gets digested by the gut.

All carbohydrate, in whatever form it is ingested, gets converted to glucose in the gut and is absorbed as such. Protein is digested into amino acids in the gut and amino acids will produce an insulin response through gluconeogenesis which is a generation of glucose from non-carbohydrate sources. Because this process occurs in the liver and therefore relatively slowly, the subsequent rise in blood glucose and therefore the insulin response is relatively shallow.

Similarly, fat is digested in the gut and absorbed as triglycerides. The latter are broken down in the liver into free fatty acids and glycerol. It is the glycerol component that once again enters the gluconeogenesis pathway in the liver and releases a low level of glucose and an attenuated insulin response as a consequence.

The main function of insulin once it has been released by the pancreas is to push glucose into the cells for immediate utilisation, and if it cannot be utilised then it promotes the conversion of glucose into triglycerides which is then stored as adipose tissue. So, this is a normal homeostatic mechanism that ensures we have an immediate supply of substrate for the generation of energy.

But it also ensures that none of this substrate is wasted and the storage facility of course exists in the event that the individual was forced to go without food for anything more than a few days at a time. And this of course probably happened on a regular basis with primitive man whose food sources were far from consistent and reliable.

At a cellular level the entry of glucose into the cell is facilitated by the insulin receptor. As a normal homeostatic function the cell has developed a mechanism such that the cell will not be flooded with glucose in the event that supply is indeed plentiful. Instead it will attempt to restrict it and it does so through down-regulation of the insulin receptor and this precisely the phenomenon of insulin resistance.

The cell therefore has to have a system whereby it knows automatically that it is being flooded with glucose and it is almost certainly the increased quantities of insulin itself that is responsible for its down-regulation. And this is exactly how you would expect the cells and the human body to respond – it is simply another example of a superbly orchestrated homeostatic mechanism designed to ensure the survival of the species.

Move forward a period of several hundred thousand years and we have the current situation where modern man has a plentiful supply of food. However, because of evolution and the way the body has evolved, these homeostatic mechanisms still exist and now operate perversely. So, every time blood insulin is elevated which of course happens in particular in response to high GI foods such as refined carbohydrate, this promotes insulin resistance.

So, the next time that a similar type of food is taken in, more insulin is required to produce the desired effect, namely to keep blood glucose within the strict parameters of 4.4 to 6.2 mmol/L. However, at some point, when it is producing maximal amounts this will not be sufficient and the glucose levels will exceed the upper limit of normal and this of course results in diabetes.

So in summary insulin resistance is a result of too much insulin and insulin itself results in further insulin resistance so a vicious circle is set up. Insulin resistance of course goes hand in hand with obesity simply because the insulin is no longer pushing the glucose into the cells. Instead it is converting the glucose into triglycerides and promoting obesity. This therefore explains why the only way biologically to prevent obesity in the first place is to limit insulin production. How do you limit insulin production? – stop ingesting food, in particular refined carbohydrate.

The really good thing however is that this does not need to equate to starvation. Starvation is bad for the body in that the body senses almost immediately that there is a restriction in the intake of calories and it responds by dropping the basal metabolic rate down to a level that will match the intake. It is extremely important that calorie intake is maintained at approximately 2500 calories for males and 2000 calories for females in order to maintain a normal basal metabolic rate.

And this is the rational for point 1 of the Nysteia Formula, namely intermittent fasting. For 18 hours of the day, ideally, there is no ingestion of food and the pancreas is not releasing any insulin. This allows the cells to regain their insulin sensitivity. It also gives the individual sufficient time, i.e. 6 hours, in which to ingest their normal daily calorie requirement to maintain their BMR.

Intermittent fasting of course also allows the body to utilise its alternative energy substrate namely fatty acids, which it is perfectly capable of doing and is a normal homeostatic mechanism. And it will obtain this from stored adipose tissue which will result in a kilogram of weight loss on average per week. Lipolysis, which is the body’s normal mechanism for releasing fatty acids from stored adipose tissue, can only happen in the absence of insulin. As soon as anything is taken into the gut there is an insulin response and this will switch off lipolysis straight away and with it the opportunity for fat burning and therefore weight loss.