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Kendrick on...the fact obesity does not cause diabetes

Our clinical columnist, Dr Malcolm Kendrick, challenges another sacred cow – questioning whether obesity and diabetes really are linked

Our clinical columnist, Dr Malcolm Kendrick, challenges another sacred cow – questioning whether obesity and diabetes really are linked

Obesity, we're told, represents the next great disease epidemic and GPs should get on and treat it. This is despite the fact that all 'treatments' for obesity have been shown to be almost useless, often resulting in greater weight gain in the long-term.

Yet even if we could find some way of effectively managing weight loss, would this provide any major health benefits?

The US is in the grip of a supposed obesity epidemic – yet the rate of CHD continues to fall. And the link between obesity, measured by BMI, and type 2 diabetes is much less certain than many people have led us to believe.

One population with a very high rate of type 2 diabetes is emigrant Asian Indians – wherever they migrate to. However, their average BMIs are usually a great deal lower than other populations.

As you may already be aware, this inconvenient fact is explained away by suggesting Asian Indians are genetically susceptible to developing diabetes.

One study of Asian Indians with BMIs below 25kg/m2 suggested the definitions of 'normal' ranges of BMI and waist circumference should be revised1.

This form of post-hoc rationalisation would be recognised by Karl Popper as a form of logic used by scientists to protect lovingly held hypotheses.

He used the following dialogue as an example: 'Why is the sea so rough today?' 'Because Neptune is very angry. ''By what evidence can you support your statement that Neptune is very angry?' 'Oh, don't you see how very rough the sea is? And is it not always rough when Neptune is angry?'

In the case of Asian Indians, this form of circular logic can be redefined: 'Why do Asian Indians have such a high rate of type 2 diabetes?'' Because they are genetically susceptible. ''How do you know?'' Because they could not have such a high rate of type 2 diabetes without other risk factors if they were not genetically susceptible.'

Inarguable logic. However, a scientist should try to establish exactly how this genetic susceptibility might be identified, rather than just redefine obesity in selected populations to a level that allows the facts to fit the hypothesis.

But it is not just Asian Indians who refute the hypothesised link between obesity and type 2 diabetes. There are many others. Perhaps the most spectacular can be found in a condition known as Berardinelli-Seip syndrome.

People affected by this syndrome have very little adipose tissue. Theoretically, therefore, they should have no problems with insulin resistance or type 2 diabetes.

Not so. Every individual with Berardinelli-Seip suffers from insulin-resistant diabetes mellitus2. On the other hand, the most highly 'obese' population in the world – Sumo wrestlers – has no problems with type 2 diabetes or impaired glucose tolerance3. These are what Karl Popper would have called 'black swans' (inarguable facts that utterly refute a theory).

In reality there are two sorts of adipose tissue, which are totally different. There is subcutaneous fat, which is what Sumo wrestlers have lots of, and there is visceral or omental fat – fat around the organs.

Visceral fat is the type of fat emigrant Asian Indians have. It is also the type of fat that develops if you give people long-term steroids, or is found in Cushing's disease4.

It is found in a number of people who have HIV and take HAART5 and is more often found in men than women. It is true that visceral fat mass does bear some relationship to overall weight; if you have a high BMI, you are likely to have more visceral fat than someone who is slim.

But this does not always hold, as demonstrated by Sumo wrestlers. In fact, if you are 'obese' yet take regular exercise, you will have little visceral fat, and no metabolic problems6.

Visceral fat itself may or may not create the spectrum of disorders ranging from metabolic syndrome to type 2 diabetes. Or perhaps increased visceral fat may be a sign of a metabolic dysfunction.

The jury is still out on this. What is certain is that a raised BMI is a crude and almost useless measurement. It does not, except in the most peripheral way, relate to an increase in type 2 diabetes, CHD or overall morbidity and mortality.

Ergo, treating obesity, as defined by a raised BMI, will achieve little.

Malcolm Kendrick is a salaried GP in south Manchester

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