Outside of heart disease and statins, another area I have been studying for many years is diabetes. Not type I diabetes (caused by destruction of beta-cells in the pancreas and a lack of insulin), but type II diabetes. Type II diabetes has nothing to do with a lack of insulin, it is generally considered to be caused by insulin resistance i.e. enough insulin is produced, but there is ‘resistance’ to its effects.
This resistance firstly drives up the insulin levels. However, as it worsens, the raised insulin levels are no longer sufficient, so the blood sugar levels rise anyway. At first the fasting sugar levels may be normal, but the response to a sugar ‘test’ shows an abnormally high level about an hour later. This is why a glucose tolerance test (GTT) used to be the way of diagnosing early stage type II diabetes.
This has been superseded by the HbA1c test. This test, essentially, looks at the amount of glucose that has stuck to your red blood cells over the last month. Which gives an idea of what the ‘average’ sugar level has been over a longer time period. It is a better measure.
Anyway, without getting too bogged down in technical details, the model that is used to explain type II diabetes is very simple.
- You eat too much
- You become obese
- As you become more and more obese you become more and more insulin resistant
- Your insulin level rises to overcome this resistance
- At some point the resistance become too much
- You develop raised blood sugar levels aka type II diabetes
I call this the ‘blowing up a balloon’ model of diabetes. As the balloon expands, you need to blow harder to get more air in.
This model (or variations thereof) is almost universally agreed, by almost everyone. It should come as no surprise, therefore, that I do not agree with it. Yes, there is not the slightest doubt that diabetes and obesity are related. In fact, there is no doubt that obesity; insulin resistance and type II diabetes are closely related.
Equally, there is no doubt that if people lose weight, their diabetes can go into reverse, and ‘reversibility’ is one of the most powerful pieces of evidence possible in proving causality. So where exactly, you may think, is my problem?
My problems first started with the recognition that you can find far too many direct contradictions to this model. Just to look at two examples. First we can look at the least obese people in the world. Those unfortunates who have a condition called ‘Beradinelli-Siep generalised lipodystrophy’. In this condition you have no fat cells – at all. So, of course, the rate of type II diabetes in these people would be zero…right? Wrong, the rate of type II diabetes is 100%.
Then we have Sumo wrestlers, the single most obese group of people on earth. So, they all have severe insulin resistance and type II diabetes right…? Wrong, whilst in training, none of them have type II diabetes.
- Thinnest group of people in the word, 100% diabetes
- Fattest group of people in the world 0% diabetes
Or to put this another way round, it is clear that obesity is neither necessary, nor sufficient to cause type II diabetes. If you were a follower of Bradford Hill, or Koch, of Popper this, effectively, writes off obesity as a possible causal factor for type II diabetes.
To move sideways for a moment or two. When you first read about type I diabetes, one of the things that stands out is that those diagnosed with type I (at least in the past) lost weight very rapidly. They grew thinner and thinner, becoming almost like skeletons – before they all died. Why?
Why, is because insulin is the energy storage hormone. It does not just affect blood sugar levels. In fact, the almost obsessive focus on the interplay between insulin and blood sugar has blinded almost everyone to the fact that insulin does far more than just lower sugar levels. It affects fat, protein and sugar metabolism. It interacts with many different pathways in adipose tissue, muscle cells and the liver. Lowering blood sugar may be, in some ways, the least important thing that it does.
The reason why you die in type I diabetes has little to do with blood sugar levels. You die because, without insulin, fats escape from adipose tissue and travels to the liver as free fatty acids. In the liver these fatty acids are automatically converted into ketone bodies (which the body uses for energy in a fasting state).
The ketone bodies are, in turn, acidic, and in a high concentration they cause ‘acidosis’. This acidity overwhelms the alkali buffering systems, and you die in a keto-acidotic coma. To reiterate, it is not the high sugar that kills you in type I diabetes, it is the uncontrolled release of fats. This has nothing to do with sugar at all – except indirectly. Which, although you may not think it, returns us to the matter in hand. Namely, what is the association between obesity and diabetes?
As we have seen, without insulin, fats escape from fat cells at a high rate, so you lose weight. If we turn this though one hundred and eighty degrees, it should be clear that, if you have too much insulin in your bloodstream, fat can no longer escape from fat cells, and you will get fatter and fatter.
Essentially, insulin is obesogenic. A fancy way of saying that if you produce too much insulin you will become obese. An amazing fact ‘discovered’ in August 2014
“DALLAS – August 25, 2014 – UT Southwestern Medical Center researchers have identified a crucial link between high levels of insulin and pathways that lead to obesity, a finding that may have important implications when treating diabetes.”
Yes chaps, well done. You made a breakthrough discovery of the absolute bleeding obvious. You mean, insulin makes you fat? Well who’d a thunk? Well, lots and lots of people actually. At which point, let me introduce you to the Pima Indians of North America. This race has an almost unbelievably high rate of type II diabetes. It is greater than 50%. Perhaps more. Are they obese, yes? Of course. However, of greater interest is that Pima Indians, long before they become obese and/or diabetic, produce far, far, more insulin than any other race :
‘The normal and prediabetic Indians had fasting and stimulated insulin levels during all the tests two-to-threefold greater than the Caucasians. Differences in insulin levels between the two races could not be explained by differences in glucose level, age, or obesity.’
Interesting… It is clear that the model with the Pima Indians is, as follows:
- You produce too much insulin
- You become obese
- You become insulin resistant
- You develop type II diabetes
Of course, it is not just the Pima Indians where this happens. This causal chain works for us all. It contains most of the same ‘factors’ as the blowing up a balloon model of diabetes (although you will notice it does not contain the ‘you eat too much’ factor). However, as you can also see, the facts are in a different order. I like to call this, the correct order.
In short, yes, obesity, insulin resistance and diabetes are closely associated. But not quite in the way that everyone believes.
Moving on. What, you might think, would cause people to produce too much insulin. Well, what foodstuffs cause the greatest rise in insulin levels? Why, let me think… Yes, carbohydrates would cause the greatest rise in insulin levels. So if you eat lots of carbohydrates, you will produce lots of insulin. Insulin forces fats into fat cells and stops it escaping. Insulin is obesogenic… Join those dots ladies and gentlemen.
P.S. Pop quiz. What do you think happens if you try to force blood sugar levels down in type II diabetes by prescribing insulin?
P.P.S. So why does everyone with Beradinelli-Siep syndrome have type II diabetes? Answers on a postcard please.