The metabolic syndrome represents a vicious cycle whereby insulin resistance leads to compensatory hyperinsulinaemia, which maintains normal plasma glucose but may exacerbate insulin resistance. Excess insulin secretion may eventually reduce β-cell function due to amyloid deposition, leading to raised blood glucose and further deterioration of β-cell function and insulin sensitivity via glucose toxicity. Reducing postprandial glucose and insulin responses may be a way to interrupt this process, but there is disagreement about the dietary approach to achieve this. Glucose and insulin responses are determined primarily by the amount of carbohydrate consumed and its rate of absorption. Slowly absorbed, low glycaemic-index (GI) foods are associated with increased HDL cholesterol and reduced risk of type 2 diabetes. There is some evidence that low-GI foods improve insulin sensitivity in humans, although studies using established techniques (glucose clamp or frequently sampled intravenous glucose tolerance test) have not been done. Low carbohydrate diets have been suggested to be beneficial in the treatment of the metabolic syndrome because of reduced postprandial insulin. However, they may increase fasting glucose and impair oral glucose tolerance — effects which define carbohydrate intolerance. The effects of low carbohydrate diets on insulin sensitivity depend on what is used to replace the dietary carbohydrate, and the nature of the subjects studied. Dietary carbohydrates may affect insulin action, at least in part, via alterations in plasma free fatty acids. In normal subjects a high-carbohydrate/low-GI breakfast meal reduced free fatty acids by reducing the undershoot of plasma glucose, whereas low-carbohydrate breakfasts increased postprandial free fatty acids. It is unknown if these effects occur in insulin-resistant or diabetic subjects. Thus further work needs to be done before a firm conclusion can be drawn as to the optimal amount and type of dietary carbohydrate for the treatment of the metabolic syndrome.

Any intervention which causes negative energy balance is guaranteed to be efficacious in producing weight loss, which will continue while there is negative energy balance or be maintained as long as the new energy balance is maintained. In clinical practice compliance is rarely 100 % so the efficiency of even the most efficacious treatment is usually low. However, recent evidence-based guidelines have recognized the clinical benefits of moderate (5–10 %) weight loss, which is achievable using a variety of interventions. Long-term studies of ‘weight loss’ are, in reality, combinations of weight loss (usually completed in 1–6 months) followed by variable weight maintenance, set in the context of progressive adult weight gain in an obesogenic environment. Few studies have adopted specific and separate strategies for weight loss and weight maintenance. Meta-analyses conducted by non-expert methodologists have failed to recognize these distinctions, and have criticized the available research without understanding the different needs of studies with weight change as the outcome variable, which require randomized controlled trials (RCT), and those with weight loss as the treatment, intended to improve metabolic or biomedical outcome measures. An RCT design is inapplicable to studies of biomedical end points (e.g. cardiac risk factors) when weight loss is the treatment. Because fixed weight loss cannot be prescribed there is always a range of weight changes in any study, and single-sample studies with regression analysis provide the best design. An RCT study design does not give useful information about clinical value as the control group is always ‘treated’ to some extent. Placebo- (or control)-subtracted differences are misleading because in an RCT all subjects recruited to active treatment, including non-responders, are continued on treatment for the full duration of the study. In routine clinical practice, treatments are changed in the light of early experience as a therapeutic trial to optimize the results for each individual, and audit is required to evaluate ‘long term weight loss’.

Prevention of hypertension, and control of blood pressure in patients with hypertension, are necessary for the reduction of cardiovascular morbidity and mortality. Lifestyle modifications are one of the most important tools for effective lowering of blood pressure. Most randomized controlled studies have shown that even a modest weight loss of 3–9 % is associated with a significant reduction in systolic and diastolic blood pressure of roughly 3 mm Hg in overweight people. Limitation of sodium chloride in food has historically been considered the critical change for reducing blood pressure. Changes in sodium intake do affect blood pressure in older persons and in patients with hypertension and diabetes, whereas its role in population blood pressure has proven controversial. Recent meta-analyses indicate that adequate intake of minerals, e.g. potassium and probably calcium, rather than restriction of sodium, should be the focus of dietary recommendations. Although epidemiological data point to a direct relation between the intake of saturated fat, starch and alcohol, as well as an inverse relationship to the intake of omega-3 fatty acids and protein, our knowledge about macronutrients and blood pressure is scanty. It may well prove more productive to look at food instead of placing emphasis on single nutrients. Thus the Dietary Approaches to Stop Hypertension (DASH) demonstrates that a diet rich in fruits, vegetables, low-fat dairy products, fibre and minerals (calcium, potassium and magnesium) produces a potent antihypertensive effect. Such a diet is not very restrictive and should not produce compliance problems. Further high-quality research on the influence of macronutrients and food will yield data for updated recommendations, enabling better prevention and control of the blood pressure problem.

The increased risk of coronary heart disease associated with the metabolic syndrome may be partially explained by prothrombotic deviations of the haemostatic system. Individuals with insulin resistance, dyslipidaemia and obesity are characterized by elevated plasma fibrinogen and factor VII coagulant activity levels and raised concentrations of plasminogen-activator inhibitor, the main inhibitor of endogenous fibrinolysis. These haemostatic abnormalities may be corrected with dietary treatment of the underlying clinical disorder. Dietary trials of diseased and healthy volunteers suggest that the optimal antithrombotic diet is a low-fat diet with a high content of foods rich in complex carbohydrates and dietary fibre. The dietary fatty acid composition has a profound effect on blood lipids, but seems of minor importance for the haemostatic system.

Polymorphisms at the APOA1/C3/A4 gene cluster and the APOE gene have been extensively studied in order to examine their potential association with plasma lipid levels, coronary heart disease risk and more recently with inter-individual variability in response to dietary therapies. Although the results have not been uniform across studies, the current research supports the concept that variation at these genes explains a significant, but still rather small, proportion of the variability in fasting and postprandial plasma lipid responses to dietary interventions. This information constitutes the initial frame to develop panels of genetic markers that could be used to predict individual responsiveness to dietary therapy for the prevention of coronary heart disease. Future progress in this complex area will come from experiments carried out using animal models, and from carefully controlled dietary protocols in humans that should include the assessment of several other candidate gene loci coding for products that play a relevant role in lipoprotein metabolism (i.e. APOB, CETP, LPL, FABP2, SRBI, ABC1 and CYP7).

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.