We used to believe that type 2 diabetes was a problem of obesity: eat too much sugar and junk food and you’ll gain weight and get diabetes. Simple. But through using sophisticated scanning technology, my team has been able to show that diabetes can strike whatever your girth. Interestingly, this is never a random attack problem that only occurs if you accumulate more fat than your body can safely store.
Anyone can get type 2 diabetes, regardless of your body size, but only if you gain sufficient weight to push you through what we call your ‘personal fat threshold’. This is the metabolic tipping point based on your genetic make-up and is individual to you.
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Key to this is the discovery, by my team in Newcastle, of the precise mechanisms that prompt type 2 diabetes to take hold. When you eat a meal, the levels of glucose (sugar) in your blood will rise and insulin (produced in the pancreas) is released to make sure that glucose is taken out of the blood and stored as glycogen in temporary storage depots in the liver and in muscles around your body.
When those glycogen stores are full, excess blood sugar is instead transformed into fat to be stored elsewhere. Then, when you’re not eating (such as at night when you’re asleep) your body will tap into these glycogen stores to keep blood glucose levels topped up.
However, if, as many people do these days, you get into the habit of grazing constantly throughout the day, your blood sugar levels never drop low enough to require topping up from your glycogen stores. It becomes a perpetual one-way process: excess blood glucose converted to fat.
If this continues, at some point you will reach your own ‘personal fat threshold’ and the safe stores of fat under the skin become overfilled and start to spill over to build up in the liver and pancreas where — crucially — fat impedes the ability of these vital organs to function effectively.
When your liver is clogged with fat, it seeks to redress the balance by pumping out extra glucose into the bloodstream and passing excess fat to the pancreas. Ultimately, this fat will consume the pancreas’s insulin-producing cells, causing them to malfunction. When my team discovered this connection, it was pretty revolutionary.
Our studies have been able to show that type 2 diabetes strikes when the liver and pancreas become engorged with fat but you don’t have to be particularly overweight for this to happen. That depends on your ‘personal fat threshold’.
It also explains how some morbidly obese people can remain free from diabetes, but some apparently skinny people can get it. Whatever your size, the problems occur because you’re eating too much for yourself personally.
In the developed world, where enticing, quick-fix, calorie-dense food is everywhere, you have to be unusually disciplined to avoid putting on weight. In Western society, we gain half a kilogram a year (1lb) through most of our adult life, and we gain an average of 5kg (or three-quarters of stone) with each decade.
Because such a significant proportion of the worldwide population is overweight there’s a statistically greater chance that the numbers of those busting their personal fat threshold will have increased (and will continue to do so). That’s one reason why the incidence of type 2 diabetes is rising. But what is surprising is the fact that the majority of very heavy people do not have type 2 diabetes, and only half of all people developing the condition are obese.
SLIM ARE AT RISK TOO:
We are now very clear: you do not have to be obese to develop the condition. You simply have to be susceptible to excess fat in the wrong place. Some people have an endless storage capacity for fat under the skin. They might carry more fat than they need, but it doesn’t clog up the liver and pancreas.
But if a naturally slim person has a low ‘personal fat threshold’, they can be at equal risk of type 2 diabetes as someone twice their size. Whatever your size, if you have type 2 diabetes, your fat stores are full to the brim and you have a good chance of reversing your diagnosis with dramatic weight loss. read more at
