We are told, ad-nauseam, that obesity is the main cause of type II diabetes. This, allegedly, follows a very simple causal chain.
Obesity > insulin resistance > raised blood sugar levels
For those not familiar with the term Insulin resistance, this is the condition whereby various organs in the body become gradually more insensitive to insulin, which forces insulin levels higher to keep the blood sugar levels down.
Eventually the resistance to insulin becomes so great that the blood sugar levels rise anyway – despite the high insulin levels. Alternatively, or in parallel, the pancreas gives up fighting against the resistance and insulin production becomes ‘burnt-out’. Whichever process is dominant, they both result in sugar levels become very high, and you will be diagnosed with type II diabetes.
At this point I have to state that I have always found it weird that a raised blood sugar level can be defined as a disease, when it is clearly nothing of the sort. In my world a ‘disease’ is the underlying malfunction which causes various signs and symptoms to occur (of which a raised blood sugar level would be one).
Everyone agrees that insulin resistance is the basic underlying cause of a raised blood sugar level a.k.a. type II diabetes. Despite this we define the blood sugar level itself as the disease.
‘A high blood sugar level is type II diabetes….end of.’
‘So, if we lower the sugar level, we have cured the disease?’
‘Yes. Now do shut up.’
Clearly bonkers, but let us not expect too much in the way of logic in medicine. Anyway, that is a slight distraction from the main theme here, which is the: obesity > insulin resistance > raised blood sugar levels discussion.
Now, for reasons that I am not going to fully bore you with here (but maybe at a later date), I have always had problems with this causal chain. Primarily, that it has never made much sense to me. Insulin resistance occurs almost exclusively in two tissues; the liver and skeletal muscle, and NOT in adipose tissue. So why would having too much adipose tissue make you insulin resistant? Answers on a post-card please*.
In order to pursue this thought further I started to look at evidence from Sumo Wrestlers. These are the most obese people on the planet. At least they are if you use BMI to define obesity. Yet, none of them have type II diabetes (at least not, whilst in training). For example:
‘Abnormally large waist circumferences, which were determined by the criteria established by the Japanese Society of Internal Medicine, were present in all Sumo wrestlers (100%), and fifteen Sumo wrestlers (83%) had high abdominal visceral fat areas (>100cm2). Only 2 subjects were categorized with high serum triglyceride levels, and 5 subjects were classified with low HDL-C levels by established criteria. None of the Sumo wrestlers had fasting hyperglycemia (high blood sugar levels) (0%)’1
Interesting, is it not, that the most obese people on the planet do not have type II diabetes (although some of them have a degree of insulin resistance – for reasons that I may explain at a later date). Yes, I know exactly what you are now thinking. They do not have diabetes because they exercise a lot. It’s true, they do. But does that not make it more likely that a lack of exercise is the true of cause of insulin resistance, rather than obesity….yes, of course it could certainly mean that.
In truth, finding very obese people without diabetes does not rule out obesity as the cause of diabetes. But it does rule out obesity as being both ‘necessary’ and ‘sufficient’. At this point I need to explain the concept of necessary and/or sufficient.
It was Koch who first tried to determine a process of logic to describe whether or not something may be a true cause of a disease, or just a chance association. He introduced us to Koch’s postulates, and also the concept of necessary and/or sufficient.
For example, it is known that the bacteria vibrio cholarea causes cholera. In order to get all the signs and symptoms of cholera it is ‘necessary’ to be infected with this organism. However, infection with vibrio cholarea does not cause cholera in everyone. If you are a fit and healthy adult you can shrug off the infection with only mild symptoms. Koch proved this by drinking a glass of water known to be infected with vibrio cholarea and developing only mild symptoms of the disease
Thus it can be stated therefore that infection with vibrio cholarea is ‘necessary’ to cause cholera. However it is not, on its own, ‘sufficient.’ Other factors are needed. On the other hand, if you could find people with cholera who had not been infected with vibrio cholarea, then you would have to declare that vibrio cholarea was neither necessary, nor sufficient, to cause cholera. So it could NOT be the cause of cholera.
This is obvious, and inarguable.
So, moving back to type II diabetes. Can you find people with type II diabetes who are of normal weight? Or, to stretch this concept to the limit, can you find people with type II diabetes who have no adipose tissue at all? Surely not, you say. Surely impossible.
At this point I shall introduce you to ‘Berardinelli-Seip Congenital Lipodystrophy’. This condition affects about one in ten million people. So it is hardly common, but that is not the point. The point is that the primary abnormality in Berardinelli-Seip Congenital Lipodystrophy is a lack of functional adipocytes – which means that those who suffer from this condition do not have fat cells, and cannot store fat. Ergo, that they are extremely lean. The leanest of the lean, the least obese of the least obese.
From time to time I describe this condition to doctors. At which point I somewhat cheekily ask them to guess what percentage of people with Berardinelli-Seip Congenital Lipodystrophy have type II diabetes. I say cheekily, because they inevitably get the answer wrong. They always, without exception, answer pretty much as follows:
‘Obviously, none of them.’
The correct answer is, of course, ‘Every… single…one…of…them.’ [Gasp, sounds of people collapsing to the floor in shock etc.]
Now, if you can understand why this is true, you are at least one step on the road to understanding type II diabetes. Or to be more accurate, what is the true underlying cause of insulin resistance and high blood sugar levels. You will also understand that obesity has only a small and indirect part to play in this process; that BMI has no relevance to the issue, and that the simple causal chain: Obesity > insulin resistance > raised blood sugar level……is wrong.
Of course obesity is closely associated with diabetes – to state otherwise would be nuts. However it is not the cause of type II diabetes. It is caused by it. By which I mean that obesity is (in major part) caused by that the underlying process that also leads to insulin resistance and high sugar levels. There is a causal chain here, but it is not Obesity>insulin resistance>raised blood sugar levels.
More on this later, once your brain has become unscrambled.
*Yes, for those who know about this area, you can talk about visceral fat, but this is another more interesting and completely different discussion. I am also only discussion type II diabetes, not type I (which is a completely different condition altogether).