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Diabetes: should athletes be worried? How to balance blood sugar levels

 

 

 

 

 

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 glucose1,2.

 

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 follow3.

 

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 diabetes4,5,6. 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 correlation5. 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 problem7.

 

Mechanisms leading to insulin resistance are unclear, although the abnormal accumulation of certain fats in the liver (hepatic steatosis) is a contributing factor8.

 

In a study by Pan et al9, 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 sensitivity5. Studies on humans have been inconsistent.

 

In a large cohort study by Janket et al10 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, dairy products) which is known to be associated with decreased insulin sensitivity5.

 

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 diet5.

 

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 level5,11. Neither sucrose (a disaccharide: glucose bonded to fructose) nor fructose (a monosaccharide) are 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 disease12,13,14. In addition, some of these effects were seen in men but not women13. 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 others14.

 

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 tolerance2,4,5,6.

 

An over-consumption of refined carbohydrates, over-processed foods, saturated fats and processed vegetable fats are all associated with insulin resistance6,7,11,15. 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 tolerance15.

 

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

 

-Limit sugars and high GI carbohydrates to just before, during and just after exercise.
-At other times, consume a large variety of foods avoiding repeating the same food on any one day.
-Try to include colourful foods at every meal.
-Eat fresh rather than ready-made as often as possible.
-Limit all saturated fats found in dairy products and fatty meats.
-Avoid fried foods.
-Avoid junk foods.
-Dilute fruit juices.

 

 

 

Reference:

 

 

1Sheard NF, Clark NG, Brand-Miller JC, Franz MJ, Pi-Sunyer FX, Mayer-Davis E,

Kulkarni K, Geil P (2004) Dietary carbohydrate (amount and type) in the prevention

and management of diabetes. Diabetes Care 27(9):2266-71.

 

2Salmer?n J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ,

Stampfer MJ, Wing AL, Willett WC (1997) Dietary fiber, glycaemic load, and risk of

NDDM in men. Diabetes Care 20(4): 545-550.

 

3Sievenpiper JL, Vuksan V (2004) Glycemic index in the treatment of diabetes: the

debate continues. Journal of the American College of Nutrition 23(1): 1-4.

 

4Festa A, Hanley AJG, Tracy RP, D’Agostino R, Haffner SM (2003) Inflammation in

the prediabetic state is related to increased insulin resistance rather than

decreased insulin secretion. Circulation 108(15):1822-30.

 

5Daly M (2003) Sugars, insulin sensitivity, and the postprandial state. The American

  Journal of Clinical Nutrition 78(4): 865S-872S.

 

6Liu S, Manson JE, Buring JE, Stampfer MJ, Willett WC, Ridker PM(2002) Relation

between a diet with a high glycemic load and plasma concentrations of high-

sensitivity C-reactive protein in middle-aged women. The American Journal of

  Clinical Nutrition 75:492-498.

 

7Roth JL, Clohisy M (2002) The metabolic syndrome: where are we and were do we

go? Nutrition Reviews 60(10; part 1): 335-7.

 

8Montminy M & Koo SH (2004) Outfoxing insulin resistance? Nature 432(7020):958-

959.

 

9Pan DA, Lillioja S, Kriketos AD, Milner MR, Baur LA, Bogardus C, Jenkins AB,

Storlien LH (1997) Skeletal muscle triglyceride levels are inversely related to insulin

action. Diabetes (46)6: 983-988.

 

10Janket SJ, Manson JE, Sesso H, Buring JE, Liu S (2003) A prospective study of

sugar intake and risk of type 2 diabetes in women. Diabetes Care 26(4):1008-15.

 

11Daly ME, Vale C, Walker M, Littlefield A, Alberti KGMM, Mathers JC (1998) Acute

effects on insulin sensitivity and diurnal metabolic profiles of a high-sucrose

compared with a high-starch diet. American Journal of Clinical Nutrition 67(6):

1186-96.

 

12Swanson JE, Laine DC, Thomas W, Bantle JP (1992) Metabolic effects of dietary

fructose in healthy subjects. The American Journal of Clinical Nutrition 55(4):851-

856.

 

13Bantle JP, Raatz SK, Thomas W, Georgopoulos A (2000) Effects of dietary fructose

on plasma lipids in healthy subjects. The American Journal of Clinical Nutrition

72(5):1128-34.

 

14Hollenbeck CB (1993) Dietary fructose effects on lipoprotein metabolism and risk

for coronary artery disease. The American Journal of Clinical Nutrition 58(5

Suppl):800S-809S.

 

15Hung T, Sievenpiper JL, Marchi A, Kendall CWC, Jenkins DJA (2003) Fat versus

carbohydrate in insulin resistance, obesity, diabetes and cardiovascular disease.

Current Opinion in Clinical Nutrition and Metabolic Care 6(2):165-176.

 

 

 

 

 

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