THE G.I. FACTOR: THE EFFECT OF FAT AND PROTEIN ON THE G.I. FACTOR

High fat foods that have a low G.L factor may appear in a falsely favourable light because increases in fat and protein tend to slow the rate of stomach emptying and therefore the rate at which foods are digested in the small intestine. High fat foods will therefore tend to have lower G.I. factors than their low-fat equivalents. For example, potato crisps have a lower G.I. factor (54) than potatoes baked without fat (85). Many sweet biscuits have a lower G.I. factor (55 to 65) than bread (70). But this is not a consistent finding. New boiled potatoes have a lower G.I. factor (62) than French fries (75), despite the latter’s fat content.

Remember, however, we need to eat a low-fat diet, not a high fat one. So, high fat foods of any sort, whether low or high in their G.I. factor, should only be eaten in limited amounts.

Why does pasta have a low G.I. factor? The starting point for making pasta is semolina or cracked wheat, not wheat flour. Durum wheat makes the best pasta because the grain is extremely hard and the wheat breaks cleanly into distinct small pieces. The large particle size of semolina means that starch gelatinisation is more difficult and thus enzyme attack is slowed down. The typical shape of pasta also appears to play a role in slowing down digestion. That’s why pasta of any shape and size has a fairly low G.I. factor (30 to 50). Cracked wheat and couscous used in Middle-Eastern cooking have intermediate G.I. factors.

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LIVING WITH DIABETES: HOW WAS INSULIN DISCOVERED?

The story of the discovery of insulin is a long and fascinating one and to some extent it is also the story of our understanding of diabetes itself.

As a medical condition, diabetes has been known to mankind for two thousand years and perhaps the very first known reference to diabetes is in an Egyptian papyrus thought to have been written about one thousand five hundred years ÂÑ.

Despite an awareness of diabetes and the fact that so many people have suffered from it, virtually nothing was known of the nature of the condition or its cause. Doctors had only known that it was associated with the passing of a large quantity of urine and excessive thirst and the name diabetes literally means ‘an excessive flow of fluid’.

It was not until the 17th century that an Englishman named Thomas Willis noted that the urine of persons with diabetes was sweet and tasted like honey or sugar.

Thus the name of the condition came to be ‘diabetes mellitus’, from the Latin word for honey. So it was that doctors came to realize that diabetes mellitus had something to do with sugar. The proof that this sweetness of the urine was in fact due to sugar was made by another Englishman, Matthew Dobson, and a century later. Dr Dobson also found that the blood of patients with diabetes was also sweet, and he came to the important conclusion that the sugar in the urine came because there was excessive sugar in the blood.

The next important advance was made by a French scientist, Claude Bernard. Bernard discovered that sugar was normally kept at a constant level in the bloodstream and that the regular source of sugar in the blood was derived from stores in the liver. The substance that acts as a sugar store in the liver we call Glycogen.

A most important step in our understanding of diabetes came in 1889 when a German laboratory worker called Minkowski found that removing a dog’s pancreas led to it getting severe diabetes. Thus the origin of diabetes was traced to the pancreas. This observation was taken further still in 1901 when Dr Opie in Baltimore, USA, noted that in those with diabetes certain tissue cells in the pancreas, the ‘Islets of Langerhans’, were degenerated.

In 1916 a British physiologist, Sir Edward Sharpey-Schafer, suggested that diabetes was due to a lack of a chemical substance produced by these ‘islet’ cells. This very important suggestion paved the way for the search for this chemical substance they produced.

From then on many people attempted to extract this substance from the pancreas. Dr Zuelzer, a German, treated some people with diabetes with such an extract, apparently with some response. However his experiments were not completely successful and many other people had tried the same thing and failed.

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