Diabetes is a growing problem in the population: according to Diabetes UK there are 3% (1.8 million) diagnosed cases (approximately 250 thousand with type 1 and over 1.5 million with type 2) and another estimated 750 thousand to 1 million undiagnosed cases of type 2 diabetes. No statistics are available for the athletic population.

What is diabetes?

Diabetes is a syndrome or group of symptoms arising from failure to regulate the metabolism of glucose by means of the pancreatic hormone, insulin. This occurs due to a lack of insulin because the pancreas does not produce enough, fails to produce any or the body fails to make proper use of the insulin that is available. Diabetes is classified as insulin-dependent (type 1) and non-insulin-dependent (type 2). This paper will focus on the latter and will ignore any genetic predisposition to the disease.

The glycaemic index and diabetes

The Glycaemic Index (GI) can be considered as a measure of carbohydrate quality. It measures the postprandial (after a meal) glycaemia (plasma glucose) raising potential of a single food by expressing the rise in glycaemia in response to a 50g available carbohydrate portion of that food as a percentage of the rise in response to a 50g available carbohydrate portion of a reference food (white bread or glucose).

Foods high on the GI result in a sharp rise of plasma glucose, with a high demand for insulin, followed by a more or less rapid fall of glucose. Foods that are low to moderate on the GI produce a slower rise, with a lower demand for insulin, and a more gradual decline in plasma glucose.

Those in favour of carbohydrate quality, argue that GI is a robust measurement, predicts the relative glycaemic response to mixed meals and is easy to follow and implement. In contrast, opponents who favour giving priority to carbohydrate quantity argue that GI is highly variable, not physiological, cannot reliably predict mixed meal responses and is difficult to learn or follow.

Despite some opposition to low-GI intervention in type 2 diabetes, the interventions are clinically efficacious in diabetes therapy over the mid to long-term. The Canadian Diabetes Association, Diabetes Australia, Diabetes UK and the European Association for the Study of Diabetes all support the application of the GI concept in the management of diabetes.

Insulin resistance

Insulin resistance, a component of the Insulin Resistance Syndrome, also known as Syndrome X and the Metabolic Syndrome, is associated with type 2 diabetes. No statistics for insulin resistance are available in the UK, although, according to Diabetes UK, a national register may be set up in the future.

Obesity is the most significant factor leading to insulin resistance with visceral obesity having a particularly strong negative correlation. It can be reversed with diet modification based on a low-fat intake and limiting refined carbohydrates without the need of caloric restrictions. Physical activity is an important factor in reversing the problem.

Mechanisms leading to insulin resistance are unclear, although the abnormal accumulation of certain fats in the liver (hepatic steatosis) is a contributing factor.

In a study by Pan et al, skeletal muscle triglyceride (mTG) appeared to be another important factor in predicting insulin resistance. Trained athletes and animals show the same or higher levels of muscle triglycerides as sedentary controls but have improved insulin action. The authors postulated that this could be due to the distribution of triglyceride. Endurance exercise increases both the mitochondrial volume and distribution in skeletal muscles. In trained dogs, mitochondria appear virtually in direct contact with triglyceride droplets whereas no such association with mitochondria was found in untrained animals. As a result, trained individuals may have an improved ability to mobilise fats.

Research into sucrose and fructose on animals has consistently shown that high sucrose and fructose diets decrease insulin sensitivity. Studies on humans have been inconsistent.

In a large cohort study by Janket et al, 38,480 initially healthy postmenopausal women were followed for an average of 6 years. The researchers accrued 918 incident cases of type 2 diabetes but found no definitive influence of sugar intake on the risk of developing type 2 diabetes. It was noted, however, that the median follow-up time of 6 years might not have been long enough to detect a very subtle relationship between sugar intake and incidence of type 2 diabetes.

Assessment on humans is thought to be more complicated because of other factors affecting insulin sensitivity. Some studies found that those consuming a diet consisting of large amounts of sweets and desserts were at increased risk of developing diabetes. However, the diet also included high amounts of saturated fats (red meat, fries and dairy products) which is known to be associated with decreased insulin sensitivity.

No studies have shown a negative effect of sucrose on insulin sensitivity. One explanation for this lack of correlation could be that recruitment of volunteers for nutrition studies is notoriously difficult and many studies have a young or a highly health-orientated population. Both groups are likely to be physically active. Given the strength of the positive influence of physical exertion on insulin sensitivity, such persons are inclined to be resistant to the negative effects of diet. However, this does suggest that the promotion of physical activity may have a greater influence on insulin sensitivity than diet.

Another possible explanation is that the GI concerns only the first 2 hours of the postprandial period. It is postulated that a GI defined by a 4-6 hour postprandial period would alter the ranking of sucrose in a GI table to a higher level. Neither sucrose (a disaccharide: glucose bonded to fructose) nor fructose (a monosaccharide) is high on the GI.

Studies based on high fructose versus high glucose diets have shown that the high fructose diets produce an increase in plasma triacylglycerol, plasma cholesterol, VLDL and LDL cholesterol concentrations, all of which are a risk factor in cardiovascular disease. In addition, some of these effects were seen in men but not women. The reason for this difference is not clear. Although not all studies are consistent with these findings, the positive data cannot and should not be dismissed as it may be of considerable clinical importance. It is also important to note that some individuals are more sensitive to fructose than others.

The risk for athletes

Are athletes at risk of developing type 2 diabetes as a result of their high intake of fructose, sucrose and high glycaemic foods? Although the scientific evidence to-date does not support this notion, athletes may be at risk of developing insulin resistance which is associated not only with diabetes but also with coronary heart disease, hypercholesterolaemia, hypertension, dysglycaemia, osteoarthritis and impaired glucose tolerance.

An over-consumption of refined carbohydrates, over-processed foods, saturated fats and processed vegetable fats are all associated with insulin resistance. The majority of adult athletes we have consulted to-date, over-consume the above with the possible exception of saturated fats. However all our adolescent athletes consumed large amounts of saturated fats.

Although some athletes are becoming more informed on the importance of nutrition for both their long-term health and their performance, there are still a large number who are uninformed or misinformed on nutritional issues. Particularly distressing is the lack of knowledge amongst adolescent athletes which needs to be urgently addressed, not only by nutritionists and dieticians, but also by coaches and parents.

One procedure that can be immediately implemented by everybody is that of chewing our food thoroughly and eating more slowly: it appears that prolonging absorption time by increasing the length of time to complete a meal, consuming smaller and more frequent meals or drinking a beverage over a prolonged period of time all improve glucose tolerance.

In summary, to minimise the risk of insulin resistance, the following points should be adhered to: