174 The nutrition handbook for food processors Postprandial glycaemia and distal colonic bulk are both physiological markers hat are strongly influenced by the effects of food properties on carbohydrate availability, but which cannot be reliably predicted from food composition data New nutritional information is required for control of postprandial glycaemia (Table 7. 2)and distal colonic bulk (Table 7.3), taking into account end-points biomarkers of exposure, current indices, relevant indices, their validation, and communication discussed above 7.6 Relative glycaemic potency and glycaemic-glucose Control of postprandial glycaemia-the blood glucose response to food intake is an increasingly important health issue. Diabetes mellitus, marked by an inabil ty to control blood glucose levels, is increasing rapidly in many developed countries, in which an over-supply of high energy and highly digestible carbo- hydrate foods is coupled with predisposing factors, including physical inactivity. obesity, and inheritance. Many consumers need to be able to manage postpran- caemla by selecting foods and food combinations according to glycaemic impact, but food labels at present give them little assistance 7.6.1 End-point Health consequences of hyperglycaemia are multiple and most evident in the diabetes mellitus syndrome. Persistently raised blood glucose causes protein glycation throughout the body, leading to cumulative, diffuse damage, emerging as pathology in a number of organ systems. Basal membrane damage is com- monly an underlying factor in changes to micro-vessels involving the eyes, kidneys and nerves. Intense insulin production in response to diabetic hyper- glycaemia, or to repeated acute glucose loading from large intakes of highly digestible carbohydrate, is thought to contribute to the progression of glucose intolerance, through B-cell toxicity, leading to loss of the capacity of the pancreas to produce insulin. Hyperinsulinaemia as a response to elevated blood glucose favours elevated blood lipids, obesity and hypertension, all risk factors in heart disease 49, 50,51 Post-prandial glycaemia may also lead to a number of acute and sometimes serious disorders, as the body attempts to counter the osmotic effects of high blood sugar levels. The excretion of sugar by the kidneys leads to water loss, excessive thirst, and in extreme cases, to fatal electrolyte imbalances 7.6.2 Markers As blood glucose response is causal in glycation, insulin response, osmotic effects and other aspects of diabetic pathology, it is a highly relevant marker of the fluence of foods and carbohydrates on progression towards disease end-pointsPostprandial glycaemia and distal colonic bulk are both physiological markers that are strongly influenced by the effects of food properties on carbohydrate availability, but which cannot be reliably predicted from food composition data. New nutritional information is required for control of postprandial glycaemia (Table 7.2) and distal colonic bulk (Table 7.3), taking into account end-points, biomarkers of exposure, current indices, relevant indices, their validation, and communication discussed above. 7.6 Relative glycaemic potency and glycaemic-glucose equivalents Control of postprandial glycaemia – the blood glucose response to food intake – is an increasingly important health issue. Diabetes mellitus, marked by an inabil￾ity to control blood glucose levels, is increasing rapidly in many developed countries, in which an over-supply of high energy and highly digestible carbo￾hydrate foods is coupled with predisposing factors, including physical inactivity, obesity, and inheritance.28 Many consumers need to be able to manage postpran￾dial glycaemia by selecting foods and food combinations according to glycaemic impact, but food labels at present give them little assistance. 7.6.1 End-point Health consequences of hyperglycaemia are multiple and most evident in the diabetes mellitus syndrome.28,49,50 Persistently raised blood glucose causes protein glycation throughout the body, leading to cumulative, diffuse damage, emerging as pathology in a number of organ systems. Basal membrane damage is com￾monly an underlying factor in changes to micro-vessels involving the eyes, kidneys and nerves.51 Intense insulin production in response to diabetic hyper￾glycaemia, or to repeated acute glucose loading from large intakes of highly digestible carbohydrate, is thought to contribute to the progression of glucose intolerance, through b-cell toxicity, leading to loss of the capacity of the pancreas to produce insulin.52 Hyperinsulinaemia as a response to elevated blood glucose favours elevated blood lipids, obesity and hypertension, all risk factors in heart disease.49,50,51 Post-prandial glycaemia may also lead to a number of acute and sometimes serious disorders, as the body attempts to counter the osmotic effects of high blood sugar levels. The excretion of sugar by the kidneys leads to water loss, excessive thirst, and in extreme cases, to fatal electrolyte imbalances.53 7.6.2 Markers As blood glucose response is causal in glycation, insulin response, osmotic effects and other aspects of diabetic pathology, it is a highly relevant marker of the influence of foods and carbohydrates on progression towards disease end-points 174 The nutrition handbook for food processors