Diabetes:The real culprits

Says Allen Spiegel, who heads the US National Diabetes Institute, ‘People cringe at the word epidemic, but by all criteria, we are witnessing an epidemic of diabetes.’

And, indeed, the statistics are frightening. There are now an estimated two-and-a-half million diabetics in the UK and nearly 20 million in the US – roughly 8 per cent of the population. At the current rate of increase, those numbers are expected to double by 2010 (Br J Commun Nurs, 2002; 7: 414-9).

A ‘Cinderella disease’ for decades, diabetes is finally becoming recognised as a major health problem. ‘Diabetes could become the AIDS of the 21st century,’ says Professor George Alberti, president of the International Diabetes Federation.

Diabetes used to be a disease of middle-age, but now, adolescents and even children are succumbing to it. In 1982, about 4 per cent of children in the US had diabetes but, by 1994, that figure had risen to a staggering 16 per cent. Similarly, in Britain, childhood diabetes has been increasing by 4 per cent a year since 1984 – with a staggering 11 per cent annual increase in the under-fives (BMJ, 1997; 315: 713-7).

Such a situation has been described as ‘potentially devastating’ because children with diabetes are doomed to die prematurely from heart disease or stroke – just two of the many diseases that diabetes brings in its wake.

Once a rarity in the underdeveloped countries, diabetes is on the rise in these countries too, as they begin to adopt the Western lifestyle. This was first seen in Japan after World War II, then in Korea, Taiwan, Southeast Asia, and now Mexico and the more affluent parts of North Africa (Publ Health Nutr, 2002; 5: 141-8). The generally accepted explanation is the increased food intake coupled with a more sedentary lifestyle.

That diabetes is a ‘disease of civilisation’ has been acknowledged almost since the condition was first identified. For years, obesity has been thought to be the primary risk factor because 90 per cent of diabetics are seriously overweight.

But there’s increasing evidence that this picture is incomplete. New research suggests that the obesity-diabetes connection is too simplistic. In fact, a major rethink of the whole diabetes picture is now taking place as previously unrecognised causes of the disease are beginning to be uncovered.

What is diabetes?
Diabetes is basically a disorder of the bodily system that regulates the amount of glucose in the bloodstream. Glucose is the body’s chief source of energy, and is manufactured by metabolising carbohydrates in the diet.

Despite wide variations in carbohydrate intake, the body manages to maintain glucose levels at a constant 1 gram/litre of blood. The organ responsible for this marvel of regulation is the pancreas. If blood glucose levels are too low, the pancreas makes a chemical called glucagon, which releases stored glucose. In contrast, if blood glucose levels are too high, the pancreas releases insulin, which removes the excess glucose from the blood and stores it in the muscles, liver or fat cells.

Any dysfunction in the insulin- glucose regulatory system will cause diabetes. One type of malfunction is the result of damage to the insulin-producing cells in the pancreas, leading to a dramatically reduced supply of insulin. This is called type 1 diabetes, the severe form of the disease that mainly strikes children and young adults.

The cause of type 1 diabetes is largely mysterious, but it often occurs after a viral infection, particularly of the intestines. Enteric viruses have therefore been suggested as a possible cause of damage to the insulin-producing cells of the pancreas (Clin Diag Virol, 1998; 9: 77-84). Type 1 diabetics must receive artificial insulin or they will go into a glucose-induced coma and die.

The vast majority of people with diabetes, however, don’t have this extreme form of the disease. Any dysfunction in the insulin-glucose system – all of which end up as the same basic problem – can be the cause: the body may not produce enough insulin; it may not respond to insulin properly; or it may produce too much insulin.

The classic way in which diabetes is believed to occur is that it starts as ‘insulin resistance’, where the body’s cells fail to react to insulin properly. This, in turn, causes the pancreas to produce more insulin to compensate, leading to a vicious circle that culminates in a kind of system exhaustion as the pancreas becomes overworked and ultimately stops functioning.

This kind of diabetes is called type 2, and is the sort that is increasing alarmingly not just among middle-aged adults, who are the typical sufferers, but in children as well.

If symptoms are noticed early enough, type 2 diabetics won’t need to be given artificial insulin as long as they strictly control their intake of carbohydrates. So, because of this type of diabetes, nutritionists have had to look at carbohydrates in a new light, which has led to a major rethink about the causes of diabetes.

What causes diabetes?
Originally, nutritionists analysed foods by the amount of energy they provided – in other words, their calories. Calorie levels were worked out in the laboratory rather crudely by burning foods and seeing how much heat energy they produced.

However, caloric measures are useless for diabetics, who need to know the glucose value of foods to enable them to control their blood glucose levels through their diet, and so avoid the need for insulin injections. But the glucose values of foods can’t be measured in the laboratory; they must be tested on live human beings.

So, in a painstaking series of tests carried out in the 1980s, every foodstuff was analysed for its potential to produce glucose in the bloodstream. Human guinea pigs were fasted to create a baseline to measure against, then given a single food to eat. Regular blood samples were taken over four hours to chart the changes in blood glucose levels.

The results didn’t turn out quite as expected. One surprise was the finding that all carbohydrates cause a glucose peak roughly 30 minutes after ingestion. Previously, it had been thought that simple carbohydrates (like sugar and honey) were fast-acting while complex carbohydrates (like potatoes and cereals) were slow-acting.

Nevertheless, there were dramatic differences between carbohydrates in the levels of blood glucose they produced. And as the technical term for blood glucose is glycaemia, the differences between carbohydrates were measured in terms of a ‘glycaemic index’ (GI): the higher the number, the greater the amount of blood glucose produced by the food.

Nutritionists arbitrarily gave glucose itself a GI of 100 and, not surprisingly, virtually all foods are lower than that (see box, p 4). Also as expected, the most refined carbohydrates led to the highest blood glucose levels – but there were some surprises. Cooking was found to have major effects on the GI. Carrots, for example, produce three times the blood glucose level when cooked rather than eaten raw. In fact, any cooking or processing raises the GI significantly.

The GI has now been used by French scientist Dr Michel Montignac as the basis of a successful slimming regime – although, arguably, his greater contribution to health has been to develop a new theory of the causes of diabetes.

His interest was sparked by a paper published in 1979 by Dr B. Jeanrenaud, who found that all obese people suffered from ‘a form of hyperinsulinemia’ (Diabetologia, 1979; 17: 133-8). Hyperinsulinaemia is when the pancreas overreacts to excess glucose by producing too much insulin. At the time, nutritionists looking at Jeanrenaud’s data concluded that hyperinsulinaemia was the cause of obesity – but Montignac wasn’t so sure.

Taking a sideways look at the theory, Montignac proposed that the overproduction of insulin is not caused by obesity, but by a faulty pancreas – which itself causes obesity.

Montignac’s theory remained in the wilderness until 1988, when two other French scientists discovered that hyperinsulinaemia caused ‘abnormally large amounts of recently consumed fat’ to be laid down in the body (Creff EF, Obésités, Paris: Masson, 1988).

Here, then, was a plausible mechanism for obesity, one that would help explain why some people become fat while others do not, even with exactly the same food intake. Obese people, the new findings suggested, are not secret guzzlers – they have a pancreas that produces too much insulin.

What were the implications of this for diabetes? Montignac theorised that the reason most people with adult-onset (type 2) diabetes are obese is not, as most people thought, because obesity causes diabetes. Rather, obesity and diabetes are two sides of the same coin – both are manifestations of the same underlying problem: hyperinsulinaemia resulting from a faulty pancreas.

So, does too much insulin cause diabetes? No, said Montignac, it’s a symptom of an overworked pancreas. It’s the end result of a state of almost continuous hyperglycaemia (excess glucose in the blood), which places too high a demand on the pancreas to produce insulin. Eventually, the system goes into overdrive, creating a near-constant surplus of insulin. This, in turn, causes ‘insulin resistance’, where insulin ‘switch-off’ cells overload and cease to respond, further tightening the vicious circle.

Diabetes is, therefore, due to pancreas exhaustion, says Montignac, caused by a diet containing too many carbohydrates with a high glycaemic index. He puts the blame fairly and squarely on the modern Western diet, with its high content of refined carbohydrates and sugar.

When Montignac first proposed the theory, few experts supported him. Indeed, the prevailing theory was – and still is – that sugar does not cause diabetes. However, the evidence has been mounting that he may be right.

In 1997, researchers at the Harvard School of Public Health reported the results of a study of 65,000 middle-aged women followed for over six years, by which time, over 900 of them were diabetic.

What marked those women who developed diabetes out from the others who hadn’t developed diabetes was their diet, which mostly consisted of low-fibre foods and refined carbohydrates.

Looking at individual foods, the chief culprits were found to be ‘cola beverages, white bread, white rice, french fried potatoes, and cooked potatoes’ – the very foods listed by Montignac as having a high GI. These foods more than doubled the risk of diabetes.

The Harvard researchers unequivocally supported Montignac’s theory: ‘hyperinsulinemia . . . is one of the best predictors of [type 2 diabetes]’, they wrote. ‘Our findings support the hypothesis that a diet with high glycemic load and a low cereal fiber content increases risk of [type 2 diabetes]’ (JAMA, 1997; 277: 472-7).

Virtually identical results were found by the same team in a parallel study of more than 40,000 men (Diabetes Care, 1997; 20: 545-50).

These findings are the first conclusive evidence that the major cause of adult-onset diabetes is a Western diet. Thanks to Montignac, we also now have a cogent theory to explain why it happens. It is now clear that people develop diabetes in middle-age not because of obesity, a sedentary lifestyle or stress (the conventional explanations); they become diabetic because of half a lifetime’s assault on the pancreas by a diet of refined carbohydrates and processed foods.

A dietary time bomb
But that’s not the end of the story. Adding a further twist of the knife, the Harvard nutritionists recently found even more evidence to condemn the modern diet. Analysing their data on the 65,000 women, they discovered another dietary risk factor – trans fatty acids. Also called hydrogenated fats, these are liberally added to processed foods to ‘improve texture’. Such fats appear to increase the risk of type 2 diabetes ‘substantially’ (Am J Clin Nutr, 2001; 73: 1019-26).

As yet, there is no explanation for why hydrogenated fats cause diabetes. But this latest evidence, taken with the earlier findings for refined carbohydrates, is a damning explanation for the huge rise in diabetes in the young. It is yet another health time bomb lobbed at us by the food industry, as if cancer and heart disease are not already enough.

Another risk factor for the disease may be milk. Ten years ago, evidence was already accumulating that babies fed on cow’s milk formulas are more likely to develop type 1 diabetes (Diabetes Care, 1994; 17: 13-9). Although the increased risk seems relatively small, it is magnified among children with diabetic siblings.

A Finnish study has shown that feeding such infants cow’s milk formula during early infancy results in a fivefold increase in the risk of diabetes (Diabetes, 2000; 49: 912-7).

Why this should happen is not completely understood, but the culprit is believed to be the insulin content of cow’s milk, which makes the infant create human antibodies to the bovine insulin. The theory is that the baby’s insulin antibodies then react against the insulin-producing cells in the pancreas, thus damaging the cells and triggering type 1 diabetes (Diabetes, 2000; 49: 1657-65).

Factors in cow’s milk have also been suggested as the reason why type 1 diabetes is more prevalent in the northern Europe. In such countries, Friesian cows predominate as they are more suited to colder, wetter climates. It is believed that the milk of Friesian cows may contain a diabetes-precipitating protein that other cow species do not produce.

Nevertheless, that is only one of many theories regarding the environmental causes of type 1 diabetes, which still remain obscure.

However, type 2 diabetes is now much less mysterious – thanks largely to the pioneering work of Dr Michel Montignac and the remarkable way he has stood conventional thinking about the disease on its head.
Tony Edwards

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Written by What Doctors Don't Tell You

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