When Banting and Macleod won the Nobel Prize for the discovery and purification of insulin in 1923, a very great thing had been achieved. Many, many lives have since been saved, and there is no doubt that the prize was justified. Even if Banting and Best did their furious best to write Macleod (A Scotsman, of course) out of the history books, and trash his reputation. Oh yes, how horrible people are to each other in the world of science.

However, as the same time as this great thing happened, something else, silently, took place. Insulin and sugar become so closely intertwined in the minds of everyone, that we got stuck. Thinking got stuck… into the following paradigm

When blood sugar goes up, insulin is released to bring it down.

Without insulin we develop diabetes

If the blood sugar drops too much, it is because there is too much insulin, and we get the patient to eat more sugar

You treat people with high sugar levels with insulin etc.

This is a paradigm with only two variables. Blood sugar*, and insulin. Type I diabetes is due to a lack of insulin, Type II is due to a relative lack of insulin caused by ‘insulin resistance’ whereby enough insulin is produced, but its effects are blocked. Insulin sugar, sugar insulin. End of.

I think of this as the super-simplistic model of diabetes. Of course insulin and blood sugar are connected, but this model is inadequate. A violin with only one string, playing a hopelessly restricted tune. For those who did watch Professor Unger’s YouTube lecture, you will be aware that this ‘insulino-centric’ model of diabetes is, in many ways, just plain wrong.

He has, for example, done experiments on mice whereby he completely destroyed the beta cells in the pancreas, conducted a glucose tolerance test, and found that the resulting glucose levels followed almost exactly the same pattern as in mice with intact beta cells. In short, insulin is not required to keep blood sugar levels under control after a glucose meal.

For those who have watched the video, you will be aware that this statement is true, but I have left out something rather critical. However, the main part of the statement is still correct. Despite what we are repeatedly told, you don’t need insulin to keep your blood sugar levels under control – the body can do this almost as well using other systems. Shock, horror, the body does not need insulin to absorb and store sugar.

This even trumps a statement that I have made repeatedly in other writing. Namely, keeping blood sugar under control is probably the least important thing that insulin does. You may just think that I am talking nonsense at this point. Without insulin, you die. That is what happened to all type 1 diabetics before insulin was discovered, isn’t it. So, why are you trying to tell me that insulin is not hugely important?

Well it is, but it is only important in that, without insulin, we do not control glucagon levels. Ah yes, glucagon, something most doctors heard about in the second year of medical school, then forgot that it ever existed. Except that, if a diabetic gets very low blood sugars levels you can inject glucagon and the sugar level bounces right back up.

However, despite that fact that most people have never heard of it, and most doctors have forgotten that it exists, glucagon is critical, and the interplay between insulin and glucagon is hugely, hugely, important. It is not a lack of insulin that causes catastrophically high sugar levels in type I diabetes. It is the overdrive of glucagon that does this. Equally, if you do not produce glucagon, you cannot get high blood sugar levels. End of.

Ah yes, so we have another player in the game of diabetes. Insulin, sugar… glucagon. And this, ladies and gentlemen is merely the start. Now, just as a teaser, I will introduce you to the critical importance of visceral fat in diabetes. Here is a little snippet from a study on mice:

‘In the present study, DIO [diet induced obesity – my comment] and diabetes mellitus were achieved in 100% of the mice after 8 weeks of treatment. At this point, some animals were submitted to visceral fat removal and the metabolic and molecular consequences of this procedure were evaluated. First, we observed that, 8 days after the surgical procedure, the mice were no longer diabetic

…Thus, we conclude that, in an animal model of DIO and diabetes mellitus, the removal of visceral fat is effective for rapidly reducing the blood levels of glucose. This is accompanied by improved in vivo and molecular actions of insulin and is paralleled by a favorable modulation of the levels of adipokines.1’

Remove visceral fat and diabetes is gone. So, here is another massive variable in the old obesity, diabetes, insulin model. This variable is visceral fat, not be confused with subcutaneous fat – the type that Sumo wrestlers have tons of. Indeed, visceral fat is so different, metabolically, to subcutaneous fat that we shouldn’t really call it fat. It is something else entirely, a different organ.

Visceral fat is also another vitally important player in type II diabetes. As is, of course, adipokine production… which you will be no doubt glad to hear I shall talk no more about for the moment. As you may have guessed, I am not providing any answers in this blog about type II (insulin resistant) diabetes – or indeed type I. I am just trying to make it very clear that the model containing two players, insulin and sugar, is a complete barrier to understanding what is going on. You must remove it from your mind.

I will also state that I have most certainly not got it all figured out, fully. So, you are not going to get a definitive answer here – although perhaps some better answer. I keep thinking I have got all the pieces in place, then another bit of information appears and my carefully constructed model splinters apart. Try, for example, looking up the effect of insulin and cortisol on visceral fat, and see if you can make sense of what the hell is going on there. If you do, please let me know.

No, the reason for writing this blog is to continue with my endless theme. Please think for yourselves, and do NOT accept what you are told. This is most especially true in the area of obesity and diabetes.

1: http://joe.endocrinology-journals.org/content/191/3/699.long

*I use the word sugar to mean, mostly, glucose