Body Chemistry


Insulin is a major player in how you use your energy sources and so in turn a major player in obesity chronic illness.

It is made by beta cells in the pancreas.

High blood sugars causes the release of insulin. 

Carbohydrates are the main cause of a quick increase in blood sugar and therefore insulin release.

But, eating protein also causes insulin to rise to some degree, though eating protein doesn’t really impact on our blood sugars. 

Eating fat causes minimal increases in insulin and  no increase in blood sugar. 

So, insulin levels change, to varying degrees whatever you eat.

 It moves glucose (sugar) from the bloodstream into tissues that need them for energy – your muscles to be stored for use, to your liver to be stored for use- they are stored in these two places as something called glycogen. 

 If these two places are full up , it sends this glucose to be changed into  something called a  triglyceride ( a type of fat) and puts  it in your fat stores – visceral and subcutaneous adipose tissue. It also stops those fat stores ( your adipose tissue) releasing their fat stores that could be used as energy. 

So insulin sends the glucose in your blood to either a tissue that can use it for energy or to your storage depot for later use.  Its presence also stops us going to our energy storage depot ( our fat cells ) and breaking down that fat ( lipolysis) to use for energy.

We need our circulating insulin levels to be generally low, spike in relation to food, and we want that spike to be small and short lived, we don’t want a lot of insulin floating around in our blood constantly ( this is known as hyperinsulinaemia), eating frequently through the day, especially eating frequent, high refined carbohydrate, processed foods results in hyperinsulinaemia.  It is beneficial for us to have very efficient insulin! At the end of our lives the least amount of insulin we’ve needed, the better.

WHAT IS Insulin Resistance?

So now we  know what insulin does it easier to understand what insulin resistance is and also get closer to understanding about metabolic dysfunction and metabolic flexibility. 

When a person is insulin resistance the insulin doesn’t have he same effect on any of the tissues it is destined to have and effect on.

The insulin doesn’t move glucose out of the blood in to the muscles or liver as effectively as it could. The receptors that the insulin is meant to bind to on these cells don’t click with the insulin  and the glucose isn’t allowed into the cell – like a bouncer at the door of a club that is having a very bad day and just won’t let many people ( glucose) in!

The pancreas, puzzled by this makes MORE insulin, figuring if more people turn up at the door of the club, they have to let more people in!

This happens even if we haven’t eaten anything else, in an effort to try and force the glucose into cells ( muscle or liver, adipocytes). This results in people with insulin resistance having high levels of insulin constantly, unrelated to eating- HYPERINSULINAEMIA. 

Eventually this situation can result in disease states such as  Type 2 Diabetes. In type 2 diabetes the insulin we make is it isn’t very effective at all anymore and the tissues just don’t respond to it. 

Insulin resistance, hyperinsulinamia are now understood to be a baseline, very important mechanistic cause of thousands of chronic diseases and wellness issues -type 2 diabetes, dementia, cancer, heary=t dsiease, strokes, erectile dysfunctions, mood disorders, gut disorders, the list goes on.

Different cells  can have different amounts of insulin resistance – your muscles can be more or less insulin resistant than your liver or your kidney , all can have different results in tests that we may do, but they all are caused but the same thing and can result in different problems.

Your insulin resistance is directly related to the SIZE of your adipocytes (fat cells).  The bigger your adipocytes are the more insulin resistant you.

As we know we push excess energy that our livers or muscles aren’t storing into our fat stores.  We can do this in two ways – either by jamming as much extra triglyceride into our fat cells – needing more and more insulin to do this ( hyperinsulinaemia) and keeping insulin levels high to keep the fat jammed in there. 

OR we can make more fat cells.

The people who make more fat cells seem to have issues with obesity but less issues with hyperinsulinaemia , insulin resistance and metabolic changes.

That is – Those of us that don’t make more fat cells try and jam the fat in the cells we have exhibit signs of  metabolic dysfunction.

This Personal Fat Threshold is genetic. Once we reach this threshold we cant jam any more fat into our fat cells, we have high insulin levels to try and close the door shut on the fat in the cells ( like sitting on an overfilled suitcase trying to close it). This extra fat then gets deposited in the liver , the muscles and everywhere its not meant to be = Insulin resistance.

Those with a genetic predisposition to being able to make more and more fat cells can get bigger and bigger without insulin resistance because they have lots of new small fat cells to accommodate the triglycerides.

This is an example of why you can have a “normal weight” and still be  insulin resistant, its just no=one flags you up as high risk so you don’t know about it until its too late- you’ve had a heart attack or a stroke, or your memory starts to change. So health isn’t all about weight.


This hormone is also made in the pancreas in its alpha cells.

Its effects are opposite to those of insulin.

It is released in response to lower blood glucose levels and it stimulates the liver to breakdown its glycogen stores ( stored glucose), it activates ‘gluconeogenesis’- new glucose production by the liver and breaks down stored fat ( triglycerides in your fat cells).  

All this results in increasing blood glucose levels.

SO we are capable of increasing our blood glucose levels without ingesting any carbohydrate and for quite some time, without any food.


Leptin is made by adipocytes ( fat cells). It has an effect on the brain, in an area called the hypothalamus and affects hunger and energy use.

It is an important hormone in periods of inadequate food intake. Leptin levels go down when we fast or on a low calorie diet and stimulate hunger whilst making sure we expend less energy – store more fat. So, low levels occur when there isn’t much food around, stimulating us to eat and to store the calories as fat.

However, the more fat stores we have, the higher levels of leptin there are. This should mean that we feel less hungry and burn more energy.  There is a theory that obese/overweight individuals , or individuals with hyperinsuinaemia, may be leptin resistant. when we are leptin resistant, the leptin doesn’t bind to its receptors properly and so the body thinks that there are low levels of it- stimulating hunger and storage of body fat.


Made mostly in the stomach, often called the hunger hormone, it stimulates appetite, increase food intake and promotes fat storage. 

If we have regular eating pattern Ghrelin levels will rise before eating and go down after eating. Ghrelin levees rise with chronic calorie restriction, explaining why lots of simple calorie restrictive diet fail in the long term. 


Sometimes dubbed “ the stress hormone”.

It is normally secreted throughout the day in a diurnal pattern – that means its levels vary according to the time of day- NORMALLY they are highest in the morning and lowest at night – getting us ready for our waking ours when we are productive and falling before we sleep.  In people who work night shifts this pattern can be reversed. 

Made in the adrenal glands just above our kidneys it is part of a feedback loop involving the hypothalamus, the pituitary gland and the adrenal gland,  it has an effect on lot of different things- blood sugar, metabolism, water balance, blood pressure.

If you can imagine what the ideal state would be just before we wake up, it would be to have a surge of hormones that make us feel less sleepy and start moving energy out of storage ( stat cells, liver cells, muscles)  and into the blood stream ready for us to use.

So, in normal conditions of good sleep, a nutrient dense diet that works for you and minimal stressors, insulin and cortisol have opposing effects.

Unfortunately chronic, non physical, psychological stress can chronically increase our cortisol levels- work , relationships, financial worries, sleep deprivation. 

In these situations our blood glucose remains higher than it would normally be , constantly triggering higher insulin levels – hyperinsulinaemia.  

High cortisol levels encourage fat storage around the organs – visceral fat- the fat that causes metabolic issues.

This is the same reason why doctors worry about long term  steroid use for illness.  The chronically elevated insulin levels can result in insulin resistance and then sometimes diabetes.