The aim of the Finnish Diabetes Prevention Study is to assess the efficacy of an intensive diet–exercise programme in preventing or delaying type 2 diabetes in individuals with impaired glucose tolerance (IGT) and to evaluate the effect of the programme on the risk factors of atherosclerotic vascular diseases and the incidence of cardiovascular events. In this ongoing study, a total of 523 overweight subjects with IGT based on two oral glucose tolerance tests were randomized to either an intervention group or a control group. The main measure in the intervention group is individual dietary advice aimed at reducing weight and intake of saturated fat and increasing intake of dietary fibre. The intervention subjects are individually guided to increase their level of physical activity. The control group receives general information about the benefits of weight reduction, physical activity and healthy diet in the prevention of diabetes. A pilot study began in 1993, and recruitment ended in 1998. By the end of April 1999 there were 65 new cases of diabetes, 34 drop-outs and one death. The weight reduction was greater (-4.6 kg) at 1 year in the intervention group (n = 152) than in the control group (n = 143, -0.9 kg, P < 0.0001), and this difference was sustained in the second year of follow-up. At 1 year 43.4 % and at 2 years 41.8 % of the intervention subjects had achieved a weight reduction of at least 5 kg, while the corresponding figures for the control subjects were 14.0 and 12.0 % (P < 0.001 between the groups). At 1 year the intervention group showed significantly greater reductions in 2 h glucose, fasting and 2 h insulin, systolic and diastolic blood pressure, and serum triglycerides. Most of the beneficial changes in cardiovascular risk factors were sustained for 2 years. These interim results of the ongoing Finnish Diabetes Prevention Study demonstrate the efficacy and feasibility of the lifestyle intervention programme.

The treatment of the metabolic syndrome aims to improve insulin sensitivity and correct/prevent the associated metabolic and cardiovascular abnormalities. Since many individuals with the metabolic syndrome are overweight, dietary treatment should be primarily focused on weight reduction. This approach can improve insulin sensitivity and exert beneficial effects on all the other abnormalities clustering in the syndrome. Insulin sensitivity can also be influenced by diet composition. In this respect, the specific effects of the quality of dietary fat are of great interest, given the considerable evidence in experimental animals that saturated fat in the diet may lead to insulin resistance. In man, there is indirect evidence that a higher saturated fat intake is associated with impaired insulin action. Human studies have also attempted to evaluate the relationship between total fat intake and insulin sensitivity. They are consistent in showing that fat intake is correlated with both plasma insulin values (positively) and insulin sensitivity (negatively). However, these correlations are largely mediated by body weight. Conversely, intervention studies are consistent in showing that when total fat intake is moderately increased (from 20 to 40 %), no major effect is observed on insulin sensitivity. We have recently undertaken a large, multicentre intervention study in 162 healthy individuals given either a high-saturated-fat or a high-monounsaturated-fat diet for 3 months. It shows that a high-monounsaturated-fat diet significantly improves insulin sensitivity compared to a high-saturated-fat diet. However, this beneficial effect of monounsaturated fat disappears when total fat intake exceeds 38 % of total energy. Independently of its effects on insulin sensitivity, diet composition can influence the factors clustering in the metabolic syndrome. Dietary carbohydrate increases blood glucose levels, particularly in the postprandial period, and consequently also insulin levels and plasma triglycerides. The detrimental effects of a high-carbohydrate diet on plasma glucose/insulin, triglyceride/HDL or fibrinolysis occur only when carbohydrate foods with a high glycaemic index are consumed, while they are abolished if the diet is based largely on fibre-rich, low-glycaemic-index foods. In conclusion, weight reduction is a powerful measure for the treatment of metabolic syndrome. Moreover, the diet for the treatment of the metabolic syndrome should be limited in the intake of saturated fat, while high fibre/low-glycaemic-index foods should be used without specific limitations. Moderate amounts of monounsaturated fat could be permitted as they do not induce detrimental metabolic effects.

Accumulating data indicate that a diet characterized by low glycaemic-index (GI) foods not only improves certain metabolic ramifications of insulin resistance, but also reduces insulin resistance per se. Epidemiological data also suggest a protective role against development of non-insulin-dependent diabetes mellitus and cardiovascular disease. A major disadvantage in this connection is the shortage of low-GI foods, and many common starchy staple foods, such as bread products, breakfast cereals and potato products, have a high GI. Studies in our laboratory show that it is possible to significantly lower the GI of starchy foods, for example by choice of raw material and/or by optimizing the processing conditions. Such low-GI foods may or may not influence glucose tolerance at a subsequent meal. Consequently, certain low-GI breakfasts capable of maintaining a net increment in blood glucose and insulin at the time of the next meal significantly reduced post-prandial glycaemia and insulinaemia following a standardized lunch meal, whereas others had no ‘second-meal’ impact. These results imply that certain low-GI foods may be more efficient in modulating metabolism in the long term. Although the literature supports a linear correlation between the GI and insulinaemic index (II) of foods, this is not always the case. Consequently, milk products elicited elevated IIs, indistinguishable from a white bread reference meal, despite GIs in the lower range. This inconsistent behaviour of milk products has not been acknowledged, and potential metabolic consequences remain to be elucidated.

Several epidemiological studies link consumption of fibre-rich foods to a reduced risk of type 2 diabetes and CHD. The ‘fibre hypothesis’ suggested that this was a direct effect of fibre. However, fibre-rich foods contain different types of fibre as well as other potentially beneficial compounds, and many foods naturally high in fibre have low glycaemic and insulinaemic indices, possibly due to food form. The question therefore emerges as to the effect of isolated fibre per se on insulin sensitivity, lipids and other risk factors associated with the metabolic syndrome. Many beneficial effects are seen with pharmacological doses of isolated viscous soluble fibre, including improved insulin sensitivity, decreased LDL-cholesterol levels and decreased clotting factors. Similar effects are seen with low glycaemic-index foods. In contrast, insoluble non-viscous cereal fibre is not seen to act directly on risk factors when taken in refined foods such as in milled flour. Since cereal fibre, the major type of fibre in western diets, does not directly act on the risk factors for the metabolic syndrome, the question remains as to possible mechanisms. Until now, fibre and the nature and processing of the starch and particle size have been seen as the main determinants of the metabolic response to starchy foods. However, fibre-rich foods also have an increased protein-to-carbohydrate ratio. Hence we suggest that the protective effect of fibre may also be due to increased vegetable protein content, which may act directly to reduce clotting factors and oxidized LDL-cholesterol levels.

Changing dietary intake is a major challenge to individuals, households and the general public. Promoting the consumption of diets that are low in fat and high in fruits, vegetables and starchy carbohydrate, and managing overweight and central obesity, are important dietary strategies for the prevention of metabolic syndrome. Educational, behavioural and motivational tactics are required to help people achieve overall dietary change. These strategies might usefully be based on intervention models which incorporate behavioural theories and goals through personal, multiple contact with individuals or in small groups, using active involvement and specific behaviour-change strategies. Two particular aspects, namely the impact of computer-generated, personalized nutrition education and social support networks (e.g. family, health centre and community) provide useful adjuncts to traditional dietary counselling and might usefully be incorporated into diet- and lifestyle-change programmes for community-based and individualized approaches for disease prevention. The use of moderate energy-deficit diets, modest targets for weight loss (and maintenance) which can be sustained over the long term, and increased physical activity probably offers the most feasible approach for intervention aimed at reducing overall body weight.

Insulin sensitivity is potentially enhanced by a range of diet-related changes including reduction of visceral adiposity, a reduction in saturated fatty acids, and possibly a redistribution of the proportions of various unsaturated fatty acids. While there is evidence to suggest that lifestyle changes can reduce the risk of progression of impaired glucose tolerance to type 2 diabetes, there are no clinical trials which have conclusively demonstrated that any measure can reduce insulin resistance in the long term to an extent that can prevent the development of type 2 diabetes and other clinical complications. Evidence concerning the possibilities for reducing visceral adiposity and altering the nature of dietary fat are therefore considered. Attempts to achieve prolonged and substantial weight reduction in adults have not been encouraging, and it may be that preventing further weight gain is the most realistic target in this age group. In childhood the attempts have been more successful. The development of new approaches to achieving behavioural change and an environment which facilitates physical activity and appropriate food choices will be essential for more successful individual and population attempts to facilitate reduction in insulin resistance by weight loss. Changes in the nature of dietary fat appear to be more easily achieved. This is already a component of dietary advice aimed at cardiovascular risk reduction, and should be reinforced now with a view to also achieving a reduction in insulin resistance.

The food industry has five important roles in facilitating needed dietary and behavioural changes. Two of these roles are direct ones. Industry can increase the availability of a wide variety of basic commodities and new foods that help consumers meet dietary recommendations. It is also responsible for developing and formulating appealing, healthy and effective food products that decrease risks of chronic degenerative disease. Industry also plays an indirect role in facilitating dietary change by motivating consumers to select and prepare foods that will result in healthy dietary patterns. It can also participate in coalitions to facilitate other behaviours that decrease risks. Finally, it can collaborate actively in applied and fundamental research to further our understanding of the associations between food and health.

The remarkable increase over the past 40 years in some chronic diseases, including the metabolic syndrome, has increased the demand for government and international policies to encourage various approaches to decrease the risk of these diseases. There are some prerequisites for working out successful national food and nutrition policies. Firstly, it is necessary to have a clear picture of the dietary pattern in a country and its associated public health problems. Based on these data, nutrient recommendations and goals are formulated by international or national scientific committees. Governments should translate these nutrient goals into food goals and eventually into national dietary guidelines. The means by which the national authorities can implement a nutrition policy include fortification and supplementation. Equally important are educational and informative tools, such as labelling on the packed food products including information about ingredients and nutrient content. With respect to the metabolic syndrome, this implies nutrient recommendations regarding the intake of fat and carbohydrates (energy per cent) and dietary fibre; dietary guidelines regarding balance between energy intake and expenditure; decreased consumption of products rich in fat and increased consumption of cereals and other products rich in dietary fibre, etc.; recommendations from the authorities regarding nutrient labelling (content of fat and dietary fibre) on relevant products; and nutrient and health claims and other aids (symbols) as tools to make it easier for consumers to select the appropriate food products.