5. Population nutrient intake goals for preventing diet-related chronic diseases

5.1 Overall goals

5.1.1 Background

Population nutrient intake goals represent the population average intake that is judged to be consistent with the maintenance of health in a population. Health, in this context, is marked by a low prevalence of diet-related diseases in the population.

Seldom is there a single “best value” for such a goal. Instead, consistent with the concept of a safe range of nutrient intakes for individuals, there is often a range of population averages that would be consistent with the maintenance of health. If existing population averages fall outside this range, or trends in intake suggest that the population average will move outside the range, health concerns are likely to arise. Sometimes there is no lower limit; this implies that there is no evidence that the nutrient is required in the diet and hence low intakes should not give rise to concern. It would be of concern if a large proportion of values were outside the defined goals.

5.1.2 Strength of evidence

Ideally the definition of an increased or a decreased risk should be based on a relationship that has been established by multiple randomized controlled trials of interventions on populations that are representative of the target of a recommendation, but this type of evidence is often not available. The recommended dietary/nutrition practice should modify the attributable risk of the undesirable exposure in that population.

The following criteria are used to describe the strength of evidence in this report. They are based on the criteria used by the World Cancer Research Fund (1), but have been modified by the Expert Consultation to include the results of controlled trials where relevant and available. In addition, consistent evidence on community and environmental factors which lead to behaviour changes and thereby modify risks has been taken into account in categorizing risks. This applies particularly to the complex interaction between environmental factors that affect excess weight gain, a risk factor which the Consultation recognized as contributing to many of the problems being considered.

• Convincing evidence. Evidence based on epidemiological studies showing consistent associations between exposure and disease, with little or no evidence to the contrary. The available evidence is based on a substantial number of studies including prospective observational studies and where relevant, randomized controlled trials of sufficient size, duration and quality showing consistent effects. The association should be biologically plausible.

• Probable evidence. Evidence based on epidemiological studies showing fairly consistent associations between exposure and disease, but where there are perceived shortcomings in the available evidence or some evidence to the contrary, which precludes a more definite judgement. Shortcomings in the evidence may be any of the following: insufficient duration of trials (or studies); insufficient trials (or studies) available; inadequate sample sizes; incomplete follow-up. Laboratory evidence is usually supportive. Again, the association should be biologically plausible.

• Possible evidence. Evidence based mainly on findings from case-control and cross-sectional studies. Insufficient randomized controlled trials, observational studies or non-randomized controlled trials are available. Evidence based on non-epidemiological studies, such as clinical and laboratory investigations, is supportive. More trials are required to support the tentative associations, which should also be biologically plausible.

• Insufficient evidence. Evidence based on findings of a few studies which are suggestive, but are insufficient to establish an association between exposure and disease. Limited or no evidence is available from randomized controlled trials. More well designed research is required to support the tentative associations.

The strength of evidence linking dietary and lifestyle factors to the risk of developing obesity, type 2 diabetes, CVD, cancer, dental diseases, osteoporosis, graded according to the above categories, is summarized in tabular form, and attached to this report as an Annex.

5.1.3 A summary of population nutrient intake goals

The population nutrient intake goals for consideration by national and regional bodies establishing dietary recommendations for the prevention of diet-related chronic diseases are presented in Table 6. These recommendations are expressed in numerical terms, rather than as increases or decreases in intakes of specific nutrients, because the desirable change will depend upon existing intakes in the particular population, and could be in either direction.

In Table 6, attention is directed towards the energy-supplying macronutrients. This must not be taken to imply a lack of concern for the other nutrients. Rather, it is a recognition of the fact that previous reports issued by FAO and WHO have provided limited guidance on the meaning of a “balanced diet” described in terms of the proportions of the various energy sources, and that there is an apparent consensus on this aspect of diet in relation to effects on the chronic non-deficiency diseases.

This report therefore complements these existing reports on energy and nutrient requirements issued by FAO and WHO (2-4). In translating these goals into dietary guidelines, due consideration should be given to the process for setting up national dietary guidelines (5).

Table 6. Ranges of population nutrient intake goals

^a This is calculated as: total fat - (saturated fatty acids + polyunsaturated fatty acids + trans fatty acids).

^b The percentage of total energy available after taking into account that consumed as protein and fat, hence the wide range.

^c The term “free sugars” refers to all monosaccharides and disaccharides added to foods by the manufacturer, cook or consumer, plus sugars naturally present in honey, syrups and fruit juices.

^d The suggested range should be seen in the light of the Joint WHO/FAO/UNU Expert Consultation on Protein and Amino Acid Requirements in Human Nutrition, held in Geneva from 9 to 16 April 2002 (2).

^e Salt should be iodized appropriately (6). The need to adjust salt iodization, depending on observed sodium intake and surveillance of iodine status of the population, should be recognized.

^f See page 58, under “Non-starch polysaccharides”.

Total fat

The recommendations for total fat are formulated to include countries where the usual fat intake is typically above 30% as well as those where the usual intake may be very low, for example less than 15%. Total fat energy of at least 20% is consistent with good health. Highly active groups with diets rich in vegetables, legumes, fruits and wholegrain cereals may, however, sustain a total fat intake of up to 35% without the risk of unhealthy weight gain.

For countries where the usual fat intake is between 15% and 20% of energy, there is no direct evidence for men that raising fat intake to 20% will be beneficial (7, 8). For women of reproductive age at least 20% has been recommended by the Joint FAO/WHO Expert Consultation on Fats and Oils in Human Nutrition that met in 1993 (3).

Free sugars

It is recognized that higher intakes of free sugars threaten the nutrient quality of diets by providing significant energy without specific nutrients. The Consultation considered that restriction of free sugars was also likely to contribute to reducing the risk of unhealthy weight gain, noting that:

• Free sugars contribute to the overall energy density of diets.

• Free sugars promote a positive energy balance. Acute and short-term studies in human volunteers have demonstrated increased total energy intake when the energy density of the diet is increased, whether by free sugars or fat (9-11). Diets that are limited in free sugars have been shown to reduce total energy intake and induce weight loss (12, 13).

• Drinks that are rich in free sugars increase overall energy intake by reducing appetite control. There is thus less of a compensatory reduction of food intake after the consumption of high-sugars drinks than when additional foods of equivalent energy content are provided (11, 14-16). A recent randomized trial showed that when soft drinks rich in free sugars are consumed there is a higher energy intake and a progressive increase in body weight when compared with energy-free drinks that are artificially sweetened (17). Children with a high consumption of soft drinks rich in free sugars are more likely to be overweight and to gain excess weight (16).

The Consultation recognized that a population goal for free sugars of less than 10% of total energy is controversial. However, the Consultation considered that the studies showing no effect of free sugars on excess weight have limitations. The CARMEN study (Carbohydrate Ratio Management in European National diets) was a multicentre, randomized trial that tested the effects on body weight and blood lipids in overweight individuals of altering the ratio of fat to carbohydrate, as well as the ratio of simple to complex carbohydrate per se. A greater weight reduction was observed with the high complex carbohydrate diet relative to the simple carbohydrate one; the difference, however was not statistically significant (18). Nevertheless, an analysis of weight change and metabolic indices for those with metabolic syndrome revealed a clear benefit of replacing simple by complex carbohydrates (19). The Consultation also examined the results of studies that found an inverse relationship between free sugars intakes and total fat intake. Many of these studies are methodologically inappropriate for determining the causes of excess weight gain, since the percentage of calories from fat will decrease as the percentage of calories from carbohydrates increases and vice versa. Furthermore, these analyses do not usually distinguish between free sugars in foods and free sugars in drinks. Thus, these analyses are not good predictors of the responses in energy intake to a selective reduction in free sugars intake.

Non-starch polysaccharides (NSP)

Wholegrain cereals, fruits and vegetables are the preferred sources of non-starch polysaccharides (NSP). The best definition of dietary fibre remains to be established, given the potential health benefits of resistant starch. The recommended intake of fruits and vegetables (see below) and consumption of wholegrain foods is likely to provide >20 g per day of NSP (>25 g per day of total dietary fibre).

Fruits and vegetables

The benefit of fruits and vegetables cannot be ascribed to a single or mix of nutrients and bioactive substances. Therefore, this food category was included rather than the nutrients themselves. The category of tubers (i.e. potatoes, cassava) should not be included in fruits and vegetables.

Body mass index (BMI)

The goal for body mass index (BMI) included in this report follows the recommendations made by the WHO Expert Consultation on Obesity that met in 1997 (20). At the population level, the goal is for an adult median BMI of 21-23 kg/m2. For individuals, the recommendation is to maintain a BMI in the range 18.5-24.9 kg/m2 and to avoid a weight gain greater than 5 kg during adult life.

Physical activity

The goal for physical activity focuses on maintaining healthy body weight. The recommendation is for a total of one hour per day on most days of the week of moderate-intensity activity, such as walking. This level of physical activity is needed to maintain a healthy body weight, particularly for people with sedentary occupations. The recommendation is based on calculations of energy balance and on an analysis of the extensive literature on the relationships between body weight and physical activity. This recommendation is also presented elsewhere (21). Obviously, this quantitative goal cannot be considered as a single “best value” by analogy with the nutrient intake goals. Furthermore, it differs from the following widely accepted public health recommendation (22):

For better health, people of all ages should include a minimum of 30 minutes of physical activity of moderate intensity (such as brisk walking) on most, if not all, days of the week. For most people greater health benefits can be obtained by engaging in physical activity of more vigorous intensity or of longer duration. This cardio respiratory endurance activity should be supplemented with strength-developing exercises at least twice a week for adults in order to improve musculo skeletal health, maintain independence in performing the activities of daily life and reduce the risk of falling.

The difference between the two recommendations results from the difference in their focus. A recent symposium on the dose-response relationships between physical activity and health outcomes found evidence that 30 minutes of moderate activity is sufficient for cardiovascular/metabolic health, but not for all health benefits. Because prevention of obesity is a central health goal, the recommendation of 60 minutes a day of moderate-intensity activity is considered appropriate. Activity of moderate intensity is found to be sufficient to have a preventive effect on most, if not all, cardiovascular and metabolic diseases considered in this report. Higher intensity activity has a greater effect on some, although not all, health outcomes, but is beyond the capacity and motivation of a large majority of the population.

Both recommendations include the idea that the daily activity can be accomplished in several short bouts. It is important to point out that both recommendations apply to people who are otherwise sedentary. Some occupational activities and household chores constitute sufficient daily physical exercise.

In recommending physical activity, potential individual risks as well as benefits need to be assessed. In many regions of the world, especially but not exclusively in rural areas of developing countries, an appreciable proportion of the population is still engaged in physically demanding activities relating to agricultural practices and domestic tasks performed without mechanization or with rudimentary tools. Even children may be required to undertake physically demanding tasks at very young ages, such as collecting water and firewood and caring for livestock. Similarly, the inhabitants of poor urban areas may still be required to walk long distances to their jobs, which are usually of a manual nature and often require a high expenditure of energy. Clearly, the recommendation for extra physical activity is not relevant for these sectors of the population.

References

1. World Cancer Research Fund. Food, nutrition and the prevention of cancer: a global perspective. Washington, DC, American Institute for Cancer Research, 1997.

2. Protein and amino acid requirements inhuman nutrition. Report of a Joint WHO/FAO/UNU Expert Consultation. Geneva, World Health Organization, 2003 (in press).

3. Fats and oils in human nutrition. Report of a Joint FAO/WHO Expert Consultation. Rome, Food and Agriculture Organization of the United Nations, 1994 (FAO Food and Nutrition Paper, No. 57).

4. Carbohydrates in human nutrition. Report of a Joint FAO/WHO Expert Consultation. Rome, Food and Agriculture Organization of the United Nations, 1998 (FAO Food and Nutrition Paper, No. 66).

5. Preparation and use of food-based dietary guidelines. Report of a Joint FAO/ WHO Consultation. Geneva, World Health Organization, 1998 (WHO Technical Report Series, No. 880).

6. WHO/UNICEF/ICCIDD. Recommended iodine levels in salt and guidelines for monitoring their adequacy and effectiveness. Geneva, World Health Organization, 1996 (document WHO/NUT/96.13).

7. Campbell TC, Parpia B, Chen J. Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China study. American Journal of Cardiology, 1998, 82:18T-21T.

8. Campbell TC, Junshi C. Diet and chronic degenerative diseases: perspectives from China. American Journal of Clinical Nutrition, 59(Suppl. 5):S1153-S1161.

9. Stubbs J, Ferres S, Horgan G. Energy density of foods: effects on energy intake. Critical Reviews in Food Science and Nutrition, 2000, 40:481-515.

10. Rolls BJ, Bell EA. Dietary approaches to the treatment of obesity. Medical Clinics of North America, 2000, 84:401-418.

11. Rolls BJ. Fat and sugar substitutes and the control of food intake. Annals of the New York Academy of Sciences, 1997, 819:180-193.

12. Mann JI et al. Effects on serum-lipids in normal men of reducing dietary sucrose or starch for five months. Lancet, 1970, 1:870-872.

13. Smith JB, Niven BE, Mann JI. The effect of reduced extrinsic sucrose intake on plasma triglyceride levels. European Journal of Clinical Nutrition, 1996, 50:498-504.

14. Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. Journal of American Medical Association, 2002, 287:2414-2423.

15. Ebbeling CB, Ludwig DS. Treating obesity in youth: should dietary glycemic load be a consideration? Advances in Pediatrics, 2001, 48:179-212.

16. Ludwig DS, Peterson KE, Gormakaer SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet, 2001, 357:505-508.

17. Raben A et al. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. American Journal of Clinical Nutrition, 2002, 76:721-729.

18. Saris WH et al. Randomized controlled trial of changes in dietary carbohydrate/ fat ratio and simple vs complex carbohydrates on body weight and blood lipids: the CARMEN study. The Carbohydrate Ratio Management in European National diets. International Journal of Obesity and Related Metabolic Disorders, 2000, 24:1310-1318.

19. Poppitt SD et al. Long-term effects of ad libitum low-fat, high-carbohydrate diets on body weight and serum lipids in overweight subjects with metabolic syndrome. American Journal of Clinical Nutrition, 2002, 75:11-20.

20. Obesity: preventing and managing the global epidemic. Report of a WHO Consultation. Geneva, World Health Organization, 2000 (WHO Technical Report Series, No. 894).

21. Weight control and physical activity. Lyon, International Agency for Research on Cancer, 2002 (IARC Handbooks of Cancer Prevention, Vol. 6).

22. Physical activity and health: a report of the Surgeon General. Atlanta, GA, US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996.

5.2 Recommendations for preventing excess weight gain and obesity

5.2.1 Background

Almost all countries (high-income and low-income alike) are experiencing an obesity epidemic, although with great variation between and within countries. In low-income countries, obesity is more common in middle-aged women, people of higher socioeconomic status and those living in urban communities. In more affluent countries, obesity is not only common in the middle-aged, but is becoming increasingly prevalent among younger adults and children. Furthermore, it tends to be associated with lower socioeconomic status, especially in women, and the urban-rural differences are diminished or even reversed.

It has been estimated that the direct costs of obesity accounted for 6.8% (or US$ 70 billion) of total health care costs, and physical inactivity for a furtherUS$24 billion, in the United States in 1995. Although direct costs in other industrialized countries are slightly lower, they still consume a sizeable proportion of national health budgets (1). Indirect costs, which are far greater than direct costs, include workdays lost, physician visits, disability pensions and premature mortality. Intangible costs such as impaired quality of life are also enormous. Because the risks of diabetes, cardiovascular disease and hypertension rise continuously with increasing weight, there is much overlap between the prevention of obesity and the prevention of a variety of chronic diseases, especially type 2 diabetes. Population education strategies will need a solid base of policy and environment-based changes to be effective in eventually reversing these trends.

5.2.2 Trends

The increasing industrialization, urbanization and mechanization occurring in most countries around the world is associated with changes in diet and behaviour, in particular, diets are becoming richer in high-fat, high energy foods and lifestyles more sedentary. In many developing countries undergoing economic transition, rising levels of obesity often coexist in the same population (or even the same household) with chronic undernutrition. Increases in obesity over the past 30 years have been paralleled by a dramatic rise in the prevalence of diabetes (2).

5.2.3 Diet, physical activity and excess weight gain and obesity

Mortality rates increase with increasing degrees of overweight, as measured by BMI. As BMI increases, so too does the proportion of people with one or more comorbid conditions. In one study in the USA (3), over half (53%) of all deaths in women with a BMI>29 kg/m² could be directly attributed to their obesity. Eating behaviours that have been linked to overweight and obesity include snacking/eating frequency, binge-eating patterns, eating out, and (protectively) exclusive breastfeeding. Nutrient factors under investigation include fat, carbohydrate type (including refined carbohydrates such as sugar), the glycaemic index of foods, and fibre. Environmental issues are clearly important, especially as many environments become increasingly “obesogenic” (obesity-promoting).

Physical activity is an important determinant of body weight. In addition, physical activity and physical fitness (which relates to the ability to perform physical activity) are important modifiers of mortality and morbidity related to overweight and obesity. There is firm evidence that moderate to high fitness levels provide a substantially reduced risk of cardiovascular disease and all-cause mortality and that these benefits apply to all BMI levels. Furthermore, high fitness protects against mortality at all BMI levels in men with diabetes. Low cardiovascular fitness is a serious and common comorbidity of obesity, and a sizeable proportion of deaths in overweight and obese populations are probably a result of low levels of cardio-respiratory fitness rather than obesity per se. Fitness is, in turn, influenced strongly by physical activity in addition to genetic factors. These relationships emphasize the role of physical activity in the prevention of overweight and obesity, independently of the effects of physical activity on body weight.

The potential etiological factors related to unhealthy weight gain are listed in Table 7.

5.2.4 Strength of evidence

Convincing etiological factors

Regular physical activity (protective) and sedentary lifestyles (causative). There is convincing evidence that regular physical activity is protective against unhealthy weight gain whereas sedentary lifestyles, particularly sedentary occupations and inactive recreation such as watching television, promote it. Most epidemiological studies show smaller risk of weight gain, overweight and obesity among persons who currently engage regularly in moderate to large amounts of physical activity (4). Studies measuring physical activity at baseline and randomized trials of exercise programmes show more mixed results, probably because of the low adherence to long-term changes. Therefore, it is ongoing physical activity itself rather than previous physical activity or enrolment in an exercise programme that is protective against unhealthy weight gain. The recommendation for individuals to accumulate at least 30 minutes of moderate-intensity physical activity on most days is largely aimed at reducing cardiovascular diseases and overall mortality. The amount needed to prevent unhealthy weight gain is uncertain but is probably significantly greater than this. Preventing weight gain after substantial weight loss probably requires about 60-90 minutes per day. Two meetings recommended by consensus that about 45-60 minutes of moderate-intensity physical activity is needed on most days or every day to prevent unhealthy weight gain (5, 6). Studies aimed at reducing sedentary behaviours have focused primarily on reducing television viewing in children. Reducing viewing times by about 30 minutes a day in children in the United States appears feasible and is associated with reductions in BMI.

Table 7. Summary of strength of evidence on factors that might promote or protect against weight gain and obesity^a

^a Strength of evidence: the totality of the evidence was taken into account. The World Cancer Research Fund schema was taken as the starting point but was modified in the following manner: randomized controlled trials were given prominence as the highest ranking study design (randomized controlled trials were not a major source of cancer evidence); associated evidence and expert opinion was also taken into account in relation to environmental determinants (direct trials were usually not available).

^b Specific amounts will depend on the analytical methodologies used to measure fibre.

^c Energy-dense and micronutrient-poor foods tend to be processed foods that are high in fat and/or sugars. Low energy-dense (or energy-dilute) foods, such as fruit, legumes, vegetables and whole grain cereals, are high in dietary fibre and water.

^d Associated evidence and expert opinion included.

A high dietary intake of non-starch polysaccharides (NSP)/dietary fibre (protective). The nomenclature and definitions of NSP (dietary fibre) have changed with time, and many of the available studies used previous definitions, such as soluble and insoluble fibre. Nevertheless, two recent reviews of randomized trials have concluded that the majority of studies show that a high intake of NSP (dietary fibre) promotes weight loss.

Pereira & Ludwig (7) found that 12 out of 19 trials showed beneficial objective effects (including weight loss). In their review of 11 studies of more than 4 weeks duration, involving ad libitum eating Howarth Saltzman & Roberts (8) reported a mean weight loss of 1.9 kg over 3.8 months. There were no differences between fibre type or between fibre consumed in food or as supplements.

High intake of energy-dense micronutrient-poor foods (causative).

There is convincing evidence that a high intake of energy-dense foods promotes weight gain. In high-income countries (and increasingly in low income countries) these energy-dense foods are not only highly processed (low NSP) but also micronutrient-poor, further diminishing their nutritional value. Energy-dense foods tend to be high in fat (e.g. butter, oils, fried foods), sugars or starch, while energy-dilute foods have a high water content (e.g. fruits and vegetables). Several trials have covertly manipulated the fat content and the energy density of diets, the results of which support the view that so-called “passive over consumption” of total energy occurs when the energy density of the diet is high and that this is almost always the case in high-fat diets. A meta-analysis of 16 trials of ad libitum high-fat versus low-fat diets of at least 2 months duration suggested that a reduction in fat content by 10% corresponds to about a 1 MJ reduction in energy intake and about 3 kg in body weight (9). At a population level, 3 kg equates to about one BMI unit or about a 5% difference in obesity prevalence. However, it is difficult to blind such studies and other non-physiological effects may influence these findings (10). While energy from fat is no more fattening than the same amount of energy from carbohydrate or protein, diets that are high in fat tend to be energy-dense. An important exception to this is diets based predominantly on energy-dilute foods (e.g. vegetables, legumes, fruits) but which have a reasonably high percentage of energy as fat from added oils.

The effectiveness over the long term of most dietary strategies for weight loss, including low-fat diets, remains uncertain unless accompanied by changes in behaviour affecting physical activity and food habits. These latter changes at a public health level require an environment supportive of healthy food choices and an active life. High quality trials to address these issues are urgently needed. A variety of popular weight-loss diets that restrict food choices may result in reduced energy intake and short term weight loss in individuals but most do not have trial evidence of long-term effectiveness and nutritional adequacy and therefore cannot be recommended for populations.

Probable etiological factors

Home and school environments that promote healthy food and activity choices for children (protective). Despite the obvious importance of the roles that parents and home environments play on children’s eating and physical activity behaviours, there is very little hard evidence available to support this view. It appears that access and exposure to a range of fruits and vegetables in the home is important for the development of preferences for these foods and that parental knowledge, attitudes and behaviours related to healthy diet and physical activity are important in creating role models (11). More data are available on the impact of the school environment on nutrition knowledge, on eating patterns and physical activity at school, and on sedentary behaviours at home. Some studies (12), but not all, have shown an effect of school-based interventions on obesity prevention. While more research is clearly needed to increase the evidence base in both these areas, supportive home and school environments were rated as a probable etiological influence on obesity.

Heavy marketing of fast-food outlets and energy-dense, micronutrient-poor foods and beverages (causative). Part of the consistent, strong relationships between television viewing and obesity in children may relate to the food advertising to which they are exposed (13-15). Fast-food restaurants, and foods and beverages that are usually classified under the “eat least” category in dietary guidelines are among the most heavily marketed products, especially on television. Young children are often the target group for the advertising of these products because they have a significant influence on the foods bought by parents (16). The huge expenditure on marketing fast-foods and other “eat least” choices (US$ 11 billion in the United States alone in 1997) was considered to be a key factor in the increased consumption of food prepared outside the home in general and of energy-dense, micronutrient-poor foods in particular. Young children are unable to distinguish programme content from the persuasive intent of advertisements. The evidence that the heavy marketing of these foods and beverages to young children causes obesity is not unequivocal. Nevertheless, the Consultation considered that there is sufficient indirect evidence to warrant this practice being placed in the “probable” category and thus becoming a potential target for interventions (15-18).

A high intake of sugars-sweetened beverages (causative). Diets that are proportionally low in fat will be proportionally higher in carbohydrate (including a variable amount of sugars) and are associated with protection against unhealthy weight gain, although a high intake of free sugars in beverages probably promotes weight gain. The physiological effects of energy intake on satiation and satiety appear to be quite different for energy in solid foods as opposed to energy in fluids. Possibly because of reduced gastric distension and faster transit times, the energy contained in fluids is less well “detected” by the body and subsequent food intake is poorly adjusted to account for the energy taken in through beverages (19). This is supported by data from cross-sectional, longitudinal, and cross-over studies (20-22). The high and increasing consumption of sugars-sweetened drinks by children in many countries is of serious concern. It has been estimated that each additional can or glass of sugars-sweetened drink that they consume every day increases the risk of becoming obese by 60% (19). Most of the evidence relates to soda drinks but many fruit drinks and cordials are equally energy-dense and may promote weight gain if drunk in large quantities. Overall, the evidence implicating a high intake of sugars-sweetened drinks in promoting weight gain was considered moderately strong.

Adverse socioeconomic conditions, especially for women in high-income countries (causative). Classically the pattern of the progression of obesity through a population starts with middle-aged women in high-income groups but as the epidemic progresses, obesity becomes more common in people (especially women) in lower socioeconomic status groups. The relationship may even be bi-directional, setting up a vicious cycle (i.e. lower socioeconomic status promotes obesity, and obese people are more likely to end up in groups with low socioeconomic status). The mechanisms by which socioeconomic status influences food and activity patterns are probably multiple and need elucidation. However, people living in circumstances of low socioeconomic status may be more at the mercy of the obesogenic environment because their eating and activity behaviours are more likely to be the “default choices” on offer. The evidence for an effect of low socioeconomic status on predisposing people to obesity is consistent (in higher income countries) across a number of cross-sectional and longitudinal studies (23), and was thus rated as a “probable” cause of increased risk of obesity.

Breastfeeding (protective). Breastfeeding as a protective factor against weight gain has been examined in at least 20 studies involving nearly 40 000 subjects. Five studies (including the two largest) found a protective effect, two found that breastfeeding predicted obesity, and the remainder found no relationships. There are probably multiple effects of confounding in these studies; however, the reduction in the risk of developing obesity observed in the two largest studies was substantial (20-37%). Promoting breastfeeding has many benefits, the prevention of childhood obesity probably being one of them.

Possible etiological factors

Several other factors were defined as “possible” protective or causative in the etiology of unhealthy weight gain.

Low-glycaemic foods have been proposed as a potential protective factor against weight gain and there are some early studies that support this hypothesis. More clinical trials are, however, needed to establish the association with greater certainty.

Large portion sizes are a possible causative factor for unhealthy weight gain (24). The marketing of “supersize” portions, particularly in fast-food outlets, is now common practice in many countries. There is some evidence that people poorly estimate portion sizes and that subsequent energy compensation for a large meal is incomplete and therefore is likely to lead to overconsumption.

In many countries, there has been a steady increase in the proportion of food eaten that is prepared outside the home. In the United States, the energy, total fat, saturated fat, cholesterol and sodium content of foods prepared outside the home is significantly higher than that of home-prepared food. People in the United States who tend to eat in restaurants have a higher BMI than those who tend to eat at home (25).

Certain psychological parameters of eating patterns may influence the risk of obesity. The “flexible restraint” pattern is associated with lower risk of weight gain, whereas the “rigid restraint/periodic disinhibition” pattern is associated with a higher risk.

Several other factors were also considered but the evidence was not thought to be strong enough to warrant defining them as protective or causative. Studies have not shown consistent associations between alcohol intake and obesity despite the high energy density of the nutrient (7 kcal/g). There are probably many confounding factors that influence the association. While a high eating frequency has been shown in some studies to have a negative relationship with energy intake and weight gain, the types of foods readily available as snack foods are often high in fat and a high consumption of foods of this type might predispose people to weight gain. The evidence regarding the impact of early nutrition on subsequent obesity is also mixed, with some studies showing relationships for high and low birth weights.

5.2.5 General strategies for obesity prevention

The prevention of obesity in infants and young children should be considered of high priority. For infants and young children, the main preventive strategies are:

- the promotion of exclusive breastfeeding;

- avoiding the use of added sugars and starches when feeding formula;

- instructing mothers to accept their child’s ability to regulate energy intake rather than feeding until the plate is empty;

- assuring the appropriate micronutrient intake needed to promote optimal linear growth.

For children and adolescents, prevention of obesity implies the need to:

- promote an active lifestyle;

- limit television viewing;

- promote the intake of fruits and vegetables;

- restrict the intake of energy-dense, micronutrient-poor foods (e.g. packaged snacks);

- restrict the intake of sugars-sweetened soft drinks.

Additional measures include modifying the environment to enhance physical activity in schools and communities, creating more opportunities for family interaction (e.g. eating family meals), limiting the exposure of young children to heavy marketing practices of energy-dense, micronutrient-poor foods, and providing the necessary information and skills to make healthy food choices.

In developing countries, special attention should be given to avoidance of overfeeding stunted population groups. Nutrition programmes designed to control or prevent undernutrition need to assess stature in combination with weight to prevent providing excess energy to children of low weight-for-age but normal weight-for-height. In countries in economic transition, as populations become more sedentary and able to access energy-dense foods, there is a need to maintain the healthy components of traditional diets (e.g. high intake of vegetables, fruits and NSP). Education provided to mothers and low socioeconomic status communities that are food insecure should stress that overweight and obesity do not represent good health.

Low-income groups globally and populations in countries in economic transition often replace traditional micronutrient-rich foods by heavily marketed, sugars-sweetened beverages (i.e. soft drinks) and energy-dense fatty, salty and sugary foods. These trends, coupled with reduced physical activity, are associated with the rising prevalence of obesity. Strategies are needed to improve the quality of diets by increasing consumption of fruits and vegetables, in addition to increasing physical activity, in order to stem the epidemic of obesity and associated diseases.

5.2.6 Disease-specific recommendations

Body mass index (BMI)

BMI can be used to estimate, albeit crudely, the prevalence of overweight and obesity within a population and the risks associated with it. It does not, however, account for the wide variations in obesity between different individuals and populations. The classification of overweight and obesity, according to BMI, is shown in Table 8.

Table 8. Classification of overweight in adults according to BMI^a

^a These BMI values are age-independent and the same for both sexes. However, BMI may not correspond to the same degree of fatness in different populations due, in part, to differences in body proportions. The table shows a simplistic relationship between BMI and the risk of comorbidity, which can be affected by a range of factors, including the nature and the risk of comorbidity, which can be affected by a range of factors, including the nature of the diet, ethnic group and activity level. The risks associated with increasing BMI are continuous and graded and begin at a BMI below 25. The interpretation of BMI gradings in relation to risk may differ for different populations. Both BMI and a measure of fat distribution (waist circumference or waist: hip ratio (WHR)) are important in calculating the risk of obesity comorbidities.

Source: reference 26.

In recent years, different ranges of BMI cut-off points for overweight and obesity have been proposed, in particular for the Asia-Pacific region (27). At present available data on which to base definitive recommendations are sparse.^[4] Nevertheless, the consultation considered that, to achieve optimum health, the median BMI for the adult population should be in the range 21-23 kg/m², while the goal for individuals should be to maintain BMI in the range 18.5-24.9 kg/m².

Waist circumference

Waist circumference is a convenient and simple measure which is unrelated to height, correlates closely with BMI and the ratio of waist-to-hip circumference, and is an approximate index of intra-abdominal fat mass and total body fat. Furthermore, changes in waist circumference reflect changes in risk factors for cardiovascular disease and other forms of chronic diseases, even though the risks seem to vary in different populations. There is an increased risk of metabolic complications for men with a waist circumference ³ 102 cm, and women with a waist circumference ³ 88 cm.

Physical activity

A total of one hour per day of moderate-intensity activity, such as walking on most days of the week, is probably needed to maintain a healthy body weight, particularly for people with sedentary occupations.^[5]

Total energy intake

The fat and water content of foods are the main determinants of the energy density of the diet. A lower consumption of energy-dense (i.e. high-fat, high-sugars and high-starch) foods and energy-dense (i.e. high free sugars) drinks contributes to a reduction in total energy intake. Conversely, a higher intake of energy-dilute foods (i.e. vegetables and fruits) and foods high in NSP (i.e. wholegrain cereals) contributes to a reduction in total energy intake and an improvement in micronutrient intake. It should be noted, however, that very active groups who have diets high in vegetables, legumes, fruits and wholegrain cereals, may sustain a total fat intake of up to 35% without the risk of unhealthy weight gain.

References

1. Colditz G. Economic costs of obesity and inactivity. Medicine and Science in Sport and Exercise, 1999, 31(Suppl. 11):S663-S667.

2. The world health report 2002: reducing risks, promoting healthy life. Geneva, World Health Organization, 2002.

3. Manson JE et al. Body weight and mortality among women. New England Journal of Medicine, 1995, 333:677-685.

4. Fogelholm M, Kukkonen-Harjula K. Does physical activity prevent weight gain - a systematic review. Obesity Reviews, 2000, 1:95-111.

5. Weight control and physical activity. Lyon, International Agency for Research on Cancer, 2002 (IARC Handbooks of Cancer Prevention, Vol. 6).

6. Saris WHM. Dose-response of physical activity in the treatment of obesity-How much is enough to prevent unhealthy weight gain. Outcome of the First Mike Stock Conference. International Journal of Obesity, 2002, 26(Suppl. 1):S108.

7. Pereira MA, Ludwig DS. Dietary fiber and body-weight regulation. Observations and mechanisms. Pediatric Clinics of North America, 2001, 48:969-980.

8. Howarth NC, Saltzman E, Roberts SB. Dietary fiber and weight regulation. Nutrition Reviews, 2001, 59:129-139.

9. Astrup A et al. The role of low-fat diets in body weight control: a meta-analysis of ad libitum dietary intervention studies. International Journal of Obesity, 2000, 24:1545-1552.

10. Willett WC. Dietary fat plays a major role in obesity: no. Obesity Reviews, 2000, 3:59-68.

11. Campbell K, Crawford D. Family food environments as determinants of preschool-aged children’s eating behaviours: implications for obesity prevention policy. A review. Australian Journal of Nutrition and Dietetics, 2001, 58:19-25.

12. Gortmaker S et al. Reducing obesity via a school-based interdisciplinary intervention among youth: Planet Health. Archives of Pediatrics and Adolescent Medicine, 1999, 153:409-418.

13. Nestle M. Food politics. Berkeley, CA, University of California Press, 2002.

14. Nestle M. The ironic politics of obesity. Science, 2003, 299:781.

15. Robinson TN. Does television cause childhood obesity? Journal of American Medical Association, 1998, 279:959-960.

16. Borzekowski DL, Robinson TN. The 30-second effect: an experiment revealing the impact of television commercials on food preferences of preschoolers. Journal of the American Dietetic Association, 2001, 101:42-46.

17. Lewis MK, Hill AJ. Food advertising on British children’s television: a content analysis and experimental study with nine-year olds. International Journal of Obesity, 1998, 22:206-214.

18. Taras HL, Gage M. Advertised foods on children’s television. Archives of Pediatrics and Adolescent Medicine, 1995, 149:649-652.

19. Mattes RD. Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrate in fluids. Physiology and Behaviour, 1996, 59:179-187.

20. Tordoff MG, Alleva AM. Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight. American Journal of Clinical Nutrition, 1990, 51:963-969.

21. Harnack L, Stang J, Story M. Soft drink consumption among US children and adolescents: nutritional consequences. Journal of the American Dietetic Association, 1999, 99:436-441.

22. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet, 2001, 357:505-508.

23. Peña M, Bacallao J. Obesity and poverty: a new public health challenge. Washington, DC, Pan American Health Organization, 2000 (Scientific Publication, No. 576).

24. Nielsen SJ, Popkin BM. Patterns and trends in food portion sizes, 1977-1998. Journal of the American Medical Association, 2003, 289:450-453.

25. Jeffery RW, French SA. Epidemic obesity in the United States: are fast foods and television viewing contributing? American Journal of Public Health, 1998, 88:277-280.

26. Obesity: preventing and managing the global epidemic. Report of a WHO Consultation. Geneva, World Health Organization, 2000 (WHO Technical Report Series, No. 894).

27. WHO Regional Office for the Western Pacific/International Association for the Study of Obesity/International Obesity Task Force. The Asia-Pacific perspective: redefining obesity and its treatment. Sydney, Health Communications Australia, 2000.

5.3 Recommendations for preventing diabetes

5.3.1 Background

Type 2 diabetes, formerly known as non-insulin-dependent diabetes (NIDDM), accounts for most cases of diabetes worldwide. Type 2 diabetes develops when the production of insulin is insufficient to overcome the underlying abnormality of increased resistance to its action. The early stages of type 2 diabetes are characterized by overproduction of insulin. As the disease progresses, process insulin levels may fall as a result of partial failure of the insulin producing b cells of the pancreas. Complications of type 2 diabetes include blindness, kidney failure, foot ulceration which may lead to gangrene and subsequent amputation, and appreciably increased risk of infections, coronary heart disease and stroke. The enormous and escalating economic and social costs of type 2 diabetes make a compelling case for attempts to reduce the risk of developing the condition as well as for energetic management of the established disease (1, 2).

Lifestyle modification is the cornerstone of both treatment and attempts to prevent type 2 diabetes (3). The changes required to reduce the risk of developing type 2 diabetes at the population level are, however, unlikely to be achieved without major environmental changes to facilitate appropriate choices by individuals. Criteria for the diagnosis of type 2 diabetes and for the earlier stages in the disease process - impaired glucose tolerance and impaired fasting glucose - have recently been revised (4, 5).

Type 1 diabetes, previously known as insulin-dependent diabetes, occurs much less frequently and is associated with an absolute deficiency of insulin, usually resulting from autoimmune destruction of the b cells of the pancreas. Environmental as well as genetic factors appear to be involved but there is no convincing evidence of a role for lifestyle factors which can be modified to reduce the risk.

5.3.2 Trends

Although increases in both the prevalence and incidence of type 2 diabetes have occurred globally, they have been especially dramatic in societies in economic transition in much of the newly industrialized world and in developing countries (1, 6-9). Worldwide, the number of cases of diabetes is currently estimated to be around 150 million. This number is predicted to double by 2025, with the greatest number of cases being expected in China and India. These numbers may represent an underestimate and there are likely to be many undiagnosed cases. Previously a disease of the middle-aged and elderly, type 2 diabetes has recently escalated in all age groups and is now being identified in younger and younger age groups, including adolescents and children, especially in high-risk populations.

Age-adjusted mortality rates among people with diabetes are 1.5-2.5 times higher than in the general population (10). In Caucasian populations, much of the excess mortality is attributable to cardiovascular disease, especially coronary heart disease (11, 12); amongst Asian and American Indian populations, renal disease is a major contributor (13, 14), whereas in some developing nations, infections are an important cause of death (15). It is conceivable that the decline in mortality due to coronary heart disease which has occurred in many affluent societies may be halted or even reversed if rates of type 2 diabetes continue to increase. This may occur if the coronary risk factors associated with diabetes increase to the extent that the risk they mediate outweighs the benefit accrued from improvements in conventional cardiovascular risk factors and the improved care of patients with established cardiovascular disease (3).

5.3.3 Diet, physical activity and diabetes

Type 2 diabetes results from an interaction between genetic and environmental factors. The rapidly changing incidence rates, however, suggest a particularly important role for the latter as well as a potential for stemming the tide of the global epidemic of the disease. The most dramatic increases in type 2 diabetes are occurring in societies in which there have been major changes in the type of diet consumed, reductions in physical activity, and increases in overweight and obesity. The diets concerned are typically energy-dense, high in saturated fatty acids and depleted in NSP.

In all societies, overweight and obesity are associated with an increased risk of type 2 diabetes, especially when the excess adiposity is centrally distributed. Conventional (BMI) categories may not be an appropriate means of determining the risk of developing type 2 diabetes in individuals of all population groups because of ethnic differences in body composition and because of the importance of the distribution of excess adiposity. While all lifestyle-related and environmental factors which contribute to excess weight gain may be regarded as contributing to type 2 diabetes, the evidence that individual dietary factors have an effect which is independent of their obesity promoting effect, is inconclusive. Evidence that saturated fatty acids increase risk of type 2 diabetes and that NSP are protective is more convincing than the evidence for several other nutrients which have been implicated. The presence of maternal diabetes, including gestational diabetes and intrauterine growth retardation, especially when associated with later rapid catch-up growth, appears to increase the risk of subsequently developing diabetes.

5.3.4 Strength of evidence

The association between excessive weight gain, central adiposity and the development of type 2 diabetes is convincing. The association has been repeatedly demonstrated in longitudinal studies in different populations, with a striking gradient of risk apparent with increasing levels of BMI, adult weight gain, waist circumference or waist-to-hip ratio. Indeed waist circumference or waist-to-hip ratio (reflecting abdominal or visceral adiposity) are more powerful determinants of subsequent risk of type 2 diabetes than BMI (16-20). Central adiposity is also an important determinant of insulin resistance, the underlying abnormality in most cases of type 2 diabetes (20). Voluntary weight loss improves insulin sensitivity (21) and in several randomized controlled trials has been shown to reduce the risk of progression from impaired glucose tolerance to type 2 diabetes (22, 23).

Longitudinal studies have clearly indicated that increased physical activity reduces the risk of developing type 2 diabetes regardless of the degree of adiposity (24-26). Vigorous exercise (i.e. training to an intensity of 80-90% of age-predicted maximum heart rate for at least 20 minutes, at least five times per week) has the potential to substantially enhance insulin sensitivity (21). The minimum intensity and duration of physical activity required to improve insulin sensitivity has not been established.

Offspring of diabetic pregnancies (including gestational diabetes) are often large and heavy at birth, tend to develop obesity in childhood and are at high risk of developing type 2 diabetes at an early age (27). Those born to mothers after they have developed diabetes have a three-fold higher risk of developing diabetes than those born before (28).

In observational epidemiological studies, a high saturated fat intake has been associated with a higher risk of impaired glucose tolerance, and higher fasting glucose and insulin levels (29-32). Higher proportions of saturated fatty acids in serum lipid or muscle phospholipid have been associated with higher fasting insulin, lower insulin sensitivity and a higher risk of type 2 diabetes (33-35). Higher unsaturated fatty acids from vegetable sources and polyunsaturated fatty acids have been associated with a reduced risk of type 2 diabetes (36, 37) and lower fasting and 2-hour glucose concentrations (32, 38). Furthermore, higher proportions of long-chain polyunsaturated fatty acids in skeletal muscle phospholipids have been associated with increased insulin sensitivity (39).

In human intervention studies, replacement of saturated by unsaturated fatty acids leads to improved glucose tolerance (40, 41) and enhanced insulin sensitivity (42). Long-chain polyunsaturated fatty acids do not, however, appear to confer additional benefit over monounsaturated fatty acids in intervention studies (42). Furthermore, when total fat intake is high (greater than 37% of total energy), altering the quality of dietary fat appears to have little effect (42), a finding which is not surprising given that in observational studies a high intake of total fat has been shown to predict development of impaired glucose tolerance and the progression of impaired glucose tolerance to type 2 diabetes (29, 43). A high total fat intake has also been associated with higher fasting insulin concentrations and a lower insulin sensitivity index (44, 45).

Considered in aggregate these findings are deemed to indicate a probable causal link between saturated fatty acids and type 2 diabetes, and a possible causal association between total fat intake and type 2 diabetes. The two randomized controlled trials which showed a potential for lifestyle modification to reduce the risk of progression from impaired glucose tolerance to type 2 diabetes included advice to reduce total and saturated fat (22, 23), but in both trials it is impossible to disentangle the effects of individual dietary manipulation.

Research relating to the association between NSP intake and type 2 diabetes is complicated by ambiguity with regard to the definitions used (the term dietary fibre and NSP are often incorrectly used interchangeably), different methods of analysis and, consequently, inconsistencies in food composition tables. Observations by Trowell in Uganda more than 30 years ago suggested that the infrequency of diabetes in rural Africa may be the result of a protective effect of substantial amounts of NSP in the diet (referred to as dietary fibre) associated with a high consumption of minimally-processed or unprocessed carbohydrate. The author also hypothesized that throughout the world, increasing intakes of highly-processed carbohydrate, depleted in NSP, had promoted the development of diabetes (46). Three cohort studies (the Health Professionals Follow-up Study of men aged 40-75 years, the Nurses’ Health Study of women aged 40-65 years, and the Iowa Women’s Health Study in women aged 55-69 years) have shown a protective effect of NSP (dietary fibre) (47-49) which was independent of age, BMI, smoking and physical activity. In many controlled experimental studies, high intakes of NSP (dietary fibre) have repeatedly been shown to result in reduced blood glucose and insulin levels in people with type 2 diabetes and impaired glucose tolerance (50). Moreover an increased intake of wholegrain cereals, vegetables and fruits (all rich in NSP) was a feature of the diets associated with a reduced risk of progression of impaired glucose tolerance to type 2 diabetes in the two randomized controlled trials previously described (22, 23). Thus the evidence for a potential protective effect of NSP (dietary fibre) appears strong. However, the fact that the experimental studies suggest that soluble forms of NSP exert benefit (50-53) whereas the prospective cohort studies suggest that it is the cereal-derived insoluble forms that are protective (47, 48) explain the “probable” rather “convincing” grading of the level of evidence.

Many foods which are rich in NSP (especially soluble forms), such as pulses, have a low glycaemic index.^[6] Other carbohydrate-containing foods (e.g. certain types of pasta), which are not especially high in NSP, also have a low glycaemic index. Low glycaemic index foods, regardless of their NSP content, are not only associated with a reduced glycaemic response after ingestion when compared with foods of higher glycaemic index, but are also associated with an overall improvement in glycaemic control (as measured by haemoglobin A1c) in people with diabetes (54-57). A low glycaemic index does not, however, per se, confer overall health benefits, since a high fat or fructose content of a food may also result in a reduced glycaemic index and such foods may also be energy-dense. Thus while this property of carbohydrate-containing foods may well influence the risk of developing type 2 diabetes, the evidence is accorded a lower level of strength than the evidence relating to the NSP content. Similarly, the level of evidence for the protective effect of n-3 fatty acids is regarded as “possible” because the results of epidemiological studies are inconsistent and the experimental data inconclusive. There is insufficient evidence to confirm or refute the suggestions that chromium, magnesium, vitamin E and moderate intakes of alcohol might protect against the development of type 2 diabetes.

A number of studies, mostly in developing countries, have suggested that intrauterine growth retardation and low birth weight are associated with subsequent development of insulin resistance (58). In those countries where there has been chronic undernutrition, insulin resistance may have been selectively advantageous in terms of surviving famine. In populations where energy intake has increased and lifestyles have become more sedentary, however, insulin resistance and the consequent risk of type 2 diabetes have been enhanced. In particular, rapid postnatal catch-up growth appears to further increase the risk of type 2 diabetes in later life. Appropriate strategies which may help to reduce type 2 diabetes risk in this situation include improving the nutrition of young children, promoting linear growth and preventing energy excess by limiting intake of energy-dense foods, controlling the quality of fat supply, and facilitating physical activity. At a population level, fetal growth may remain restricted until maternal height improves. This may take several generations to correct. The prevention of type 2 diabetes in infants and young children may be facilitated by the promotion of exclusive breastfeeding, avoiding overweight and obesity, and promoting optimum linear growth. The strength of evidence on lifestyle factors is summarized in Table 9.

Table 9. Summary of strength of evidence on lifestyle factors and risk of developing type 2 diabetes

¹ NSP, non-starch polysaccharides.

^a Includes gestational diabetes.

^b As a global public health recommendation, infants should be exclusively breastfed for the first six months of life to achieve optimal growth, development and health (59).

5.3.5 Disease-specific recommendations

Measures aimed at reducing overweight and obesity, and cardiovascular disease are likely to also reduce the risk of developing type 2 diabetes and its complications. Some measures are particularly relevant to reducing the risk for diabetes; these are listed below:

• Prevention/treatment of overweight and obesity, particularly in highrisk groups.

• Maintaining an optimum BMI, i.e. at the lower end of the normal range. For the adult population, this means maintaining a mean BMI in the range 21-23 kg/m² and avoiding weight gain (>5 kg) in adult life.

• Voluntary weight reduction in overweight or obese individuals with impaired glucose tolerance (although screening for such individuals may not be cost-effective in many countries).

• Practising an endurance activity at moderate or greater level of intensity (e.g. brisk walking) for one hour or more per day on most days per week.

• Ensuring that saturated fat intake does not exceed 10% of total energy and for high-risk groups, fat intake should be <7% of total energy.

• Achieving adequate intakes of NSP through regular consumption of wholegrain cereals, legumes, fruits and vegetables. A minimum daily intake of 20 g is recommended.

References

1. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995-2025: prevalence, numerical estimates, and projections. Diabetes Care, 1998, 21:1414-1431.

2. Amos AF, McCarty DJ, Zimmet P. The rising global burden of diabetes and its complications: estimates and projections to the year 2010. Diabetic Medicine, 1997, 14(Suppl. 5):S1-S85.

3. Mann J. Stemming the tide of diabetes mellitus. Lancet, 2000, 356:1454-1455.

4. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care, 1997, 20:1183-1197.

5. Definition, diagnosis and classification of diabetes mellitus and its complications. Report of a WHO Consultation. Part 1. Diagnosis and classification of diabetes mellitus. Geneva, World Health Organization, 1999 (document WHO/NCD/NCS/99.2).

6. Harris MI et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994. Diabetes Care, 1998, 21:518-524.

7. Flegal KM et al. Prevalence of diabetes in Mexican Americans, Cubans, and Puerto Ricans from the Hispanic Health and Nutrition Examination Survey, 1982-1984. Diabetes Care, 1991, 14:628-638.

8. Mokdad AH et al. Diabetes trends among American Indians and Alaska natives: 1990-1998. Diabetes Care, 2001, 24:1508-1509.

9. Mokdad AH et al. The continuing epidemics of obesity and diabetes in the United States. Journal of the American Medical Association, 2001, 286:1195-1200.

10. Kleinman JC et al. Mortality among diabetics in a national sample. American Journal of Epidemiology, 1988, 128:389-401.

11. Gu K, Cowie CC, Harris MI. Mortality in adults with and without diabetes in a national cohort of the US population, 1971-1993. Diabetes Care, 1998, 21:1138-1145.

12. Roper NA et al. Excess mortality in a population with diabetes and the impact of material deprivation: longitudinal, population-based study. British Medical Journal, 2001, 322:1389-1393.

13. Morrish et al. Mortality and causes of death in the WHO Multinational Study of Vascular Disease in Diabetes. Diabetologia, 2001, 44(Suppl. 2):S14-S21.

14. Sievers ML et al. Impact of NIDDM on mortality and causes of death in Pima Indians. Diabetes Care, 1992, 15:1541-1549.

15. McLarty DG, Kinabo L, Swai AB. Diabetes in tropical Africa: a prospective study, 1981-7. II. Course and prognosis. British Medical Journal, 1990, 300:1107-1110.

16. Colditz GA et al. Weight as a risk factor for clinical diabetes in women. American Journal of Epidemiology, 1990, 132:501-513.

17. Després JP et al. Treatment of obesity: need to focus on high-risk abdominally obese patients. British Medical Journal, 2001, 322:716-720.

18. Chan JM et al. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care, 1994, 17:961-969.

19. Boyko EJ et al. Visceral adiposity and risk of type 2 diabetes: a prospective study among Japanese Americans. Diabetes Care, 2000, 23:465-471.

20. Després JP. Health consequences of visceral obesity. Annals of Medicine, 2001, 33:534-541.

21. McAuley KA et al. Intensive lifestyle changes are necessary to improve insulin sensitivity. Diabetes Care, 2002, 25:445-452.

22. Tuomilehto J et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. New England Journal of Medicine, 2002, 344:1343-1350.

23. Knowler WC et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention of metformin. New England Journal of Medicine, 2002, 346:393-403.

24. Manson JE et al. A prospective study of exercise and incidence of diabetes among US male physicians. Journal of the American Medical Association, 1992, 268:63-67.

25. Kriska AM et al. The association of physical activity with obesity, fat distribution and glucose intolerance in Pima Indians. Diabetologia, 1993, 36:863-869.

26. Helmrich SP et al. Physical activity and reduced occurrence of non-insulindependent diabetes mellitus. New England Journal of Medicine, 1991, 325:147-152.

27. Pettitt DJ et al. Congenital susceptibility to NIDDM. Role of intrauterine environment. Diabetes, 1988, 37:622-628.

28. Dabelea D et al. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships. Diabetes, 2000, 49:2208-2211.

29. Feskens EJM et al. Dietary factors determining diabetes and impaired glucose tolerance. A 20-year follow-up of the Finnish and Dutch cohorts of the Seven Countries Study. Diabetes Care, 1995, 18:1104-1112.

30. Bo S et al. Dietary fat and gestational hyperglycaemia. Diabetologia, 2001, 44:972-978.

31. Feskens EJM, Kromhout D. Habitual dietary intake and glucose tolerance in euglycaemic men: the Zutphen Study. International Journal of Epidemiology, 1990, 19:953-959.

32. Parker DR et al. Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: the Normative Aging Study. American Journal of Clinical Nutrition, 1993, 58:129-136.

33. Folsom AR et al. Relation between plasma phospholipid saturated fatty acids and hyperinsulinemia. Metabolism, 1996, 45:223-228.

34. Vessby B, Tengblad S, Lithell H. Insulin sensitivity is related to the fatty acid composition of serum lipids and skeletal muscle phospholipids in 70-year-old men. Diabetologia, 1994, 37:1044-1050.

35. Vessby B et al. The risk to develop NIDDM is related to the fatty acid composition of the serum cholesterol esters. Diabetes, 1994, 43:1353-1357.

36. Salmeron J et al. Dietary fat intake and risk of type 2 diabetes in women. American Journal of Clinical Nutrition, 2001, 73:1019-1026.

37. Meyer KA et al. Dietary fat and incidence of type 2 diabetes in older Iowa women. Diabetes Care, 2001, 24:1528-1535.

38. Mooy JM et al. Prevalence and determinants of glucose intolerance in a Dutch Caucasian population. The Hoorn Study. Diabetes Care, 1995, 18:1270-1273.

39. Pan DA et al. Skeletal muscle membrane lipid composition is related to adiposity and insulin action. Journal of Clinical Investigation, 1995, 96:2802-2808.

40. Uusitupa M et al. Effects of two high-fat diets with different fatty acid compositions on glucose and lipid metabolism in healthy young women. American Journal of Clinical Nutrition, 1994, 59:1310-1316.

41. Vessby B et al. Substituting polyunsaturated for saturated fat as a single change in a Swedish diet: effects on serum lipoprotein metabolism and glucose tolerance in patients with hyperlipoproteinaemia. European Journal of Clinical Investigation, 1980, 10:193-202.

42. Vessby B et al. Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: the KANWU Study. Diabetologia, 2001, 44:312-319.

43. Marshall JA et al. Dietary fat predicts conversion from impaired glucose tolerance to NIDDM. The San Luis Valley Diabetes Study. Diabetes Care, 1994, 17:50-56.

44. Mayer EJ et al. Usual dietary fat intake and insulin concentrations in healthy women twins. Diabetes Care, 1993, 16:1459-1469.

45. Lovejoy J, DiGirolamo M. Habitual dietary intake and insulin sensitivity in lean and obese adults. American Journal of Clinical Nutrition, 1992, 55:1174-1179.

46. Trowell HC. Dietary-fiber hypothesis of the etiology of diabetes mellitus. Diabetes, 1975, 24:762-765.

47. Salmeron J et al. Dietary fiber, glycemic load and risk of NIDDM in men. Diabetes Care, 1997, 20:545-550.

48. Salmeron J et al. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. Journal of the American Medical Association, 1997, 277:472-477.

49. Meyer KA et al. Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. American Journal of Clinical Nutrition, 2000, 71:921-930.

50. Mann J. Dietary fibre and diabetes revisited. European Journal of Clinical Nutrition, 2001, 55:919-921.

51. Simpson HRC et al. A high carbohydrate leguminous fibre diet improves all aspects of diabetic control. Lancet, 1981, 1:1-5.

52. Mann J. Lawrence lecture. Lines to legumes: changing concepts of diabetic diets. Diabetic Medicine, 1984, 1:191-198.

53. Chandalia M et al. Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. New England Journal of Medicine, 2000, 342:1392-1398.

54. Frost G, Wilding J, Beecham J. Dietary advice based on the glycaemic index improves dietary profile and metabolic control in type 2 diabetic patients. Diabetic Medicine, 1994, 11:397-401.

55. Brand JC et al. Low-glycemic index foods improve long-term glycemic control in NIDDM. Diabetes Care, 1991, 14:95-101.

56. Fontvieille AM et al. The use of low glycaemic index foods improves metabolic control of diabetic patients over five weeks. Diabetic Medicine, 1992, 9:444-450.

57. Wolever TMS et al. Beneficial effect of a low glycaemic index diet in type 2 diabetes. Diabetic Medicine, 1992, 9:451-458.

58. Stern MP et al. Birth weight and the metabolic syndrome: thrifty phenotype or thrifty genotype? Diabetes/Metabolism Research and Reviews, 2000, 16:88-93.

59. Infant and young child nutrition. Geneva, World Health Organization, 2001 (document A54/2).

5.4 Recommendations for preventing cardiovascular diseases

5.4.1 Background

The second half of the 20th century has witnessed major shifts in the pattern of disease, in addition to marked improvements in life expectancy, this period is characterized by profound changes in diet and lifestyles which in turn have contributed to an epidemic of noncommunicable diseases. This epidemic is now emerging, and even accelerating, in most developing countries, while infections and nutritional deficiencies are receding as leading contributors to death and disability (1).

In developing countries, the effect of the nutrition transition and the concomitant rise in the prevalence of cardiovascular diseases will be to widen the mismatch between health care needs and resources, and already scarce resources will be stretched ever more thinly. Because unbalanced diets, obesity and physical inactivity all contribute to heart disease, addressing these, along with tobacco use, can help to stem the epidemic. A large measure of success in this area has already been demonstrated in many industrialized countries.

5.4.2 Trends

Cardiovascular diseases are the major contributor to the global burden of disease among the noncommunicable diseases. WHO currently attributes one-third of all global deaths (15.3 million) to CVD, with developing countries, low-income and middle-income countries accounting for 86% of the DALYs lost to CVD world wide in 1998. In the next two decades the increasing burden of CVD will be borne mostly by developing countries.

5.4.3 Diet, physical activity and cardiovascular disease

The “lag-time” effect of risk factors for CVD means that present mortality rates are the consequence of previous exposure to behavioural risk factors such as inappropriate nutrition, insufficient physical activity and increased tobacco consumption. Overweight, central obesity, high blood pressure, dyslipidaemia, diabetes and low cardio-respiratory fitness are among the biological factors contributing principally to increased risk. Unhealthy dietary practices include the high consumption of saturated fats, salt and refined carbohydrates, as well as low consumption of fruits and vegetables, and these tend to cluster together.

5.4.4 Strength of evidence

Convincing associations for reduced risk of CVD include consumption of fruits (including berries) and vegetables, fish and fish oils (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), foods high in linoleic acid and potassium, as well as physical activity and low to moderate alcohol intake. While vitamin E intake appears to have no relationship to risk of CVD, there is convincing evidence that myristic and palmitic acids, trans fatty acids, high sodium intake, overweight and high alcohol intake contribute to an increase in risk. A “probable” level of evidence demonstrates a decreased risk for a-linolenic acid, oleic acid, NSP, wholegrain cereals, nuts (unsalted), folate, plant sterols and stanols, and no relationship for stearic acid. There is a probable increase in risk from dietary cholesterol and unfiltered boiled coffee. Possible associations for reduced risk include intake of flavonoids and consumption of soy products, while possible associations for increased risk include fats rich in lauric acid, b-carotene supplements and impaired fetal nutrition. The evidence supporting these conclusions is summarized below.

Fatty acids and dietary cholesterol

The relationship between dietary fats and CVD, especially coronary heart disease, has been extensively investigated, with strong and consistent associations emerging from a wide body of evidence accrued from animal experiments, as well as observational studies, clinical trials and metabolic studies conducted in diverse human populations (2).

Saturated fatty acids raise total and low-density lipoprotein (LDL) cholesterol, but individual fatty acids within this group, have different effects (3-5). Myristic and palmitic acids have the greatest effect and are abundant in diets rich in dairy products and meat. Stearic acid has not been shown to elevate blood cholesterol and is rapidly converted to oleic acid in vivo. The most effective replacement for saturated fatty acids in terms of coronary heart disease outcome are polyunsaturated fatty acids, especially linoleic acid. This finding is supported by the results of several large randomized clinical trials, in which replacement of saturated and trans fatty acids by polyunsaturated vegetable oils lowered coronary heart disease risk (6).

Trans fatty acids are geometrical isomers of cis-unsaturated fatty acids that adapt a saturated fatty acid-like configuration. Partial hydrogenation, the process used to increase shelf-life of polyunsaturated fatty acids (PUFAs) creates trans fatty acids and also removes the critical double bonds in essential fatty acids necessary for the action. Metabolic studies have demonstrated that trans fatty acids render the plasma lipid profile even more atherogenic than saturated fatty acids, by not only elevating LDL cholesterol to similar levels but also by decreasing highdensity lipoprotein (HDL) cholesterol (7). Several large cohort studies have found that intake of trans fatty acids increases the risk of coronary heart disease (8, 9). Most trans fatty acids are contributed by industrially hardened oils. Even though trans fatty acids have been reduced or eliminated from retail fats and spreads in many parts of the world, deep-fried fast foods and baked goods are a major and increasing source (7).

When substituted for saturated fatty acids in metabolic studies, both monounsaturated fatty acids and n-6 polyunsaturated fatty acids lower plasma total and LDL cholesterol concentrations (10); PUFAs are somewhat more effective than monounsaturates in this respect. The only nutritionally important monounsaturated fatty acids is oleic acid, which is abundant in olive and canola oils and also in nuts. The most important polyunsaturated fatty acid is linoleic acid, which is abundant especially in soybean and sunflower oils. The most important n-3 PUFAs are eicosapentaenoic acid and docosahexaenoic acid found in fatty fish, and a-linolenic acid found in plant foods. The biological effects of n-3 PUFAs are wide ranging, involving lipids and lipoproteins, blood pressure, cardiac function, arterial compliance, endothelial function, vascular reactivity and cardiac electrophysiology, as well as potent antiplatelet and anti-inflammatory effects (11). The very long chain n-3 PUFAs (eicosapentaenoic acid and docosahexaenoic acid) powerfully lower serum triglycerides but they raise serum LDL cholesterol. Therefore, their effect on coronary heart disease is probably mediated through pathways other than serum cholesterol.

Most of the epidemiological evidence related to n-3 PUFAs is derived from studies of fish consumption in populations or interventions involving fish diets in clinical trials (evidence on fish consumption is discussed further below). Fish oils have been used in the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI) trial involving survivors of myocardial infarction (12). After 3.5 years of follow-up, the group that received fish oil had a 20% reduction in total mortality, a 30% reduction in cardiovascular death and a 45% decrease in sudden death. Several prospective studies have found an inverse association between the intake of a-linolenic acid, (high in flaxseed, canola and soybean oils), and risk of fatal coronary heart disease (13, 14).

Cholesterol in the blood and tissues is derived from two sources: diet and endogenous synthesis. Dairy fat and meat are major dietary sources. Egg yolk is particularly rich in cholesterol but unlike dairy products and meat does not provide saturated fatty acids. Although dietary cholesterol raises plasma cholesterol levels (15), observational evidence for an association of dietary cholesterol intake with CVD is contradictory (16). There is no requirement for dietary cholesterol and it is advisable to keep the intake as low as possible (2). If intake of dairy fat and meat are controlled, there is no need to severely restrict egg yolk intake, although some limitation remains prudent.

Dietary plant sterols, especially sitostanol, reduce serum cholesterol by inhibiting cholesterol absorption (17). The cholesterol-lowering effects of plant sterols has also been well documented (18) and commercial products made of these compounds are widely available, but their longterm effects remain to be seen.

NSP (dietary fibre)

Dietary fibre is a heterogeneous mixture of polysaccharides and lignin that cannot be degraded by the endogenous enzymes of vertebrate animals. Water-soluble fibres include pectins, gums, mucilages and some hemicelluloses. Insoluble fibres include cellulose and other hemicelluloses. Most fibres reduce plasma total and LDL cholesterol, as reported by several trials (19). Several large cohort studies carried out in different countries have reported that a high fibre diet as well as a diet high in wholegrain cereals lowers the risk of coronary heart disease (20-23).

Antioxidants, folate, and flavonoids

Even though antioxidants could, in theory, be protective against CVD and there is observational data supporting this theory, controlled trials employing supplements have been disappointing. The Heart Outcomes Prevention Evaluation trial (HOPE), a definitive clinical trial relating vitamin E supplementation to CVD outcomes, revealed no effect of vitamin E supplementation on myocardial infarction, stroke or death from cardiovascular causes in men or women(24). Also, the results of the Heart Protection Study indicated that no significant benefits of daily supplementation of vitamin E, vitamin C and b-carotene were observed among the high-risk individuals that were the subject of the study (25). In several studies where dietary vitamin C reduced the risk of coronary heart disease, supplemental vitamin C had little effect. Clinical trial evidence is lacking at present. Observational cohort studies have suggested a protective role for carotenoids but a meta-analysis of four randomized trials, in contrast, reported an increased risk of cardiovascular death (26).

The relationship of folate to CVD has been mostly explored through its effect on homocysteine, which may itself be an independent risk factor for coronary heart disease and probably also for stroke. Folic acid is required for the methylation of homocysteine to methionine. Reduced plasma folate has been strongly associated with elevated plasma homocysteine levels and folate supplementation has been demonstrated to decrease those levels (27). However, the role of homocysteine as an independent risk factor for CVD has been subject to much debate, since several prospective studies have not found this association to be independent of other risk factors (28, 29). It has also been suggested that elevation of plasma homocysteine is a consequence and not a cause of atherosclerosis, wherein impaired renal function resulting from atherosclerosis raises plasma homocysteine levels (30, 31). Data from the Nurses’ Health Study showed that folate and vitamin B6, from diet and supplements, conferred protection against coronary heart disease (32). A recently published metaanalysis concluded that a higher intake of folate (0.8 mg folic acid) would reduce the risk of ischaemic heart disease by 16% and stroke by 24% (33).

Flavonoids are polyphenolic compounds that occur in a variety of foods of vegetable origin, such as tea, onions and apples. Data from several prospective studies indicate an inverse association of dietary flavonoids with coronary heart disease (34, 35). However, confounding may be a major problem and may explain the conflicting results of observational studies.

Sodium and potassium

High blood pressure is a major risk factor for coronary heart disease and both forms of stroke (ischaemic and haemorrhagic). Of the many risk factors associated with high blood pressure, the dietary exposure that has been most investigated is daily sodium intake. It has been studied extensively in animal experimental models, in epidemiological studies, controlled clinical trials and in population studies on restricted sodium intake (36, 37).

All these data show convincingly that sodium intake is directly associated with blood pressure. An overview of observational data obtained from population studies suggested that a difference in sodium intake of 100 mmol per day was associated with average differences in systolic blood pressure of 5 mmHg at age 15-19 years and 10 mmHg at age 60-69 years (37). Diastolic blood pressures are reduced by about half as much, but the association increases with age and magnitude of the initial blood pressure. It was estimated that a universal reduction in dietary intake of sodium by 50 mmol per day would lead to a 50% reduction in the number of people requiring antihypertensive therapy, a 22% reduction in the number of deaths resulting from strokes and a16%reduction in the number of deaths from coronary heart disease. The first prospective study using 24-hour urine collections for measuring sodium intake, which is the only reliable measure, demonstrated a positive relationship between an increased risk of acute coronary events, but not stroke events, and increased sodium excretion (38). The association was strongest among overweight men.

Several clinical intervention trials, conducted to evaluate the effects of dietary salt reduction on blood pressure levels, have been systematically reviewed (39, 40). Based on an overview of 32 methodologically adequate trials, Cutler, Follmann & Allender (39) concluded that a daily reduction of sodium intake by 70-80 mmol was associated with a lowering of blood pressure both in hypertensive and normotensive individuals, with systolic and diastolic blood pressure reductions of 4.8/1.9 mmHg in the former and 2.5/1.1 mmHg in the latter. Clinical trials have also demonstrated the sustainable blood pressure lowering effects of sodium restriction in infancy (41, 42), as well as in the elderly in whom it provides a useful nonpharmacological therapy (43). The results of a low-sodium diet trial (44) showed that low-sodium diets, with 24-hour sodium excretion levels around 70 mmol, are effective and safe. Two population studies, in China and in Portugal, have also revealed significant reductions in blood pressure in the intervention groups (45, 46).

A meta-analysis of randomized controlled trials showed that potassium supplements reduced mean blood pressures (systolic/diastolic) by 1.8/1.0 mmHg in normotensive subjects and 4.4/2.5 mmHg in hypertensive subjects (47). Several large cohort studies have found an inverse association between potassium intake and risk of stroke (48, 49). While potassium supplements have been shown to have protective effects on blood pressure and cardiovascular diseases, there is no evidence to suggest that long-term potassium supplements should be administered to reduce the risk for CVD. The recommended levels of fruit and vegetable consumption assure an adequate intake of potassium.

Food items and food groups

While the consumption of fruits and vegetables has been widely believed to promote good health, evidence related to their protective effect against CVD has only been presented in recent years (50). Numerous ecological and prospective studies have reported a significant protective association for coronary heart disease and stroke with consumption of fruits and vegetables (50-53). The effects of increased fruit and vegetable consumption on blood pressure alone and in combination with a low-fat diet, were assessed in the Dietary Approaches to Stop Hypertension (DASH) trial (54). While the combination diet was more effective in lowering blood pressure, the fruit and vegetable diet also lowered blood pressure (by 2.8 mmHg systolic and 1.1 mmHg diastolic) in comparison to the control diet. Such reductions, while seeming modest at the individual level, would result in a substantial reduction in population-wide risk of CVD by shifting the blood pressure distribution.

Most, but not all, population studies have shown that fish consumption is associated with a reduced risk of coronary heart disease. A systematic review concluded that the discrepancy in the findings may be a result of differences in the populations studied, with only high-risk individuals benefiting from increasing their fish consumption (55). It was estimated that in high-risk populations, an optimum fish consumption of 40-60 g per day would lead to approximately a 50% reduction in death from coronary heart disease. In a diet and reinfarction trial, 2-year mortality was reduced by 29% in survivors of a first myocardial infarction in persons receiving advice to consume fatty fish at least twice a week (56). A recent study based on data from 36 countries, reported that fish consumption is associated with a reduced risk of death from all causes as well as CVD mortality (57).

Several large epidemiological studies have demonstrated that frequent consumption of nuts was associated with decreased risk of coronary heart disease (58, 59). Most of these studies considered nuts as a group, combining many different types of nuts. Nuts are high in unsaturated fatty acids and low in saturated fats, and contribute to cholesterol lowering by altering the fatty acid profile of the diet as a whole. However, because of the high energy content of nuts, advice to include them in the diet must be tempered in accordance with the desired energy balance.

Several trials indicate that soy has a beneficial effect on plasma lipids (60, 61). A composite analysis of 38 clinical trials found that an average consumption of 47 g of soy protein a day led to a 9% decline in total cholesterol and a 13% decline in LDL cholesterol in subjects free of coronary heart disease (62). Soy is rich in isoflavones, compounds that are structurally and functionally similar to estrogen. Several animal experiments suggest that the intake of these isoflavones may provide protection against coronary heart disease, but human data on efficacy and safety are still awaited.

There is convincing evidence that low to moderate alcohol consumption lowers the risk of coronary heart disease. In a systematic review of ecological, case-control and cohort studies in which specific associations were available between risk of coronary heart-disease and consumption of beer, wine and spirits, it was found that all alcoholic drinks are linked with lower risk (63). However, other cardiovascular and health risks associated with alcohol do not favour a general recommendation for its use.

Boiled, unfiltered coffee raises total and LDL cholesterol because coffee beans contain a terpenoid lipid called cafestol. The amount of cafestol in the cup depends on the brewing method: it is zero for paper-filtered drip coffee, and high in the unfiltered coffee still widely drunk in, for example, in Greece, the Middle East and Turkey. Intake of large amounts of unfiltered coffee markedly raises serum cholesterol and has been associated with coronary heart disease in Norway (64). A shift from unfiltered, boiled coffee to filtered coffee has contributed significantly to the decline in serum cholesterol in Finland (65).

5.4.5 Disease-specific recommendations

Measures aimed at reducing the risk of CVD are outlined below. The strength of evidence on lifestyle factors is summarized in Table 10.

Fats

Dietary intake of fats strongly influences the risk of cardiovascular diseases such as coronary heart disease and stroke, through effects on blood lipids, thrombosis, blood pressure, arterial (endothelial) function, arrythmogenesis and inflammation. However, the qualitative composition of fats in the diet has a significant role to play in modifying this risk.

Table 10. Summary of strength of evidence on lifestyle factors and risk of developing cardiovascular diseases

EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid; NSP, non-starch polysaccharides.

The evidence shows that intake of saturated fatty acids is directly related to cardiovascular risk. The traditional target is to restrict the intake of saturated fatty acids to less than 10%, of daily energy intake and less than 7% for high-risk groups. If populations are consuming less than 10%, they should not increase that level of intake. Within these limits, intake of foods rich in myristic and palmitic acids should be replaced by fats with a lower content of these particular fatty acids. In developing countries, however, where energy intake for some population groups may be inadequate, energy expenditure is high and body fat stores are low (BMI <18.5 kg/m2). The amount and quality of fat supply has to be considered keeping in mind the need to meet energy requirements. Specific sources of saturated fat, such as coconut and palm oil, provide low-cost energy and may be an important source of energy for the poor.

Not all saturated fats have similar metabolic effects; those with 12-16 carbons in the fatty acid chain have a greater effect on raising LDL cholesterol. This implies that the fatty acid composition of the fat source should be examined. As populations progress in the nutrition transition and energy excess becomes a potential problem, restricting certain fatty acids becomes progressively more relevant to ensuring cardiovascular health.

To promote cardiovascular health, diets should provide a very low intake of trans fatty acids (hydrogenated oils and fats). In practice, this implies an intake of less than 1% of daily energy intake. This recommendation is especially relevant in developing countries where low-cost hydrogenated fat is frequently consumed. The potential effect of human consumption of hydrogenated oils of unknown physiological effects (e.g. marine oils) is of great concern.

Diets should provide an adequate intake of PUFAs, i.e. in the range 6-10% of daily energy intake. There should also be an optimal balance between intake of n-6 PUFAs and n-3 PUFAs, i.e. 5-8% and 1-2% of daily energy intake, respectively.

Intake of oleic acid, a monounsaturated fatty acid, should make up the rest of the daily energy intake from fats, to give a daily total fat intake ranging from15%up to30%of daily energy intake. Recommendations for total fat intake may be based on current levels of population consumption in different regions and modified to take account of age, activity and ideal body weight. Where obesity is prevalent, for example, an intake in the lower part of the range is preferable in order to achieve a lower energy intake. While there is no evidence to directly link the quantity of daily fat intake to an increased risk of CVD, total fat consumption should be limited to enable the goals of reduced intake of saturated and trans fatty acids to be met easily in most populations and to avoid the potential problems of undesirable weight gain that may arise from unrestricted fat intake. It should be noted that highly active groups with diets rich in vegetables, legumes, fruits and wholegrain cereals will limit the risk of unhealthy weight gain on a diet comprising a total fat intake of up to 35%.

These dietary goals can be met by limiting the intake of fat from dairy and meat sources, avoiding the use of hydrogenated oils and fats in cooking and manufacture of food products, using appropriate edible vegetable oils in small amounts, and ensuring a regular intake of fish (one to two times per week) or plant sources of a-linolenic acid. Preference should be given to food preparation practices that employ non-frying methods.

Fruits and vegetables

Fruits and vegetables contribute to cardiovascular health through the variety of phytonutrients, potassium and fibre that they contain. Daily intake of fresh fruit and vegetables (including berries, green leafy and cruciferous vegetables and legumes), in an adequate quantity (400-500 g per day), is recommended to reduce the risk of coronary heart disease, stroke and high blood pressure.

Sodium

Dietary intake of sodium, from all sources, influences blood pressure levels in populations and should be limited so as to reduce the risk of coronary heart disease and both forms of stroke. Current evidence suggests that an intake of no more than 70 mmol or 1.7 g of sodium per day is beneficial in reducing blood pressure. The special situation of individuals (i.e. pregnant women and non-acclimated people who perform strenuous physical activity in hot environments) who may be adversely affected by sodium reduction needs to be kept in mind.

Limitation of dietary sodium intake to meet these goals should be achieved by restricting daily salt (sodium chloride) intake to less than 5 g per day. This should take into account total sodium intake from all dietary sources, for example additives such as monosodium glutamate and preservatives. Use of potassium-enriched low-sodium substitutes is one way to reduce sodium intake. The need to adjust salt iodization, depending on observed sodium intake and surveillance of iodine status of the population, should be recognized.

Potassium

Adequate dietary intake of potassium lowers blood pressure and is protective against stroke and cardiac arrythmias. Potassium intake should be at a level which will keep the sodium to potassium ratio close to 1.0, i.e. a daily potassium intake level of 70-80 mmol per day. This may be achieved through adequate daily consumption of fruits and vegetables.

NSP (dietary fibre)^[7]

Fibre is protective against coronary heart disease and has also been used in diets to lower blood pressure. Adequate intake may be achieved through fruits, vegetables and wholegrain cereals.

Fish

Regular fish consumption (1-2 servings per week) is protective against coronary heart disease and ischaemic stroke and is recommended. The serving should provide an equivalent of 200-500 mg of eicosapentaenoic and docosahexaenoic acid. People who are vegetarians are recommended to ensure adequate intake of plant sources of a-linolenic acid.

Alcohol

Although regular low to moderate consumption of alcohol is protective against coronary heart disease, other cardiovascular and health risks associated with alcohol do not favour a general recommendation for its use.

Physical activity

Physical activity is related to the risk of cardiovascular diseases, especially coronary heart disease, in a consistent inverse dose-response fashion when either volume or intensity are used for assessment. These relationships apply to both incidence and mortality rates from all cardiovascular diseases and from coronary heart disease. At present, no consistent dose-response relationship can be found between risk of stroke and physical activity. The lower limits of volume or intensity of the protective dose of physical activity have not been defined with certainty, but the current recommendation of at least 30 minutes of at least moderate-intensity physical activity on most days of the week is considered sufficient. A higher volume or intensity of activity would confer a greater protective effect. The recommended amount of physical activity is sufficient to raise cardiorespiratory fitness to the level that has been shown to be related to decreased risk of cardiovascular disease. Individuals who are unaccustomed to regular exercise or have a high-risk profile for CVD should avoid sudden and high-intensity bursts of physical activity.

References

1. Reddy KS. Cardiovascular diseases in the developing countries: dimensions, determinants, dynamics and directions for public health action. Public Health Nutrition, 2002, 5:231-237.

2. Kris-Etherton PM et al. Summary of the scientific conference on dietary fatty acids and cardiovascular health: conference summary from the nutrition committee of the American Heart Association. Circulation, 2001, 103:1034-1039.

3. Grundy SM, Vega GL. Plasma cholesterol responsiveness to saturated fatty acids. American Journal of Clinical Nutrition, 1988, 47:822-824.

4. Katan MJ, Zock PL, Mensink RP. Dietary oils, serum lipoproteins and coronary heart disease. American Journal of Clinical Nutrition, 1995, 61(Suppl. 6):1368-1373.

5. Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arteriosclerosis and Thrombosis, 1992, 12:911-919.

6. Hu FB et al. Dietary fat intake and the risk of coronary heart disease in women. New England Journal of Medicine, 1997, 337:1491-1499.

7. Katan MB. Trans fatty acids and plasma lipoproteins. Nutrition Reviews, 2000, 58:188-191.

8. Oomen CM et al. Association between trans fatty acid intake and 10-year risk of coronary heart disease in the Zutphen Elderly Study: a prospective population-based study. Lancet, 2001, 357:746-751.

9. Willett WC et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet, 1993, 341:581-585.

10. Kris-Etherton PM. Monosaturated fatty acids and risk of cardiovascular disease. Circulation, 1999, 100:1253-1258.

11. Mori TA, Beilin LJ. Long-chain omega 3 fatty acids, blood lipids and cardiovascular risk reduction. Current Opinion in Lipidology, 2001, 12:11-17.

12. GISSI-Prevenzione investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico. Lancet, 1999, 354:447-455.

13. Hu FB et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. American Journal of Clinical Nutrition, 1999, 69:890-897.

14. Ascherio A et al. Dietary fat and risk of coronary heart disease in men: cohort follow-up study in the United States. British Medical Journal, 1996, 313:84-90.

15. Hopkins PN. Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review. American Journal of Clinical Nutrition, 1992, 55:1060-1070.

16. Hu FB et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. Journal of the American Medical Association, 1999, 281:1387-1394.

17. Miettinen TA et al. Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population. New England Journal of Medicine, 1995, 333:1308-1312.

18. Law M. Plant sterols and stanol margarines and health. British Medical Journal, 2000, 320:861-864.

19. Anderson JW, Hanna TJ. Impact of nondigestible carbohydrates on serum lipoproteins and risk for cardiovascular disease. Journal of Nutrition, 1999, 129:1457-1466.

20. Truswell AS. Cereal grains and coronary heart disease. European Journal of Clinical Nutrition, 2002, 56:1-14.

21. Liu S et al. Whole-grain consumption and risk of coronary heart disease: results from the Nurses’ Health Study. American Journal of Clinical Nutrition, 1999, 70:412-419.

22. Pietinen P et al. Intake of dietary fiber and risk of coronary heart disease in a cohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Circulation, 1996, 94:2720-2727.

23. Rimm EB et al. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men. Journal of the American Medical Association, 1996, 275:447-451.

24. Yusuf S et al. Vitamin E supplementation and cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. New England Journal of Medicine, 2000, 342:154-160.

25. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20 536 high-risk individuals: a randomised placebo-controlled trial. Lancet, 2002, 360:23-33.

26. Egger M, Schneider M, Davey-Smith G. Spurious precision? Meta-analysis of observational studies. British Medical Journal, 1998, 316:140-144.

27. Brouwer IA et al. Low dose folic acid supplementation decreases plasma homocysteine concentrations: a randomized trial. American Journal of Clinical Nutrition, 1999, 69:99-104.

28. Ueland PM et al. The controversy over homocysteine and cardiovascular risk. American Journal of Clinical Nutrition, 2000, 72:324-332.

29. Nygard O et al. Total plasma homocysteine and cardiovascular risk profile. The Hordaland Homocysteine Study. Journal of the American Medical Association, 1995, 274:1526-1533.

30. Brattstrom L, Wilcken DEL. Homocysteine and cardiovascular disease: cause or effect? American Journal of Clinical Nutrition, 2000, 72:315-323.

31. Guttormsen AB et al. Kinetic basis of hyperhomocysteinemia in patients with chronic renal failure. Kidney International, 1997, 52:495-502.

32. Rimm EB et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. Journal of the American Medical Association, 1998, 279:359-364.

33. Wald DS, Law M, Morris JK. Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis. British Medical Journal, 325:1202-1208.

34. Keli SO et al. Dietary flavonoids, antioxidant vitamins, and incidence of stroke: the Zutphen study. Archives of Internal Medicine, 1996. 156:637-642.

35. Hertog MGL et al. Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly Study. Lancet, 1993, 342:1007-1011.

36. Gibbs CR, Lip GY, Beevers DG. Salt and cardiovascular disease: clinical and epidemiological evidence. Journal of Cardiovascular Risk, 2000, 7:9-13.

37. Law MR, Frost CD, Wald NJ. By how much does salt reduction lower blood pressure? III-Analysis of data from trials of salt reduction. British Medical Journal, 1991, 302:819-824.

38. Tuomilehto J et al. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet, 2001, 357:848-851.

39. Cutler JA, Follmann D, Allender PS. Randomized trials of sodium reduction: an overview. American Journal of Clinical Nutrition, 1997, 65:643-651.

40. Midgley JP et al. Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. Journal of the American Medical Association, 1996, 275:1590-1597.

41. Geleijnse JM et al. Long-term effects of neonatal sodium restriction on blood pressure. Hypertension, 1997, 29:913-917 (erratum appears in Hypertension, 1997, 29:1211).

42. Hofman A, Hazebroek A, Valkenburg HA. A randomized trial of sodium intake and blood pressure in newborn infants. Journal of the American Medical Association, 1983, 250:370-373.

43. Whelton PK et al. Sodium reduction and weight loss in the treatment of hypertension in older persons. Journal of the American Medical Association, 1998, 279:839-846 (erratum appears in Journal of the American Medical Association, 1998, 279:1954).

44. Sacks FM et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. New England Journal of Medicine, 20