5. Population Nutrient Intake Goals For Preventing Diet

5.1.1 Background



Population nutrient intake goals represent the people average intake that's judged to get consistent with the repair off health in the population. Health, on this context, is marked by the low prevalence of diet-related diseases in the population.



Seldom it is possible to single “best value” for such a goal. Instead, similar to the concept of a secure range of nutrient intakes for individuals, there exists often a array of population averages that would be in conjuction with the maintenance of health. If existing population averages fall outside this range, or trends in intake suggest that the populace average will move outside of the range, health issues are likely to arise. Sometimes there is certainly no lower limit; this implies that there is no evidence the nutrient is required within the diet so because of this low intakes must not give rise to concern. It would be of interest if a sizable proportion of values were outside of the defined goals.



5.1.2 Strength of evidence



Ideally the definition of a greater or a minimal risk needs to be based on a relationship that's been established by multiple randomized controlled trials of interventions on populations which can be representative of the objective of a recommendation, but this type of evidence is usually not available. The recommended dietary/nutrition practice should modify the attributable chance of the undesirable exposure for the reason that population.



The following criteria are employed to describe the effectiveness of evidence with this report. They are depending on the criteria utilised by the World Cancer Research Fund (1), but happen to be modified through the Expert Consultation to add 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 become taken into account in categorizing risks. This applies particularly for the complex interaction between environmental factors that affect unwanted weight gain, a risk factor that the Consultation acknowledged as contributing to many of the problems being considered.



Convincing evidence. Evidence depending on epidemiological studies showing consistent associations between exposure and disease, with little if any evidence for the contrary. The available evidence is based on a substantial quantity of studies including prospective observational studies and where relevant, randomized controlled trials of sufficient size, duration and quality showing consistent effects. The association must be biologically plausible.



Probable evidence. Evidence determined by epidemiological studies showing fairly consistent associations between exposure and disease, but high are perceived shortcomings in the available evidence or some evidence on the contrary, which precludes a much more definite judgement. Shortcomings within the evidence could be any from the following: insufficient duration of trials (or studies); insufficient trials (or studies) available; inadequate sample sizes; incomplete follow-up. Laboratory evidence is generally 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 can be obtained. Evidence determined by non-epidemiological studies, including clinical and laboratory investigations, is supportive. More trials have to support the tentative associations, which will also be biologically plausible.



Insufficient evidence. Evidence depending on findings of your few studies that are suggestive, but you are insufficient to establish an association between exposure and disease. Limited or no evidence can be acquired from randomized controlled trials. More attractive research is required to support the tentative associations.



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



5.1.3 A introduction to 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, for the reason that desirable change will be based upon existing intakes within the particular population, and might be in either direction.



In Table 6, attention is directed towards the energy-supplying macronutrients. This should not be taken to imply a lack or worry for the other nutrients. Rather, it is a recognition that previous reports issued by FAO and WHO have provided limited help with the meaning of the “balanced diet” described with regards to the proportions of the numerous energy sources, and that there's an apparent consensus with this aspect of diet in terms of effects for 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 must be given on the process for starting national dietary guidelines (5).



Table 6. Ranges of population nutrient intake goals



Dietary factor



Total fat



15 - 30%



5 - 8%



1 - 2%



Fruits and vegetables



From foodsf



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



b The area of total energy available after looking at that consumed as protein and fat, hence the big selection.



c The term “free sugars” is the term for all monosaccharides and disaccharides added to foods from the manufacturer, cook or consumer, plus sugars naturally seen in honey, syrups and fruit juices.



d The suggested range must be seen inside light with 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 ought to be iodized appropriately (6). The should adjust salt iodization, depending on observed sodium intake and surveillance of iodine status of the people, should be recognized.



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



Total fat



The strategies for total fat are formulated to add countries in which the usual fat intake is normally above 30% in addition to those the location where the usual intake may be very low, as an example less than 15%. Total fat energy with a minimum of 20% is consistent with good health. Highly active groups with diets abundant with vegetables, legumes, fruits and wholegrain cereals may, however, sustain a total fat intake all the way to 35% without the chance of unhealthy putting on weight.



For countries where the usual fat intake is between 15% and 20% of energy, there is no direct evidence for guys that raising fat intake to 20% is going to be beneficial (7, 8). For women of reproductive age at the very least 20% has become recommended through 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 significant energy without specific nutrients. The Consultation considered that restriction of free sugars has also been likely to give rise to reducing the chance of unhealthy putting on weight, noting that:



Free sugars contribute to the overall energy density of diets.



Free sugars promote an optimistic energy balance. Acute and short-term studies in human volunteers have demonstrated increased total energy intake if the energy density in the diet is increased, whether by free sugars or fat (9-11). Diets that are limited in free sugars are already shown to lessen 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 an compensatory lowering of food intake after the consumption of high-sugars drinks than when additional foods of equivalent energy content are given (11, 14-16). A recent randomized trial showed that when soft drinks abundant with free sugars are consumed there is certainly a higher energy intake along with a progressive increase in body weight when compared with energy-free drinks which can be artificially sweetened (17). Children with a high utilization of soft drinks rich in free sugars tend to be likely to be overweight and also to gain excess fat (16).



The Consultation recognized that the population goal free of charge sugars of lower than 10% of total energy is controversial. However, the Consultation considered that this studies showing no effect of free sugars on extra weight have limitations. The CARMEN study (Carbohydrate Ratio Management in European National diets) would be a multicentre, randomized trial that tested the consequences on weight and blood lipids in overweight individuals of altering precisely fat to carbohydrate, in addition to the ratio of all to easy to complex carbohydrate per se. A greater fat reduction was observed with the high complex carbohydrate diet relative on the simple carbohydrate one; the main difference, however was not statistically significant (18). Nevertheless, an analysis of weight change and metabolic indices for all those with metabolic syndrome revealed a clear benefit of replacing simple by complex carbohydrates (19). The Consultation also examined the final results of studies that found an inverse relationship between free sugars intakes and total fat intake. Many of the studies are methodologically inappropriate for determining the causes of unwanted weight gain, since the percentage of unhealthy calories will decrease as the number of calories from carbohydrates increases and the other way round. Furthermore, these analyses really don't distinguish between free sugars in foods and free sugars in drinks. Thus, these analyses are certainly not good predictors of the responses in energy intake to a selective decrease in free sugars intake.



Non-starch polysaccharides (NSP)



Wholegrain cereals, vegatables and fruits are the preferred reasons for non-starch polysaccharides (NSP). The best concise explaination dietary fibre remains to become established, in the potential health improvements of resistant starch. The recommended intake of vegetables and fruit (see below) and consumption of wholegrain foods is likely to provide >20 g every day of NSP (>25 g per day of total dietary fibre).



Fruits and vegetables



The good thing about fruits and vegetables is not ascribed to a single or mixture of nutrients and bioactive substances. Therefore, this food category was included instead of the nutrients themselves. The category of tubers (i.e. potatoes, cassava) must not be included in vegatables and fruits.



Body mass index (BMI)



The goal for body mass index (BMI) included with this report follows the advice made with the WHO Expert Consultation on Obesity that met in 1997 (20). At the people level, desire to is for a grown-up median BMI of 21-23 kg/m2. For individuals, the recommendations is to conserve a BMI in the range 18.5-24.9 kg/m2 and to avoid fat loss gain more than 5 kg during life.



Physical activity



The goal for exercise focuses on maintaining healthy weight. The recommendation is for a complete of one hour daily on most days in the week of moderate-intensity activity, including walking. This level of exercising is needed to conserve a healthy weight, particularly for people with sedentary occupations. The recommendation is based on calculations of their time balance as well as on an analysis of the extensive literature around the relationships between weight and physical activity. This recommendation can also be presented elsewhere (21). Obviously, this quantitative goal can't be considered as a single “best value” by analogy with the nutrient intake goals. Furthermore, it differs from the next widely accepted public health recommendation (22):



For better health, people of every age group should include a minimum of 30 minutes of exercising of moderate intensity (such as brisk walking) of many, if not completely, days of the week. For most people greater health advantages can be obtained by engaging in exercising of more vigorous intensity or of longer duration. This cardio respiratory endurance activity needs to be supplemented with strength-developing exercises a minimum of twice per week for adults in order to improve musculo skeletal health, maintain independence in performing the activities of everyday life and reduce the risk of falling.



The difference between the 2 recommendations results from the main difference in their focus. A recent symposium for the dose-response relationships between physical activity and health outcomes found evidence that half an hour of moderate activity is plenty for cardiovascular/metabolic health, however, not for all many benefits. Because prevention of obesity is really a central health goal, counsel of 60 minutes a day of moderate-intensity activity is regarded as appropriate. Activity of moderate intensity is found to be sufficient to get a preventive effect on most, if not completely, cardiovascular and metabolic diseases considered within this report. Higher intensity activity has a greater effect on some, however, not all, health outcomes, but is past the capacity and motivation of an large majority of the population.



Both recommendations range from the idea the daily activity could be accomplished in several short bouts. It is very important to explain that both recommendations apply to people who will be otherwise sedentary. Some occupational activities and household chores constitute sufficient daily physical exercise.



In recommending exercise, potential individual risks as well as benefits need to get assessed. In many regions of the world, especially although not exclusively in rural parts of developing countries, an appreciable proportion of people is still engaged in challenging activities associated with agricultural practices and domestic tasks performed without mechanization or with rudimentary tools. Even children may be required to undertake challenging tasks at very young ages, like collecting water and firewood and looking after livestock. Similarly, the inhabitants of poor cities may still be required to walk long distances to their jobs, that are usually of a manual nature and often require a high expenditure of their time. Clearly, the advice for extra physical exercise is not relevant because of these sectors of the population.



References



1. World Cancer Research Fund. Food, nutrition and also the prevention of cancer: a universal 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 your 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 the Joint FAO/WHO Expert Consultation. Rome, Food and Agriculture Organization from the United Nations, 1998 (FAO Food and Nutrition Paper, No. 66).



5. Preparation and make use of of food-based dietary guidelines. Report of an 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 also the etiology of heart 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 on 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 from 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 concerning obesity, diabetes, and coronary 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 in comparison with artificial sweeteners: different effects on ad libitum food consumption 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 adjustments to dietary carbohydrate/ fat ratio and simple vs complex carbohydrates on bodyweight 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 connection between ad libitum low-fat, high-carbohydrate diets on 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 your WHO Consultation. Geneva, World Health Organization, 2000 (WHO Technical Report Series, No. 894).



21. Weight control and exercise. 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 extra weight gain and obesity



5.2.1 Background



Almost all countries (high-income and low-income alike) get each year an obesity epidemic, although with great variation between and within countries. In low-income countries, obesity is a bit more common in middle-aged women, people of higher socioeconomic status and those living in urban communities. In more affluent countries, obesity just isn't only common within the middle-aged, but has become increasingly prevalent among younger adults and youngsters. Furthermore, it tends to get associated with lower socioeconomic status, particularly in women, and also the urban-rural differences are diminished as well as reversed.



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



5.2.2 Trends



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



5.2.3 Diet, physical exercise and unwanted 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 more than one comorbid conditions. In one study inside USA (3), over half (53%) of all deaths in ladies with a BMI>29 kg/m2 could possibly be directly attributed with 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 like sugar), the glycaemic index of foods, and fibre. Environmental issues are clearly important, especially as much environments become increasingly “obesogenic” (obesity-promoting).



Physical activity is an important determinant of bodyweight. In addition, exercising and physical fitness (which relates towards the ability to perform exercising) are crucial modifiers of mortality and morbidity linked to overweight and obesity. There is firm evidence that moderate to high fitness levels provide a substantially reduced probability of cardiovascular disease and all-cause mortality which these benefits sign up for all BMI levels. Furthermore, high fitness protects against mortality in any respect BMI levels in men with diabetes. Low cardiovascular fitness is often a serious and common comorbidity of obesity, as well as a sizeable proportion of deaths in overweight and obese populations are probably a response to low numbers of cardio-respiratory fitness rather than obesity per se. Fitness is, therefore, influenced strongly by exercise in addition to genetic factors. These relationships emphasize the role of physical activity in the prevention of overweight and obesity, independently from the effects of physical exercise on body mass.



The potential etiological factors related to being overweight gain are listed in Table 7.



5.2.4 Strength of evidence



Convincing etiological factors



Regular physical exercise (protective) and sedentary lifestyles (causative). There is convincing evidence that regular exercising is protective against unhealthy weight gain whereas sedentary lifestyles, particularly sedentary occupations and inactive recreation such as watching television, market it. Most epidemiological studies show smaller risk of weight gain, overweight and obesity among persons who currently engage regularly in moderate to huge amounts of physical exercise (4). Studies measuring physical exercise at baseline and randomized trials of exercise programmes show more mixed results, probably because of the low adherence to long-term changes. Therefore, it can be ongoing physical activity itself as opposed to previous exercise or enrolment in the exercise programme which is protective against unhealthy weight gain. The recommendation for folks to accumulate at least 30 minutes of moderate-intensity physical exercise on most days is basically aimed at reducing cardiovascular diseases and overall mortality. The amount required to prevent unhealthy weight gain is uncertain but may perhaps be significantly in excess of this. Preventing extra weight after substantial weight reduction probably requires about 60-90 minutes every day. Two meetings recommended by consensus that about 45-sixty minutes of moderate-intensity exercising is needed on most days or every single day to prevent being overweight gain (5, 6). Studies directed at reducing sedentary behaviours have focused mainly on reducing television viewing in youngsters. Reducing viewing times by about thirty minutes a day in children in the United States appears feasible and is related to reductions in BMI.



Table 7. Summary of strength of evidence on factors that could promote or protect against putting on weight and obesitya



Evidence



Sedentary lifestyles



Probable



Home and school environments that support appropriate food choices for childrend



Breastfeeding



High intake of sugars-sweetened sodas and juices



Adverse socioeconomic conditionsd (in developed countries, particularly for women)



Possible



Large helping sizes



High proportion of food prepared beyond your home (civilized world)



“Rigid restraint/periodic disinhibition” eating patterns



Insufficient



Alcohol



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



b Specific amounts will be based on the analytical methodologies utilized to measure fibre.



c Energy-dense and micronutrient-poor foods tend to get processed foods which might be high in fat and/or sugars. Low energy-dense (or energy-dilute) foods, including fruit, legumes, vegetables and whole fiber cereals, are loaded with 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 after a while, and many of the available studies used previous definitions, for example soluble and insoluble fibre. Nevertheless, two recent reviews of randomized trials have concluded the majority of studies show that an increased intake of NSP (dietary fibre) promotes weight reduction.



Pereira & Ludwig (7) found that 12 from 19 trials showed beneficial objective effects (including fat loss). In their review of 11 studies in excess of 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 your energy-dense foods promotes putting on weight. In high-income countries (and increasingly in low income countries) these energy-dense foods are certainly not only packaged (low NSP) and also micronutrient-poor, further diminishing their nutrients. Energy-dense foods tend to be high in fat (e.g. butter, oils, deep fried foods), sugars or starch, while energy-dilute foods have a higher water content (e.g. fruit and veggies). Several trials have covertly manipulated body fat content and the energy density of diets, the outcome of which offer the view that so-called “passive over consumption” of total energy occurs once the energy density with the diet is high understanding that this is usually the case in high-fat diets. A meta-analysis of 16 trials of ad libitum high-fat versus low-fat diets for at least 2 months duration suggested that a reduction in fat content by 10% corresponds to about a single MJ decrease in energy intake and about 3 kg in weight (9). At a population level, 3 kg equals about one BMI unit or with regards to a 5% difference in obesity prevalence. However, it's difficult to blind such studies and also other non-physiological effects may influence these findings (10). While energy from fat isn't more fattening compared to same amount of one's from carbohydrate or protein, diets which can be high in fat tend to get energy-dense. An important exception to this really is diets based predominantly on energy-dilute foods (e.g. vegetables, legumes, fruits) but who have a reasonably high percentage of your energy as fat from added oils.



The effectiveness over time of most dietary strategies for weight reduction, including low-fat diets, remains uncertain unless accompanied by changes in behaviour affecting physical exercise and food habits. These latter changes in a public health level require a breeding ground supportive of balanced diet and a dynamic life. High quality trials to handle these issues are urgently needed. A various popular weight-loss diets that restrict food choices may bring about reduced energy intake and short term weight-loss in individuals but most do not have trial proof of long-term effectiveness and nutritional adequacy and therefore can not be recommended for populations.



Probable etiological factors



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



Heavy marketing of fast-food outlets as well as-dense, micronutrient-poor foods and beverages (causative). Part in the consistent, strong relationships between television viewing and obesity in youngsters may relate on the food advertising this agreement they are exposed (13-15). Fast-food restaurants, and foods and beverages which can be usually classified within the “eat least” category in dietary guidelines are the most heavily marketed products, especially in the media. Young youngsters are often the mark group for your advertising of these products given that they have a significant influence for the foods bought by parents (16). The huge expenditure on marketing fast-foods and other “eat least” choices (US$ 11 billion within the United States alone in 1997) was considered to get a key factor inside the increased utilization of food prepared outside the home generally and of your energy-dense, micronutrient-poor foods particularly. Young children can't seem to distinguish programme content from the persuasive intent of advertisements. The evidence the heavy marketing of those foods and beverages to small children causes obesity just isn't unequivocal. Nevertheless, the Consultation considered that there is sufficient indirect evidence to warrant this practice being placed inside “probable” category thereby becoming a prospective target for interventions (15-18).



A high intake of sugars-sweetened beverages (causative). Diets which are proportionally lacking in fat will likely be proportionally higher in carbohydrate (including a variable level of sugars) and are associated with protection against being overweight gain, although an increased intake of free sugars in beverages probably promotes fat gain. The physiological effects of one's intake on satiation and satiety appear to be quite different for energy in solid foods rather than energy in fluids. Possibly as a result of reduced gastric distension and faster transit times, the energy contained in fluids is less well “detected” from the body and subsequent food intake is poorly adjusted to account for your 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 use of sugars-sweetened drinks by children in lots of countries is of significant concern. It may be estimated that each additional can or glass of sugars-sweetened drink which they consume daily increases the likelihood of becoming obese by 60% (19). Most from the evidence pertains to soda drinks but a majority of fruit drinks and cordials are equally energy-dense and might promote putting on weight if drunk large quantities. Overall, the evidence implicating an increased intake of sugars-sweetened drinks in promoting extra weight was considered moderately strong.



Adverse socioeconomic conditions, especially for women in high-income countries (causative). Classically the pattern of the progression of obesity by way of a population commences 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, starting a vicious circle (i.e. lower socioeconomic status promotes obesity, and obese everyone is more likely to end up in groups with low socioeconomic status). The mechanisms in which socioeconomic status influences food and activity patterns are usually multiple and need elucidation. However, people living in circumstances of low socioeconomic status might be more at the mercy with the obesogenic environment as their eating and activity behaviours tend to be more likely to get the “default choices” offered. The evidence for an impact of low socioeconomic status on predisposing visitors to obesity is consistent (in higher income countries) across a variety of cross-sectional and longitudinal studies (23), and was thus rated as a “probable” reason for increased probability of obesity.



Breastfeeding (protective). Breastfeeding like a protective factor against weight gain may be examined in at the very least 20 studies involving nearly 40 000 subjects. Five studies (including the 2 largest) found a protective effect, two found that breastfeeding predicted obesity, along with the remainder found no relationships. There are probably multiple results of confounding over these studies; however, the reduction within the risk of developing obesity observed in the two largest studies was substantial (20-37%). Promoting breastfeeding has many benefits, the prevention of obesity probably being one.



Possible etiological factors



Several additional factors were looked as “possible” protective or causative inside the etiology of being overweight gain.



Low-glycaemic foods happen to be proposed as a potential protective factor against fat gain and there are a handful of early studies that support this hypothesis. More clinical trials are, however, needed to establish the association with greater certainty.



Large the size of portions are a possible causative factor for being overweight gain (24). The marketing of “supersize” portions, especially in fast-food outlets, is now common practice in numerous countries. There is a evidence that people poorly estimate portion sizes and that subsequent energy compensation to get a large meal is incomplete and therefore is likely to cause overconsumption.



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



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



Several other factors were also considered but the evidence wasn't thought being strong enough to warrant defining them as protective or causative. Studies haven't shown consistent associations between alcohol intake and obesity inspite of the high energy density in the nutrient (7 kcal/g). There are probably many confounding factors that influence the association. While a top eating frequency may be shown in some studies to have a negative relationship with energy intake and extra weight, the types of foods readily available as goodies are often an excellent source of fat as well as a high utilization of foods of the type might predispose people to weight gain. The evidence regarding the impact of early nutrition on subsequent obesity can also be mixed, with a few studies showing relationships for high and low birth weights.



5.2.5 General approaches for obesity prevention



The prevention of obesity in infants and young children needs to be considered of high priority. For infants and small children, the principle preventive strategies are:



- the promotion of exclusive breastfeeding;



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



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



- assuring the correct micronutrient intake had to promote optimal linear growth.



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



- promote a dynamic lifestyle;



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



- restrict the intake of sugars-sweetened sodas.



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 supplying the necessary information and skills to make healthy food choices.



In developing countries, special attention needs to be given to avoidance of overfeeding stunted population groups. Nutrition programmes meant to control or prevent undernutrition need to assess stature along with weight to stop 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 given to mothers and low socioeconomic status communities which might be food insecure should stress that overweight and obesity usually do not represent 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, along with reduced exercise, are associated while using rising prevalence of obesity. Strategies are needed to improve the standard of diets by increasing consumption of fruits and vegetables, in addition to increasing physical exercise, as a way to stem the epidemic of obesity and associated diseases.



5.2.6 Disease-specific recommendations



Body mass index (BMI)



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



Table 8. Classification of overweight in adults as outlined by BMIa



Classification



Normal range



18.5 - 24.9



³40.0



Very severe



a These BMI values are age-independent along with the same for both sexes. However, BMI may not correspond on the same level of fatness in numerous populations due, to some extent, to differences in body proportions. The table shows a simplistic relationship between BMI and the likelihood of comorbidity, which can be affected by a range of factors, like the nature and the probability of comorbidity, which may be affected by way of a range of factors, like the nature with 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 terms of risk could differ for different populations. Both BMI along with a measure of fat distribution (waist circumference or waist: hip ratio (WHR)) are essential in calculating the chance of obesity comorbidities.



Source: reference 26.



In recent times, different ranges of BMI cut-off points for overweight and obesity are already proposed, in particular for that Asia-Pacific region (27). At present available data on which to base definitive recommendations are sparse. 4 Nevertheless, the consultation considered that, to realize optimum health, the median BMI to the adult population should be in the range 21-23 kg/m2, whilst the goal for those should be to keep BMI within the range 18.5-24.9 kg/m2.



Waist circumference



Waist circumference is a convenient as well as simple measure which can be unrelated to height, correlates closely with BMI and the ratio of waist-to-hip circumference, and it is an approximate index of intra-abdominal fat mass and total extra fat. Furthermore, alterations in waist circumference reflect changes in risk factors for cardiovascular disease and other kinds of chronic diseases, although risks appear to vary in several populations. There is a heightened risk of metabolic complications for men with a waist circumference ³ 102 cm, and women using a waist circumference ³ 88 cm.



Physical activity



A total of a single hour per day of moderate-intensity activity, for example walking on many days in the week, is most likely needed to conserve a healthy weight, particularly for people with sedentary occupations. 5



Total energy intake



The fat and water content of foods would be the main determinants with the energy density in the diet. A lower consumption of your energy-dense (i.e. high-fat, high-sugars and high-starch) foods as well as-dense (i.e. high free sugars) drinks contributes to a reduction altogether energy intake. Conversely, a greater intake of one's-dilute foods (i.e. fruit and veggies) and foods loaded with NSP (i.e. wholegrain cereals) contributes to a reduction in whole energy intake plus an improvement in micronutrient intake. It must be noted, however, that very active groups who've diets high in vegetables, legumes, fruits and wholegrain cereals, may sustain an overall total fat intake all the way to 35% without the probability 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 exercise prevent extra weight - a deliberate review. Obesity Reviews, 2000, 1:95-111.



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



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



7. Pereira MA, Ludwig DS. Dietary fiber and the 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 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 significant 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 with 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 consumption and 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 with the American Dietetic Association, 1999, 99:436-441.



22. Ludwig DS, Peterson KE, Gortmaker SL. Relation between use 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 whole 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 the size of portions, 1977-1998. Journal with the American Medical Association, 2003, 289:450-453.



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



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



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



5.3 Recommendations for preventing diabetes



5.3.1 Background



Type 2 diabetes, formerly generally known as non-insulin-dependent diabetes (NIDDM), accounts for most cases of diabetes worldwide. Type 2 diabetes develops if the production of insulin is insufficient to get over the underlying abnormality of increased effectiveness against its action. The early stages of type 2 diabetes are seen as overproduction of insulin. As the disease progresses, process insulin levels may fall as a direct result partial failure from the insulin producing b cells from the pancreas. Complications of diabetes include blindness, kidney failure, foot ulceration which may lead to gangrene and subsequent amputation, and appreciably increased probability 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 likelihood of developing the condition in addition to for energetic management of the established disease (1, 2).



Lifestyle modification could be the cornerstone of both treatment and tries to prevent diabetes (3). The changes necessary to reduce the probability of developing diabetes type 2 at the people level are, however, unlikely to be achieved without major environmental changes to facilitate appropriate choices by individuals. Criteria for the diagnosis of diabetes and for that 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 significantly less frequently and is linked to an absolute lack of insulin, usually due to autoimmune destruction from the b cells of the pancreas. Environmental as well as genetic factors appear to get involved but there's no convincing evidence of a role for lifestyle factors which might be modified to slow up the risk.



5.3.2 Trends



Although increases in both the prevalence and incidence of diabetes have occurred globally, they are actually especially dramatic in societies in economic transition in much with the newly industrialized world as well as 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, using the greatest variety 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, diabetes type 2 symptoms has recently escalated in every age groups and it is now being identified in younger and younger age brackets, including adolescents and youngsters, particularly in high-risk populations.



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



5.3.3 Diet, physical activity and diabetes



Type 2 diabetes is a result of an interaction between genetic and environmental factors. The rapidly changing incidence rates, however, suggest a particularly crucial role for your latter in addition to a prospect of stemming the tide of the global epidemic with the disease. The most dramatic increases in diabetes are occurring in societies through which there are already major changes in the type of diet consumed, reductions in physical exercise, and increases in overweight and obesity. The diets concerned are normally energy-dense, high in saturated fatty acids and depleted in NSP.



In all societies, overweight and obesity are associated with an increased risk of diabetes type 2 symptoms, especially in the event the excess adiposity is centrally distributed. Conventional (BMI) categories might not be an appropriate means of determining the likelihood of developing type 2 diabetes in individuals of most population groups as a consequence of ethnic differences in body composition and because from the importance with the distribution of excess adiposity. While all lifestyle-related and environmental factors which contribute to excess fat gain may be regarded as leading to type 2 diabetes, the data that individual dietary factors have an impact which is independent of their obesity promoting effect, is inconclusive. Evidence that saturated fat increase chance of type 2 diabetes which NSP are protective is a lot more convincing compared to evidence for many other nutrients which are already implicated. The presence of maternal diabetes, including gestational diabetes and intrauterine growth retardation, especially when linked to later rapid catch-up growth, appears to be increase the likelihood of subsequently developing diabetes.



5.3.4 Strength of evidence



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



Longitudinal research has clearly indicated that increased exercising reduces the risk of developing type 2 diabetes regardless with the degree of adiposity (24-26). Vigorous exercise (i.e. training for an intensity of 80-90% old-predicted maximum heartbeat for at the very least 20 minutes, a minimum of five times each week) has got the potential to substantially enhance insulin sensitivity (21). The minimum intensity and amount of physical activity required to improve insulin sensitivity will not be established.



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



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



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



Considered in aggregate these findings are deemed to point out a probable causal link between saturated fat and diabetes type 2, plus 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 relieve the chance of progression from impaired glucose tolerance to diabetes included advice to reduce total and saturated fats (22, 23), but both in trials it's impossible to disentangle the effects of individual dietary manipulation.



Research relating towards the association between NSP intake and type 2 diabetes is complicated by ambiguity with regard on the definitions used (the word dietary fibre and NSP will often be incorrectly used interchangeably), various methods of analysis and, consequently, inconsistencies in food composition tables. Observations by Trowell in Uganda more than three decades ago suggested the infrequency of diabetes in rural Africa could possibly be the result of a protective effect of substantial amounts of NSP inside diet (known as dietary fibre) associated with a high usage of minimally-processed or unprocessed carbohydrate. The author also hypothesized that throughout the planet, increasing intakes of highly-processed carbohydrate, depleted in NSP, had promoted the progression of diabetes (46). Three cohort studies (the Health Professionals Follow-up Study of males aged 40-75 years, the Nurses’ Health Study of ladies aged 40-65 years, and also the Iowa Women’s Health Study ladies aged 55-69 years) show a protective effect of NSP (dietary fibre) (47-49) which was separate from age, BMI, smoking and physical exercise. In many controlled experimental studies, high intakes of NSP (dietary fibre) have repeatedly been proven to result in reduced blood sugar levels and insulin levels in people with diabetes type 2 symptoms and impaired glucose tolerance (50). Moreover an elevated intake of wholegrain cereals, fruit and veggies (all abundant in NSP) was a feature with the diets connected with a reduced risk of progression of impaired glucose tolerance to type 2 diabetes within 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 declare that soluble varieties of NSP exert benefit (50-53) whereas the mark cohort studies claim that it is the cereal-derived insoluble forms that are protective (47, 48) explain the “probable” rather “convincing” grading with the level of evidence.



Many foods that are rich in NSP (especially soluble forms), including pulses, use a low glycaemic index. 6 Other carbohydrate-containing foods (e.g. some kinds of pasta), which can be not especially full of NSP, also use a low glycaemic index. Low glycaemic index foods, in spite of their NSP content, are certainly not only connected with a reduced glycaemic response after ingestion when compared to foods of upper glycaemic index, but they are also linked to an overall improvement in glycaemic control (as measured by haemoglobin A1c) in people who have diabetes (54-57). A low glycaemic index won't, however, per se, confer overall health advantages, since a top fat or fructose content of a food may also result in a very reduced glycaemic index and such foods may even be energy-dense. Thus while this property of carbohydrate-containing foods may well influence the risk of developing diabetes type 2 symptoms, the evidence is accorded a lower amount of strength than the evidence relating to the NSP content. Similarly, the degree of evidence for that protective effect of n-3 fat is regarded as “possible” because the final results of epidemiological studies are inconsistent and the experimental data inconclusive. There is insufficient evidence to make sure that or refute the suggestions that chromium, magnesium, vitamin E and moderate intakes of alcohol might protect against the development of diabetes type 2.



A quantity of studies, mostly in developing countries, have suggested that intrauterine growth retardation and low birth weight are associated with subsequent progression of insulin resistance (58). In those countries where there has become chronic undernutrition, insulin resistance may have been selectively advantageous regarding surviving famine. In populations where energy intake has risen and lifestyles have be sedentary, however, insulin resistance along with the consequent probability of type 2 diabetes are actually enhanced. In particular, rapid postnatal catch-up growth appears to be further increase the probability of type 2 diabetes in later life. Appropriate strategies which may help to reduce diabetes risk in this situation include enhancing the nutrition of small children, promoting linear growth and preventing energy excess by limiting intake of your energy-dense foods, controlling the caliber of fat supply, and facilitating physical exercise. At a population level, fetal growth may remain restricted until maternal height improves. This may take several generations to improve. The prevention of diabetes type 2 in infants and young children could possibly be facilitated through 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 likelihood of developing diabetes type 2



Evidence



Physical activity



1 NSP, non-starch polysaccharides.



a Includes gestational diabetes.



b As a worldwide public health recommendation, infants must be exclusively breastfed for the first few months of life to accomplish optimal growth, development and health (59).



5.3.5 Disease-specific recommendations



Measures targeted at reducing overweight and obesity, and cardiovascular disease will certainly also reduce the probability of developing diabetes type 2 symptoms and its complications. Some measures are particularly relevant to lowering the risk for diabetes; these are generally listed below:



Prevention/treatments for overweight and obesity, particularly in highrisk groups.



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



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



Practising an endurance activity at moderate or greater degree of intensity (e.g. brisk walking) for one hour or more each day on most days weekly.



Ensuring that fats intake won't exceed 10% of total energy as well as high-risk groups, fat intake needs to be <7% of total energy.



Achieving adequate intakes of NSP through regular use of wholegrain cereals, legumes, vegetables and fruit. A minimum daily intake of 20 g is usually 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 particular complications: estimates and projections on 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 around the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care, 1997, 20:1183-1197.



5. Definition, diagnosis and classification of diabetes mellitus and it is 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 with the American Medical Association, 2001, 286:1195-1200.



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



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



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



13. Morrish et al. Mortality to cause of death inside 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 results in 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 like a risk factor for clinical diabetes in females. 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 males. Diabetes Care, 1994, 17:961-969.



19. Boyko EJ et al. Visceral adiposity and likelihood 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 changes in lifestyle are necessary to improve insulin sensitivity. Diabetes Care, 2002, 25:445-452.



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



23. Knowler WC et al. Reduction inside incidence of diabetes type 2 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 from the American Medical Association, 1992, 268:63-67.



25. Kriska AM et al. The association of exercising 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 experience of diabetes conveys risks for type 2 diabetes and obesity: a report 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 in 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 fat 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 with the serum cholesterol esters. Diabetes, 1994, 43:1353-1357.



36. Salmeron J et al. Dietary fat intake and likelihood of type 2 diabetes in ladies. 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 younger ladies. 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 very Swedish diet: effects on serum lipoprotein metabolic process 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 some 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 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 with the etiology of diabetes mellitus. Diabetes, 1975, 24:762-765.



47. Salmeron J et al. Dietary fiber, glycemic load and likelihood 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 in the American Medical Association, 1997, 277:472-477.



49. Meyer KA et al. Carbohydrates, soluble 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 facets 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 connection between high fibers intake in patients with diabetes type 2 mellitus. New England Journal of Medicine, 2000, 342:1392-1398.



54. Frost G, Wilding J, Beecham J. Dietary advice using 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-list foods improve long-term glycemic control in NIDDM. Diabetes Care, 1991, 14:95-101.



56. Fontvieille AM et al. The using 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 the low glycaemic index diet in diabetes type 2. Diabetic Medicine, 1992, 9:451-458.



58. Stern MP et al. Birth weight along with 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 with the 20th century has witnessed major shifts in the pattern of disease, together with marked improvements in life expectancy, this period is seen as an profound adjustments to diet and lifestyles which subsequently have contributed for an epidemic of noncommunicable diseases. This epidemic is emerging, as well as 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 with the nutrition transition and the concomitant rise in the prevalence of cardiovascular diseases is going to be to widen the mismatch between health care needs and resources, and already scarce resources will likely be stretched a lot more thinly. Because unbalanced diets, obesity and physical inactivity all bring about heart disease, addressing these, in addition to tobacco use, will help stem the epidemic. A large measure of success with this area has already been demonstrated in lots of industrialized countries.



5.4.2 Trends



Cardiovascular diseases include the major contributor towards the global burden of disease among the noncommunicable diseases. WHO currently attributes one-third coming from all global deaths (15.3 million) to CVD, with developing countries, low-income and middle-income countries making up 86% in the DALYs lost to CVD globally in 1998. In the next twenty years the increasing burden of CVD will probably be borne mostly by developing countries.



5.4.3 Diet, exercising and heart problems



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



5.4.4 Strength of evidence



Convincing associations for reduced probability of CVD include use of fruits (including berries) and vegetables, fish and fish oils (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), foods high in linoleic acid and potassium, in addition to physical activity and low to moderate alcohol intake. While vitamin E intake seems to have no relationship to chance of CVD, there's convincing evidence that myristic and palmitic acids, trans fatty acids, high sodium intake, overweight and high alcohol intake contribute to an surge in risk. A “probable” amount of evidence demonstrates a decreased risk for any-linolenic acid, oleic acid, NSP, wholegrain cereals, nuts (unsalted), folate, plant sterols and stanols, no relationship for stearic acid. There can be a probable rise 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 abundant with 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 heart disease, has been extensively investigated, with strong and consistent associations emerging from a wide body of evidence accrued from animal experiments, along with observational studies, many studies and metabolic studies conducted in diverse human populations (2).



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



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



When substituted for saturated fat in metabolic studies, both monounsaturated fatty acids and n-6 polyunsaturated efas lower plasma total and LDL cholesterol concentrations (10); PUFAs are somewhat more efficient than monounsaturates with this respect. The only nutritionally important monounsaturated efas is oleic acid, which can be abundant in olive and canola oils and in addition in nuts. The most important polyunsaturated fatty acid is linoleic acid, that's abundant specially in soybean and sunflower oils. The most important n-3 PUFAs are eicosapentaenoic acid and docosahexaenoic acid present in fatty fish, and a-linolenic acid within plant foods. The biological outcomes of n-3 PUFAs are wide ranging, involving lipids and lipoproteins, hypertension, cardiac function, arterial compliance, endothelial function, vascular reactivity and cardiac electrophysiology, in addition to 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 impact on coronary heart disease is probably mediated through pathways apart from serum cholesterol.



Most in the epidemiological evidence associated with n-3 PUFAs is derived from studies of fish consumption in populations or interventions involving fish diets in many studies (evidence on fish consumption is discussed further below). Fish oils are actually used in the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI) trial involving survivors of myocardial infarction (12). After 3.several years of follow-up, the group that received omega3 had a 20% reduction in total mortality, a 30% decrease in cardiovascular death along with a 45% decrease in sudden death. Several prospective research has found an inverse association between your intake of your-linolenic acid, (loaded with flaxseed, canola and soybean oils), and chance of fatal cardiovascular disease (13, 14).



Cholesterol within the blood and tissues hails 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 doesn't provide saturated fat. Although dietary cholesterol raises plasma levels of cholesterol (15), observational evidence for an association of dietary cholesterol intake with CVD is contradictory (16). There is not any requirement for dietary cholesterol and it's advisable to maintain the intake to a minimum (2). If intake of dairy fat and meat are controlled, there exists no need to severely restrict egg yolk intake, even though some limitation remains prudent.



Dietary plant sterols, especially sitostanol, reduce serum cholesterol by inhibiting cholesterol absorption (17). The cholesterol-lowering connection between plant sterols been specifically well documented (18) and commercial products made of those compounds are widely available, on the other hand longterm effects remain to become seen.



NSP (dietary fibre)



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



Antioxidants, folate, and flavonoids



Even though antioxidants could, in theory, be protective against CVD and there's observational data supporting this theory, controlled trials employing supplements happen to be disappointing. The Heart Outcomes Prevention Evaluation trial (HOPE), a definitive medical 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 outcomes of the Heart Protection Study indicated that no significant great things about daily supplementation of vitamin E, vitamin C and b-carotene were observed one of many high-risk people who were the subject from the study (25). In several studies where dietary vitamin C reduced the probability of coronary heart problems, supplemental vitamin C had little effect. Clinical trial evidence is lacking at the moment. Observational cohort research has suggested a protective role for carotenoids but a meta-analysis of four years old randomized trials, in comparison, reported a greater risk of cardiovascular death (26).



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



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



Sodium and potassium



High blood pressure is a major risk factor for cardiovascular disease and both types of stroke (ischaemic and haemorrhagic). Of the many risk factors related to high blood pressure levels, the dietary exposure which has been most investigated is daily sodium intake. It continues to be studied extensively in animal experimental models, in epidemiological studies, controlled many studies and in population studies on restricted sodium intake (36, 37).



All these data show convincingly that sodium intake is directly related to blood pressure. An overview of observational data purchased from population studies suggested a difference in sodium intake of 100 mmol daily was related to average differences in systolic blood pressure of 5 mmHg at 15-19 a few years 10 mmHg at 60-69 years (37). Diastolic blood pressures are reduced by about 50 % as much, though the association increases as they age and magnitude in the initial hypertension. It was estimated which a universal decrease in dietary intake of sodium by 50 mmol every day would lead to a 50% reduction in the number of men and women requiring antihypertensive therapy, a 22% reduction inside number of deaths as a result of strokes and a16%reduction in the number of deaths from cardiovascular disease. The first prospective study using 24-hour urine collections for measuring sodium intake, that's the only reliable measure, demonstrated an optimistic relationship between an increased risk of acute coronary events, however, 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 level levels, happen to be systematically reviewed (39, 40). Based on an introduction to 32 methodologically adequate trials, Cutler, Follmann & Allender (39) concluded that a daily reduction of sodium intake by 70-80 mmol was linked to a lowering of blood pressure levels both in hypertensive and normotensive individuals, with systolic and diastolic blood pressure levels reductions of 4.8/1.9 mmHg in the former and two.5/1.1 mmHg inside the latter. Clinical trials in addition have demonstrated the sustainable blood pressure levels lowering connection between sodium restriction in infancy (41, 42), as well as inside the elderly in whom it possesses a useful nonpharmacological therapy (43). The results of an low-sodium diet trial (44) demonstrated that low-sodium diets, with 24-hour sodium excretion levels around 70 mmol, are impressive and safe. Two population studies, in China along with Portugal, have revealed significant reductions in blood pressure inside the intervention groups (45, 46).



A meta-analysis of randomized controlled trials indicated 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 numerous studies have found an inverse association between potassium intake and probability of stroke (48, 49). While potassium supplements are actually shown to own protective effects on blood pressure levels and cardiovascular diseases, there is certainly no evidence to suggest that long-term potassium supplements must be administered to slow up the risk for CVD. The recommended degrees of fruit and vegetable consumption assure an adequate intake of potassium.



Food items and food groups



While the consumption of fruits and vegetables continues to be widely shown to promote health, evidence related on their protective effect against CVD has only been presented in modern times (50). Numerous ecological and prospective numerous studies have reported a tremendous protective association for heart disease and stroke with utilization of fruits and vegetables (50-53). The effects of increased fruit and vegetable consumption on hypertension alone as well as in combination with a low-fat diet, were assessed within the Dietary Approaches to Stop Hypertension (DASH) trial (54). While the combination diet was more efficient in lowering hypertension, the fruit and vegetable diet also lowered hypertension (by 2.8 mmHg systolic and 1.1 mmHg diastolic) in comparison towards the control diet. Such reductions, while seeming modest with the individual level, would result in the substantial decline in population-wide chance of CVD by shifting the blood pressure level distribution.



Most, but not all, population studies demonstrate that fish consumption is linked to a reduced likelihood of coronary heart disease. A systematic review concluded that this discrepancy inside findings may be a results of differences inside 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 usage of 40-60 g per day would result in approximately a 50% lowering of death from cardiovascular disease. In dieting and reinfarction trial, 2-year mortality was reduced by 29% in survivors of an first myocardial infarction in persons receiving advice to consume fatty fish no less than twice every week (56). A recent study based on data from 36 countries, reported that fish consumption is related to a reduced chance of death from all causes along with CVD mortality (57).



Several large epidemiological reports have demonstrated that frequent consumption of nuts was related to decreased chance of coronary cardiovascular disease (58, 59). Most of the studies considered nuts like a group, combining various sorts of nuts. Nuts are an excellent source of unsaturated essential fatty acids and low in saturated fats, and contribute to cholesterol lowering by altering the fatty acid profile in the diet being a whole. However, because of the high energy content of nuts, advice to feature them within the diet should be tempered in accordance with the desired energy balance.



Several trials indicate that soy carries a beneficial effect on plasma lipids (60, 61). A composite analysis of 38 clinical trials discovered that an average consumption of 47 g of soy protein each day led to your 9% decline in whole cholesterol as well as a 13% decline in LDL cholesterol in subjects free of cardiovascular disease (62). Soy is abundant with isoflavones, compounds that are structurally and functionally much like estrogen. Several animal experiments claim that the intake of the isoflavones may shield you against cardiovascular disease, but human data on efficacy and safety remain awaited.



There is convincing evidence that low to moderate having a drink lowers the risk of coronary cardiovascular disease. In a systematic report on ecological, case-control and cohort studies in which specific associations were available between probability of coronary heart-disease and usage of beer, wine and spirits, it was discovered that all alcoholic drinks are associated with lower risk (63). However, other cardiovascular and health risks linked to alcohol tend not to favour an over-all recommendation for the use.



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



5.4.5 Disease-specific recommendations



Measures geared towards reducing the probability 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 probability of cardiovascular diseases including coronary coronary disease and stroke, through effects on blood lipids, thrombosis, blood pressure levels, arterial (endothelial) function, arrythmogenesis and inflammation. However, the qualitative composition of fats within the diet includes a significant role to learn in modifying this risk.



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



Evidence



Vegetables and fruits (including berries)



Potassium



Vitamin E supplements



Probable



Impaired fetal nutrition



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



The evidence implies that intake of saturated fatty acids is directly related to cardiovascular risk. The traditional target would be to restrict the intake of saturated fat to under 10%, of daily energy intake and lower than 7% for high-risk groups. If populations are consuming lower than 10%, they shouldn't increase that a higher level intake. Within these limits, intake of foods abundant in myristic and palmitic acids ought to be replaced by fats with a lower content of the particular essential fatty acids. In developing countries, however, where energy intake for many population groups could possibly be inadequate, energy expenditure is high and body fat stores are low (BMI <18.5 kg/m2). The amount superiority fat supply has to become considered keeping in mind the requirement to meet energy requirements. Specific reasons for saturated fat, including coconut and palm oil, provide low-cost energy and could possibly be an important method to obtain energy for that poor.



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



To promote cardiovascular health, diets should provide a very low intake of trans fat (hydrogenated oils and fats). In practice, what this means is an intake of lower than 1% of daily energy intake. This recommendation is very relevant in developing countries where low-cost hydrogenated fat is generally consumed. The potential effect of human use of hydrogenated oils of unknown physiological effects (e.g. marine oils) is of deep concern.



Diets should provide an adequate intake of PUFAs, i.e. within the range 6-10% of daily energy intake. There should be also 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 form the rest of the daily energy intake from fats, to give an everyday total fat intake ranging from15%up to30%of daily energy intake. Recommendations for total fat intake may be depending on current degrees of population consumption in numerous regions and modified to consider account of age, activity and ideal bodyweight. Where obesity is prevalent, for instance, an intake within the lower part with the range is preferable in order to achieve a lower energy intake. While there's no evidence to directly link the amount of daily fat intake to an elevated risk of CVD, total fat consumption should be limited to enable the goals of reduced intake of saturated and trans fatty acids to get met easily in many populations also to avoid the possible problems of undesirable extra weight that may arise from unrestricted fat intake. It ought to be noted that highly active groups with diets full of vegetables, legumes, fruits and wholegrain cereals will limit the probability of unhealthy weight gain on an eating plan comprising an overall total fat intake all the way to 35%.



These dietary goals may be met by limiting the intake of fat from dairy and meat sources, avoiding the usage of hydrogenated oils and fats in cooking and manufacture of food products, using appropriate edible vegetable oils in a small amount, and ensuring a regular intake of fish (1 or 2 times per week) or plant sources of the-linolenic acid. Preference must be given to preparing food practices that employ non-frying methods.



Fruits and vegetables



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



Sodium



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



Limitation of dietary sodium intake to meet these goals needs to be achieved by restricting daily salt (sodium chloride) intake to lower than 5 g each day. This should consider total sodium intake all dietary sources, as an example additives such as monosodium glutamate and preservatives. Use of potassium-enriched low-sodium substitutes is one way to cut back sodium intake. The should adjust salt iodization, depending on observed sodium intake and surveillance of iodine status of the population, ought to be recognized.



Potassium



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



NSP (dietary fibre) 7



Fibre is protective against cardiovascular 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 which is recommended. The serving usually supplies 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 utilization of alcohol is protective against cardiovascular disease, other cardiovascular and health risks connected with alcohol do not favour an overall recommendation due to the use.



Physical activity



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



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5.5 Recommendations for preventing cancer



5.5.1 Background



Cancer is caused by the variety of identified and unidentified factors. The most important established source of cancer is tobacco smoking. Other important determinants of cancer risk include diet, alcohol and exercising, infections, hormonal factors and radiation. The relative importance of cancers being a cause of death is increasing, mostly because from the increasing proportion of those who are old, as well as in part as a consequence of reductions in mortality from some other causes, especially infectious diseases. The incidence of cancers with the lung, colon and rectum, breast and prostate generally increases in parallel with economic development, as the incidence of stomach cancer usually declines with development.



5.5.2 Trends



Cancer is now an important cause of mortality throughout the planet and, within the developed world, is normally exceeded only by cardiovascular diseases. An estimated ten million new cases well as over 6 million deaths from cancer took place 2000 (1). As developing countries become urbanized, patterns of cancer, including those most strongly connected with diet, often shift towards that regarding economically developed countries. Between 2000 and 2020, the total number of cases of cancer inside the developing world is predicted to improve by 73% and, inside developed world, to improve by 29%, largely as a consequence of an increase inside the number of old people (1).



5.5.3 Diet, exercise and cancer



Dietary factors are estimated to account for approximately 30% of cancers in industrialized countries (2), making diet second and then tobacco as being a theoretically preventable reason behind cancer. This proportion is thought to get about 20% in developing countries (3), but may grow with dietary change, particularly if the importance of other causes, especially infections, declines. Cancer rates change as populations move between countries and adopt different dietary (and also other) behaviours, further implicating dietary factors within the etiology of cancer.



Body weight and physical inactivity together are estimated to take into account approximately one-fifth to one-third of several in the most common cancers, specifically cancers from the breast (postmenopausal), colon, endometrium, kidney and oesophagus (adenocarcinoma) (4).



5.5.4 Strength of evidence



Research to date has uncovered few definite relationships between diet and cancer risk. Dietary factors for which there is certainly convincing evidence for an surge in risk are overweight and obesity, plus a high consumption of alcoholic beverages, aflatoxins, and some kinds of salting and fermenting fish. There is additionally convincing evidence to point out that exercise decreases the probability of colon cancer. Factors which probably increase risk include high dietary intake of preserved meats, salt-preserved foods and salt, and intensely hot (thermally) drinks and food. Probable protective factors are usage of fruits and vegetables, and physical exercise (for breast cancers). After tobacco, overweight and obesity appear to get the most important known avoidable reasons behind cancer.



The role of diet inside the etiology of the major cancers



Cancers with the oral cavity, pharynx and oesophagus. In western world the main risk factors for cancers with the oral cavity, pharynx and oesophagus are alcohol and tobacco, or more to 75% of which cancers are due to these two lifestyle factors (5). Overweight and obesity have established yourself risk factors designed for adenocarcinoma (however, not squamous cell carcinoma) with the oesophagus (6-8). In developing countries, around 60% of cancers from the oral cavity, pharynx and oesophagus are thought being a results of micronutrient deficiencies related to your restricted diet that is certainly low in vegatables and fruits and animal products (5, 9). The relative roles of assorted micronutrients usually are not yet clear (5, 9). There can also be consistent evidence that consuming drinks and foods at the very high temperature increases the risk of these cancers (10). Nasopharyngeal cancer is specially common in South-East Asia (11), and has been clearly associated with a high intake of Chinese-style salted fish, especially during early childhood (12, 13), in addition to with infection using the Epstein-Barr virus (2).



Stomach cancer. Until about 20 years ago stomach cancer was the most common cancer within the world, but mortality rates are already falling in all of the industrialized countries (14) and stomach cancer happens to be much more prevalent in Asia than in North America or Europe (11). Infection with all the bacterium Helicobacter pylori can be an established risk factor, and not a sufficient cause, for your development of stomach cancer (15). Diet is thought being important within the etiology of this disease; substantial evidence shows that risk is increased by high intakes of some traditionally preserved salted foods, especially meats and pickles, sufficient reason for salt per se, and that risk is decreased by high intakes of vegetables and fruit (16), perhaps as a consequence of their vitamin C content. Further prospective data are needed, especially to examine whether some with the dietary associations could be partly confounded by Helicobacter pylori infection and whether dietary factors may modify the association of Helicobacter pylori with risk.



Colorectal cancer. Colorectal cancer incidence rates are approximately ten-fold higher in developed compared to developing countries (11), and it may be suggested that diet-related factors mayaccount for up to80%in the differences in rates between countries (17). The best established diet-related risk factor is overweight/obesity (8) and physical activity has been consistently related to a reduced risk of colon cancer (although not of rectal cancer) (8, 18). These factors together, however, don't explain the massive variation between populations in colorectal cancer rates. There is almost universal agreement that some aspects of the “westernized” diet are an important determinant of risk; as an example, there is some evidence that risk is increased by high intakes of meat and fat, knowning that risk is decreased by high intakes of fruits and vegetables, dietary fibre, folate and calcium, but none of these hypotheses may be firmly established.



International correlation studies show a strong association between per capita utilization of meat and colorectal cancer mortality (19), as well as a recent systematic review concluded that preserved meat is associated with a greater risk for colorectal cancer but that fresh meat is just not (20). However, most reports have not observed positive associations with poultry or fish (9). Overall, the data suggests that high use of preserved and steak probably enhances the risk for colorectal cancer.



As with meat, international correlation studies show a strong association between per capita consumption of fat and colorectal cancer mortality (19). However, the outcomes of observational studies of fat and colorectal cancer have, overall, not been supportive of a connection with fat intake (9, 21).



Many case-control numerous studies have observed a weak association between the likelihood of colorectal cancer and high use of fruits and vegetables and/or dietary fibre (22, 23), but the final results of recent large prospective studies are already inconsistent (24-26). Furthermore, results from randomized controlled trials have not shown that intervention more than a 3-4 year period with supplemental fibre or even a diet lower in fat and high in fibre and fruits and vegetables can lessen the recurrence of colorectal adenomas (27-29). It is likely that some in the inconsistencies are a result of differences between studies in the types of fibre eaten and inside methods for classifying fibre in food tables, or how the association with fruit and veggies arises principally from an surge in risk at very low numbers of consumption (30). On balance, the evidence that is certainly currently available shows that intake of fruit and veggies probably reduces the risk for colorectal cancer.



Recent research has suggested that vitamins and minerals might influence the chance for colorectal cancer. Some prospective numerous studies have suggested that a high intake of folate from diet or nutritional vitamin supplements is linked to a reduced risk for colon cancer (31-33). Another promising hypothesis is that relatively high intakes of calcium may slow up the risk for colorectal cancer; several observational research has supported this hypothesis (9, 34), and a couple trials have indicated that supplemental calcium may possess a modest protective effect about the recurrence of colorectal adenomas (29, 35).



Liver cancer. Approximately 75% of cases of liver cancer exist in developing countries, and liver cancer rates vary over 20-fold between countries, being much higher in sub-Saharan Africa and South-East Asia than in North America and Europe (11). The major risk factor for hepatocellular carcinoma, the primary type of liver cancer, is chronic infection with hepatitis B, also to a lesser extent, hepatitis C virus (36). Ingestion of foods contaminated while using mycotoxin, aflatoxin is a crucial risk factor among people in developing countries, along with active hepatitis virus infection (13, 37). Excessive consumption of alcohol is the key diet-related risk factor for liver cancer in industrialized countries, probably via the growth and development of cirrhosis and alcoholic hepatitis (5).



Pancreatic cancer. Cancer with the pancreas is much more common in industrialized countries in comparison to developing countries (11, 38). Overweight and obesity possibly improve the risk (9, 39). Some numerous studies have suggested that risk is increased by high intakes of meat, and reduced by high intakes of vegetables, these data usually are not consistent (9).



Lung cancer. Lung cancer could be the most common cancer in the world (11). Heavy smoking boosts the risk by around 30-fold, and smoking causes over 80% of lung cancers in western world (5). Numerous observational studies have found that lung cancer patients typically report a reduced intake of fruits, vegetables and related nutrients (such as b-carotene) than controls (9, 34). The only one of these factors to are already tested in controlled trials, namely b-carotene, has, however, didn't produce any benefit when given like a supplement for 12 years (40-42). The possible effect of diet on cancer of the lung risk remains controversial, as well as the apparent protective effect of fruits and vegetables could be largely the result of residual confounding by smoking, since smokers generally consume less fruit and vegetables than non-smokers. In public health terms, the overriding priority for preventing lung cancer is always to reduce the prevalence of smoking.



Breast cancer. Breast cancer could be the second most frequent cancer in the world as well as the most common cancer among women. Incidence rates are about half a dozen times higher in industrialized countries in comparison to less civilized world and Japan (11). Much of the international variation is really a result of differences in established reproductive risk factors like age at menarche, parity and age at births, and breastfeeding (43, 44), but differences in dietary habits and exercising may also contribute. In fact, age at menarche is partly driven by dietary factors, in this restricted dietary intake during childhood and adolescence contributes to delayed menarche. Adult height, also, is weakly positively associated with risk, which is partly dependant on dietary factors during childhood and adolescence (43). Estradiol and perhaps other hormones play a key role inside etiology of breast cancers (43), and it is possible that any more dietary effects on risk are mediated by hormonal mechanisms.



The only dietary factors which are already shown to increase the risk for cancer of the breast are obesity and alcohol. Obesity increases breast cancers risk in postmenopausal women by around 50%, probably by increasing serum concentrations of free estradiol (43). Obesity won't increase risk among premenopausal women, but obesity in premenopausal women is likely to lead to obesity throughout life and so to an eventual increase in breast cancer risk. For alcohol, there's now a sizable body of information from well-designed studies which consistently shows a small boost in risk with increasing consumption, with about a 10% rise in risk for an average of 1 alcoholic drink daily (45). The mechanism for this association just isn't known, but may involve increases in estrogen levels (46).



The outcomes of studies of other dietary factors including fat, meat, dairy products, vegetables and fruit, fibre and phyto-estrogens are inconclusive (9, 34, 47, 48).



Endometrial cancer. Endometrial cancer risk is around three-fold higher in obese women compared to lean women (8, 49), probably because in the effects of obesity on alteration in hormones (50). Some case-control numerous studies have suggested that diets high in fruits and vegetables may reduce risk which diets an excellent source of saturated or total fat may increase risk, but the quantity of available details are limited (9).



Prostate cancer. Prostate cancer incidence rates are strongly suffering from diagnostic practices and therefore difficult to interpret, but mortality rates demonstrate that death from prostate cancer is approximately 10 times more common in North America and Europe when compared to Asia (11).



Little may be known about the etiology of prostate cancer, although ecological studies advise that it is positively linked to a “westernized” diet (19). The data from prospective numerous studies have not established causal or protective associations for specific nutrients or dietary factors (9, 34). Diets full of red meat, dairy food and animal fat have frequently been implicated inside development of cancer of prostate, even though data aren't entirely consistent (9, 51-53). Randomized controlled trials have provided substantial, consistent evidence that supplements of b-carotene tend not to alter the danger for prostate type of cancer (40, 41, 54) but have suggested that vitamin E (54) and selenium (55) might have a protective effect. Lycopene, primarily from tomatoes, may be associated with a reduced risk in some observational studies, but the data are not consistent (56). Hormones control the growth of the prostate, and diet might influence cancer of prostate risk by affecting hormonal changes.



Kidney cancer. Overweight and obesity are in place risk factors for cancer with the kidney, and may take into account up to 30% of kidney cancers in men and some women (57).



Table 11 provides a summary of strength of evidence with regard to the role of varied risk factors inside the development of cancer.



Table 11. Summary of strength of evidence on lifestyle factors and the chance of developing cancer



Evidence



Alcohol (oral cavity, pharynx, larynx, oesophagus, liver, breast)



Aflatoxin (liver)



Physical activity (breast)



Preserved meat (colorectum)



Very hot (thermally) drinks and food (oral cavity, pharynx, oesophagus)



Possible/insufficient



Fibre



Soya



Fish



Calcium, zinc and selenium



Animal fats



Heterocyclic amines



Nitrosamines



a The “convincing” and “probable” categories within this report correspond for the “sufficient” category from the IARC directory weight control and exercise (4) due to the public health insurance policy implications.



b For colorectal cancer, a protective effect of fruit and vegetable intake has become suggested by many case-control studies but this has not been sustained by results of various large prospective studies, suggesting that in case a benefit does exist it can be likely being modest.



The Consultation recognized the problems posed by the lack of knowledge on diet and cancer in the developing world. There are very limited data from Africa, Asia and Latin America, yet these regions represent two-thirds or more with the world population. There is thus an urgent requirement of epidemiological research on diet and cancer over these regions. The have to evaluate the role of food processing methods, traditional and industrial, seemed to be identified. Microbiological and chemical food contaminants may also contribute to carcinogenicity of diets.



The nutrition transition is accompanied by modifications in prevalence of specific cancers. For some cancers, like stomach cancer, this could possibly be beneficial while persons, like colorectal and breast cancers, the modifications are adverse.



5.5.5 Disease-specific recommendations



The main strategies for reducing the chance of developing cancer are listed below:



Maintain weight (among adults) in a way that BMI is in the range of 18.5-24.9 kg/m2 and avoid extra weight (>5 kg) during adult life (58).



Maintain regular physical exercise. The primary goal should be to perform physical activity on most days of the week; 60 minutes each day of moderate-intensity activity, like walking, could possibly be needed to keep up healthy body weight in otherwise sedentary people. More vigorous activity, such as fast walking, may give some additional benefits for cancer prevention (4).



Consumption of alcoholic beverages is just not recommended: if consumed, tend not to exceed two units 8 per day.



Chinese-style fermented salted fish should only be consumed in moderation, especially during childhood. Overall use of salt-preserved foods and salt ought to be moderate.



Minimize experience aflatoxin in foods.



Have a diet which includes at least 400 g each day of total vegatables and fruits.



Those who are certainly not vegetarian are advised to moderate utilization of preserved meat (e.g. sausages, salami, bacon, ham). 9



Do not consume foods or drinks when they are in a very hot (scalding hot) temperature.



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16. Palli D. Epidemiology of gastric cancer: the test of available evidence. Journal of Gastroenterology, 2000, 35(Suppl. 12):S84-S89.



17. Cummings JH, Bingham SA. Diet and the prevention of cancer. British Medical Journal, 1998, 317:1636-1640.



18. Hardman AE. Physical activity and cancer risk. Proceedings with the Nutrition Society, 2001, 60:107-113.



19. Armstrong B, Doll R. Environmental factors and cancer incidence and mortality in numerous countries, with special mention of the dietary practices. International Journal of Cancer, 1975, 15:617-631.



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21. Howe GR et al. The relationship between fat molecules intake and probability of colorectal cancer: evidence from your combined analysis of 13 case-control studies. Cancer Causes and Control, 1997, 8:215-228.



22. Potter JD, Steinmetz K. Vegetables, fruit and phytoestrogens as preventive agents. In: Stewart BW, McGregor D, Kleihues P, eds. Principles of chemoprevention. Lyon, International Agency for Research on Cancer, 1996:61-90 (IARC Scientific Publications, No. 139).



23. Jacobs DR Jr et al. Whole-grain intake and cancer: an expanded review and meta-analysis. Nutrition and Cancer, 1998, 30:85-96.



24. Bueno de Mesquita HB, Ferrari P, Riboli E (on the part of EPIC Working Group on Dietary Patterns). Plant foods and the likelihood of colorectal cancer in Europe: preliminary findings. In: Riboli E, Lambert R, eds. Nutrition and lifestyle: opportunities for cancer prevention. Lyon, International Agency for Research on Cancer, 2002:89-95 (IARC Scientific Publications, No. 156).



25. Fuchs CS et al. Dietary fiber and the likelihood of colorectal cancer and adenoma in ladies. New England Journal of Medicine, 1999, 340:169-176.



26. Michels KB et al. Prospective study of fruit and vegetable consumption and incidence of colon and rectal cancers. Journal from the National Cancer Institute, 2000, 92:1740-1752.



27. Schatzkin A et al. Lack of effect of a low-fat, high-fiber diet on the recurrence of colorectal adenomas. Polyp Prevention Trial Study Group. New England Journal of Medicine, 2000, 342:1149-1155.



28. Alberts DSet al. Lack of effect of the high-fiber cereal supplement for the recurrence of colorectal adenomas. Phoenix Colon Cancer Prevention Physicians’ Network. New England Journal of Medicine, 2000, 342:1156-1162.



29. Bonithon-Kopp C et al. Calcium and fibre supplementation in prevention of colorectal adenoma recurrence: a randomised intervention trial. European Cancer Prevention Organisation Study Group. Lancet, 2000, 356:1300-1306.



30. Terry P et al. Fruit, vegetables, fiber, and likelihood of colorectal cancer. Journal with the National Cancer Institute, 2001, 93:525-533.



31. Giovannucci E et al. Alcohol, low-methionine, low-folate diets, and chance of colon cancer that face men. Journal with the National Cancer Institute, 1995, 87:265-273.



32. Glynn SA et al. Alcohol consumption and likelihood of colorectal cancer inside a cohort of Finnish men. Cancer Causes and Control, 1996, 7:214-223.



33. Giovannucci E et al. Multivitamin use, folate, and colon cancer in women within the Nurses’ Health Study. Annals of Internal Medicine, 1998, 129:517-524.



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35. Baron JA et al. Calcium supplements and colorectal adenomas. Polyp Prevention Trial Study Group. Annals from the New York Academy of Sciences, 1999, 889:138-145.



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37. Saracco G. Primary liver cancer is of multifactorial origin: importance of hepatitis B virus infection and dietary aflatoxin. Journal of Gastroenterology and Hepatology, 1995, 10:604-608.



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39. Michaud DS et al. Physical activity, obesity, height, and the risk of pancreatic cancer. Journal of the American Medical Association, 2001, 286:921-929.



40. Hennekens CH et al. Lack of effect of long-term supplementation with betacarotene for the incidence of malignant neoplasms and heart problems. New England Journal of Medicine, 1996, 334:1145-1149.



41. Omenn GS et al. Effects of the combination of beta carotene and vitamin A on carcinoma of the lung and cardiovascular disease. New England Journal of Medicine, 1996, 334:1150-1155.



42. Beta Carotene Cancer Prevention Study Group The Alpha-Tocopherol. The effect of vitamin E and beta carotene around the incidence of lung cancer and other cancers in male smokers. New England Journal of Medicine, 1994, 330:1029-1035.



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44. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and breastfeeding: collaborative reanalysis of person data from 47 epidemiological studies in 30 countries, including 50 302 women with breast cancers and 96 973 women devoid of the disease. Lancet, 2002, 360:187-195.



45. Smith-Warner SA et al. Alcohol and breast cancer in females: a pooled analysis of cohort studies. Journal from the American Medical Association, 1998, 279:535-540.



46. Dorgan JF et al. Serum hormones as well as the alcohol-cancer of the breast association in postmenopausal women. Journal in the National Cancer Institute, 2001, 93:710-715.



47. Key TJ, Allen NE. Nutrition and breast cancers. Breast, 2001, 10(Suppl. 3):S9-S13.



48. Smith-Warner SA et al. Intake of vegatables and fruits and likelihood of breast cancer: a pooled analysis of cohort studies. Journal with the American Medical Association, 2001, 285:769-776.



49. Bergstrom A et al. Overweight just as one avoidable reason for cancer in Europe. International Journal of Cancer, 2001, 91:421-430.



50. Key TJ, Pike MC. The dose-effect relationship between “unopposed” oestrogens and endometrial mitotic rate: its central role in explaining and predicting endometrial cancer risk. British Journal of Cancer, 1988, 57:205-212.



51. Schuurman AG et al. Animal products, calcium and protein and prostate cancer risk in The Netherlands Cohort Study. British Journal of Cancer, 1999, 80:1107-1113.



52. Chan JM et al. Dairy products, calcium, and cancer of the prostate risk inside Physicians’ Health Study. American Journal of Clinical Nutrition, 2001, 74:549-554.



53. Michaud DS et al. A prospective study on intake of animal products and probability of prostate cancer. Cancer Causes and Control, 2001, 12:557-567.



54. Heinonen OP et al. Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial. Journal with the National Cancer Institute, 1998, 90:440-446.



55. Clark LC et al. Decreased incidence of cancer of the prostate with selenium supplementation: results of a double-blind cancer prevention trial. British Journal of Urology, 1998, 81:730-734.



56. Kristal AR, Cohen JH. Invited commentary: tomatoes, lycopene, and cancer of the prostate. How strong is evidence, American Journal of Epidemiology, 2000, 151:124-127.



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5.6 Recommendations for preventing dental diseases



5.6.1 Background



Oral health is associated with diet in several ways, as an example, through nutritional influences on cranio-facial development, oral cancer and oral infectious diseases. The purpose with this review, however, would be to focus on the nutritional aspects of dental diseases. Dental diseases include dental caries, developmental defects of enamel, dental erosion and periodontal disease. Dental diseases can be a costly burden to medical services, making up between 5% and 10% of total healthcare expenditures and exceeding the price tag on treating heart problems, cancer and osteoporosis in industrialized countries (1). In low-income countries, the cost of traditional restorative management of dental disease may possibly exceed the free resources for health care. Dental health promotion and preventive strategies are clearly cheaper and sustainable.



Although not life-threatening, dental diseases use a detrimental impact on quality of life in early childhood through to senior years, having an impact on self-esteem, eating ability, nutrition and health. In modern society, a substantial role of teeth is to enhance appearance; facial appearance is very essential in determining an individual’s integration into society, and teeth also play a vital role in speech and communication. Oral diseases are connected with considerable pain, anxiety and impaired social functioning (2, 3). Dental decay may lead to tooth loss, which reduces the opportunity to eat a nutritious diet, the enjoyment of food, the confidence to socialize and also the quality of life (4-6).



5.6.2 Trends



The quantity of dental decay is measured while using the dmf/DMF index, a count of the quantity of teeth or surfaces inside a person’s mouth which can be decayed, missing or filled as a direct result caries in primary dentition/ permanent dentition. An additional dental status indicator may be the proportion of the population who are edentulous (haven't any natural teeth).



In most low-income countries, the prevalence rate of dental caries is comparatively low and over 90% of caries are untreated. Available data (7) show that the mean number of decayed, missing or filled permanent teeth (DMFT) at age 12 years in low-income countries is 1.9, 3.3 in middle-income countries and a pair of.one out of high-income countries (Table 12).



Data about the level of dental caries within the permanent dentition of 12-yearolds show two distinct trends. First, a fall inside the prevalence of dental caries in western world, and second an increase inside the prevalence in the disease in certain developing countries which have increased their usage of sugars and have never yet been introduced on the presence of adequate numbers of fluoride. Despite the marked overall decline in dental caries in the last 30 years, the prevalence of dental caries remains unacceptably full of many developed countries. Even in countries with low average DMFT scores, a tremendous proportion of kids have relatively high amounts of dental caries. Moreover, there exists some indication the favourable trends in amounts of dental caries in permanent teeth have come to a halt (8).



Table 12. Trends in amounts of dental caries in 12-year-olds (mean DMFT per person aged 12 years)



Country or area



1971



0.1



1982



0.3



1987



0.4-1.1



Source: reference 7.



Many developing countries have low decayed, missing, filled primary teeth (dmft) values but a high prevalence of dental caries in the primary dentition. Data on 5-year-old children in Europe suggest that the trend towards reduced prevalence of dental decay has halted (9-11). In children aged 5-7 years, average dmft values of below 2.0 are actually reported for Denmark, England, Finland, Italy, Netherlands and Norway (12). Higher dmft values were reported recently for Belarus (4.7) (13), Hungary (4.5) (14), Romania (4.3) (15) and the Russian Federation (4.7) (16).



Being free from caries when he was 12 years does not imply being caries-free for life. The mean DMFT in countries of the European Union after 1988 varied between 13.4 and 20.8 at 35-44 years (17). The WHO guidelines on teeth's health state that when he was 35-44 years a DMFT score of 14 or above is considered high. In most developing countries, the level of caries in adults with this age group is leaner, for instance, 2.one in China (18) and 5.7 in Niger (19). Few data can be purchased on the prevalence and seriousness of root caries in older adults, but while using increasingly ageing population and greater retention of teeth, the situation of root caries is planning to become a tremendous public health concern in the future.



The number of edentulous persons has declined over the past 20-30 years in a number of industrialized countries (3). Despite overall gains however, there exists still a sizable proportion of older adults who will be edentulous or partially dentate and as the people continues to age loss of tooth will affect a growing amount of persons worldwide. Table 13 summarizes the accessible information about the prevalence of edentulousness in old-age populations throughout the planet.



Dental erosion is a relatively new dental problem in many countries throughout the world, and is linked to diet. There is anecdotal evidence that prevalence is increasing in industrialized countries, but there won't be any data over time to suggest patterns of the disease. There are insufficient data accessible to comment on worldwide trends; in certain populations, however, it is thought that approximately50%of youngsters are affected (20).



5.6.3 Diet and dental disease



Nutritional status affects the teeth pre-eruptively, even if this influence is a smaller amount important as opposed to post-eruptive local effect of diet around the teeth (21). Deficiencies of vitamins D and A and protein-energy malnutrition have been associated with enamel hypoplasia and salivary gland atrophy (which decreases the mouth’s power to buffer plaque acids), which render the teeth more susceptible to decay. In developing countries, within the absence of dietary sugars, undernutrition just isn't associated with dental caries. Undernutrition coupled with an increased intake of sugars may exacerbate the risk of caries.



There is a few evidence to claim that periodontal disease progresses more quickly in undernourished populations (22); the key role of nutrition in maintaining an adequate host immune response may explain this observation. Apart from severe vitamin C deficiency, which might result in scurvy-related periodontitis, there's little evidence currently for a link between diet and periodontal disease. Current research is investigating the possibility role from the antioxidant nutrients in periodontal disease. Poor oral hygiene will be the most important risk factor within the development of periodontal disease (21). Undernutrition exacerbates the seriousness of oral infections (e.g. acute necrotizing ulcerative gingivitis) and may even eventually result in their evolution into life-threatening diseases for example noma, a dehumanizing oro-facial gangrene (23).



Table 13. Prevalence of edentulousness the over 60's throughout the world



Country or area



Prevalence of edentulousness (%)



Age group (years)



Source: reference 7.



Dental caries occur due to demineralization of enamel and dentine by organic acids formed by bacteria in dental plaque with the anaerobic metabolism of sugars derived from the diet (24). Organic acids increase the solubility of calcium hydroxyapatite inside dental hard tissues and demineralization occurs. Saliva is super-saturated with calcium and phosphate at pH 7 which promotes remineralization. If the oral pH remains high enough for sufficient time then complete remineralization of enamel may occur. If the acid challenge is to great, however, demineralization dominates and the enamel gets to be more porous right up until a carious lesion forms (25). The development of caries requires the existence of sugars and bacteria, but is influenced through the susceptibility of the tooth, the bacterial profile, and the quantity and quality with the saliva.



Dietary sugars and dental caries



There is a wealth of evidence from many different types of investigation, including human studies, animal experiments and experimental studies in vivo as well as in vitro showing the role of dietary sugars inside the etiology of dental caries (21). Collectively, data from these studies provide an overall picture from the cariogenic potential of carbohydrates. Sugars are undoubtedly the key dietary factor inside the development of dental caries. Here, the phrase “sugars” is the term for all monosaccharides and disaccharides, even though the term “sugar” refers only to sucrose. The term “free sugars” is the term for all monosaccharides and disaccharides added to foods with the manufacturer, cook or consumer, plus sugars naturally within honey, fresh fruit juices and syrups. The term “fermentable carbohydrate” refers to free sugars, glucose polymers, oligosaccharides and highly refined starches; it excludes non-starch polysaccharides and raw starches.



Worldwide epidemiological studies have compared sugar consumption and numbers of dental caries in the between-country level. Sreebny (26, 27) correlated the dental caries experience (DMFT) of 12-year-olds with data on sugar supplies of 47 countries and found a tremendous correlation (+0.7); 52% of the variation in the level of caries was explained by the per capita accessibility to sugar. In countries with a consumption level of sugar <18 kg per person a year caries experience was consistently


Miyazaki & Morimoto (29) reported an important correlation (r = +0.91) between sugar availability in Japan and DMFT at age 12 years between 1957 and 1987. Populations which had experienced a lower sugar availability throughout the Second World War showed a lowering of dental caries which subsequently increased again if the restriction was lifted (30-32). Although the data pre-date the widespread usage of fluoride dentifrice, Weaver (33) observed a decline in dental caries between 1943 and 1949 in aspects of northern England with both high and low concentrations of fluoride in drinking-water.



Isolated communities using a traditional method of life and a consistently low intake of sugars have very low amounts of dental caries. As economic levels such societies rise, the volume of sugar along with other fermentable carbohydrates inside the diet increases and this is frequently associated with a marked surge in dental caries. Examples of the trend are actually reported on the list of Inuit in Alaska, USA (34), as well as in populations in Ethiopia (35), Ghana (36), Nigeria (37), Sudan (38), and about the Island of Tristan da Cunha, St Helena (39).



There is evidence to reveal that many groups of men and women with high experience of sugars have levels of caries higher than people average. Examples include children with chronic diseases requiring long-term sugar-containing medicines (40), and confectionery workers (41-44). Likewise, connection with dental caries has seldom been reported in groups of folks who possess a habitually low intake of sugars, as an example, children of dentists (45, 46) and youngsters in institutions where strict dietary regimens are inflicted (47, 48). A weakness of population studies with this type is that adjustments to intake of sugars often occur concurrently with changes inside the intake of refined starches, which makes it impossible to attribute adjustments to dental caries solely to changes in the intake of sugars. An exception to this would be the data from studies of children with hereditary fructose intolerance (HFI). Studies have shown that people with HFI have a low intake of sugars and a higher than average intake of starch, but use a low dental caries experience (49).



Human intervention studies are rare, and people that have been reported are decades old and were conducted in the pre-fluoride era prior to the strong link between sugars intake and dental caries levels was established. It would not be possible to repeat such studies today due to ethical constraints. The Vipeholm study, conducted in a grownup mental institution in Sweden between 1945 and 1953 (50), investigated the end results of consuming sugary foods of varying stickiness and at different times through the entire day on the development of caries. It was found that sugar, even when consumed in a lot, had little influence on caries increment if it absolutely was ingested up to your maximum of four times every day at mealtimes only. Increased frequency of usage of sugar between meals was, however, linked to a marked surge in dental caries. It has also been found that the increase in dental caries activity disappears on withdrawal of sugar-rich foods. Despite the complicated nature with the study the conclusions are valid, but they apply to the pre-fluoride era. The Turku study would be a controlled dietary intervention study completed on adults in Finland in the 1970s which indicated that almost total substitution of sucrose within the diet with xylitol (a non-cariogenic sweetener) resulted within an 85% decline in dental caries over the 2-year period (51).



Numerous cross-sectional epidemiological reports have compared sugars intake with dental caries levels in lots of countries of the world. Those conducted ahead of the early 1990s have been summarized by Rugg-Gunn (21). Nine from 21 studies that compared amount of sugars consumed with caries increment found significant associations, as the other 12 didn't. Moreover, 23 from 37 studies that investigated the association between frequency of sugars consumption and caries levels found significant relationships, while 14 didn't find this kind of associations.



A cross-sectional study within the United States of 2514 people aged 9-29 years conducted between 1968 and 1970 found that this dental caries experience with adolescents eating the highest levels of sugars (upper 15% in the sample) was twice that of those eating the cheapest amounts (lower 15% in the sample) (52). Granath et al. (53) indicated that intake of sugars was the most important factor connected with caries inside the primary dentition of preschool children in Sweden. When the results of oral hygiene and fluoride were kept constant, the children which has a low intake of sugars between meals had as much as 86% less caries than those with high intakes of sugars. Other reports have found fluoride exposure and oral hygiene to get more strongly linked to caries than sugars consumption (54, 55). A recent study in the United Kingdom of an representative sample of youngsters aged 4-18 years showed no significant relationship between caries experience and level of intake of free sugars; inside the age group 15-18 years, however, the top of band of free sugars consumers were more more likely to have decay compared to lower band (70% in comparison with 52%) (20).



Many other cross-sectional studies have demostrated a relationship between sugars consumption and degrees of caries inside primary and/or permanent dentitions in countries or areas throughout the world, including China (56), Denmark (57), Madagascar (58, 59), Saudi Arabia (60), Sweden (61, 62), Thailand (63) and the United Kingdom (64).



When investigating the association between diet along with the development of dental caries it is much more appropriate to employ a longitudinal study design where sugars consumption habits after a while are related to changes in dental caries experience. Such studies demonstrate a significant relationship between caries development and sugars intake (65-67). In a comprehensive study of over 400 children in England aged 11-12 years, a small but significant relationship is discovered between intake of total sugars and caries increment over a couple of years (r = +0.2) (67). The Michigan Study inside the United States investigated the relationship between sugars intake and dental caries increment over 3 years in kids initially aged 10-15 years (66). A weak relationship was found between your amount of dietary sugars consumed and dental caries experience.



In a report on longitudinal studies, Marthaler (68) analysed the relationship between dietary sugars and caries activity in countries in which the availability of sugars is high and also the use of fluoride is extensive. He figured in modern societies that make usage of prevention, the connection between sugars consumption and dental caries was still evident (68). He also figured many older studies had did not show a relationship between sugars intake and development of dental caries simply because they were of poor methodological design, used unsuitable methods of dietary analysis or were of insufficient power (68). Correlations between individuals’ sugars consumption and dental caries increments may be weak if the range of sugars intake inside the study inhabitants are small. That would be to say, when all people inside a population are exposed towards the disease risk factor, the relationship relating to the risk factor and also the disease will not be apparent (69).



Frequency and level of sugars consumption. Several studies, including the above-mentioned Vipeholm study in Sweden, have indicated that caries experience increases markedly in the event the frequency of sugars intake exceeds four times every day (50, 70-72). The significance about frequency versus the total quantity of sugars is difficult to evaluate since the two variables take time and effort to distinguish from each other. Data from animal reports have indicated the need for frequency of sugars intake within the development of dental caries (73, 74). Some human research has also shown how the frequency of sugars intake is a vital etiological factor for caries development (75). Many research has related the frequency of intake of sugars or sugars-rich food to caries development but have not simultaneously investigated the relationship between level of sugars consumed and dental caries, and so no conclusion about the relative importance of these two variables can be drawn from these studies (76-78).



Animal numerous studies have also shown a relationship between amount of sugars consumed as well as the development of dental caries (79-82). Several longitudinal studies in humans have indicated how the amount of sugars consumed is a bit more important as opposed to frequency (66, 67, 83, 84), while Jamel et al. (85) discovered that both the frequency and the amount of sugars intake are crucial.



The strong correlation between the amount and frequency of sugars consumption has become demonstrated by a number of investigators in different countries (67, 86-88). It is therefore highly likely that, in terms of caries development, both variables are potentially important.



Relative cariogenicity of various sugars and food consistency. Therelative acidogenicity of numerous monosaccharides and disaccharides may be investigated in plaque pH studies, who have shown that lactose is less acidogenic than other sugars (89). Animal studies have provided no clear evidence that, with all the exception of lactose, the cariogenicity of monosaccharides and disaccharides differs. The above-mentioned study in Turku, Finland, found no difference in caries development between subjects on diets sweetened with sucrose in contrast to those whose diet ended up sweetened with fructose (51). Invert sugar (50% fructose + 50% glucose) is less cariogenic than sucrose (90).



The adhesiveness or stickiness of an food is not necessarily in connection with either oral retention time or cariogenic potential. For example, consumption of sugars-containing drinks (i.e. non-sticky) is linked to increased chance of dental caries (85, 88)



Potential impact of sugars reduction on other dietary components. It is very important to consider the possible impact of the reduction in free sugars on other components with the diet. Simple, cross-sectional analysis of dietary data from populations has demonstrated an inverse relationship relating to the intake of free sugars along with the intake of fat (91), suggesting that reducing free sugars might lead to an surge in fat intake. There is, however, an increasing body of evidence from studies with time that shows that changes in intake of fat and free sugars are certainly not inversely related, which reductions in intake of fat are offset by increases in intakes of starch instead of free sugars (92, 93). Cole-Hamilton et al. (94) found that the intake of both fat and added sugars simultaneously decreased as fibre intake increased. Overall dietary goals that promote increased intake of wholegrain staple foods, fruits and vegetables along with a reduced utilization of free sugars are thus unlikely to lead to a greater consumption of fat.



Influence of fluoride. Fluoride undoubtedly protects against dental caries (95). The inverse relationship between fluoride in drinking-water and dental caries, as an illustration, is more developed. Fluoride reduces caries in children by between 20% and 40%, but won't eliminate dental caries altogether.



Over 800 controlled trials in the effect of fluoride administration on dental caries happen to be conducted; collectively these studies demonstrate that fluoride could be the most effective preventive agent against caries (95). Several reports have that indicated that the relationship between sugars intake and caries still exists inside the presence of adequate fluoride exposure (33, 71, 96, 97). In two major longitudinal studies in youngsters, the observed relationships between sugars intake and progression of dental caries remained even though controlling for utilization of fluoride and dental hygiene practices (66, 67). As mentioned earlier, following a writeup on available longitudinal studies, Marthaler (68) concluded that, even when preventive measures including use of fluoride are employed, a relationship between sugars intake and caries still exists. He also stated that in industrialized countries where there's adequate contact with fluoride, no further reduction inside the prevalence and severity of dental caries will probably be achieved unless the intake of sugars is reduced.



A recent systematic review that investigated the significance about sugars intake in caries etiology in populations encountered with fluoride concluded that where there is adequate experience of fluoride, sugars consumption can be a moderate risk factor for caries in most people; moreover sugars consumption is likely to get a more powerful indicator for probability of caries in persons who don't have regular experience of fluoride. Thus, restricting sugars consumption still carries a role to play within the prevention of caries in situations where there is certainly widespread usage of fluoride but this role is not as strong as it can be without experience fluoride (98). Despite the indisputable preventive role of fluoride, there's no strong evidence of an clear relationship between oral cleanliness and degrees of dental caries (99-100).



Excess ingestion of fluoride during enamel formation can lead to dental fluorosis. This condition is observed specifically in countries which may have high degrees of fluoride in water supplies (95).



Starches and dental caries



Epidemiological studies demonstrate that starch is of low risk to dental caries. People who consume high-starch/low-sugars diets have low levels of caries, whereas people that consume low-starch/highsugars diets have high degrees of caries (39, 48, 49, 51, 67, 101, 102). In Norway and Japan the intake of starch increased through the Second World War, the occurrence of caries was reduced.



The heterogeneous nature of starch (i.e. a higher level refinement, botanical origin, raw or cooked) is of particular relevance when assessing its potential cariogenicity. Several kinds of experiment have shown that raw starch is of low cariogenicity (103-105). Cooked starch is all about onethird to one-half as cariogenic as sucrose (106, 107). Mixtures of starch and sucrose are, however, potentially more cariogenic than starch alone (108). Plaque pH studies, having an indwelling oral electrode, demonstrate starch-containing foods reduce plaque pH to below 5.5, but starches are less acidogenic than sucrose. Plaque pH studies measure acid production from your substrate in lieu of caries development, and take no account from the protective factors found in a few starch-containing foods or of the effect of foods on stimulation of salivary flow.



Glucose polymers and pre-biotics are increasingly being combined with foods in industrialized countries. Evidence about the cariogenicity of such carbohydrates is sparse and emanates from animal studies, plaque pH studies and studies in vitro which claim that maltodextrins and glucose syrups are cariogenic (109-111). Plaque pH studies and experiments in vitro suggest that isomalto-oligosaccharides and gluco-oligosaccharides may be less acidogenic than sucrose (112-114). There is, however, evidence that fructo-oligosaccharides are as acidogenic as sucrose (115, 116).



Fruit and dental caries



As habitually consumed, there is certainly little evidence to reveal that fruit is an important factor inside the development of dental caries (67, 117-119). A amount of plaque pH reports have found fruit to become acidogenic, although less so than sucrose (120-122). Animal studies have shown that when fruit is consumed in quite high frequencies (e.g. 17 times every day) it might induce caries (123, 124), but less so than sucrose. In the only epidemiological study in which a link between fruit consumption and DMFT was found (125), fruit intakes were very high (e.g. 8 apples or 3 bunches of grapes every day) and also the higher DMFT in fruit farm workers compared with grain farm workers arose solely from differences in the numbers of missing teeth.



Dietary factors which control dental caries



Some dietary components protect against dental caries. The cariostatic nature of cheese continues to be demonstrated in several experimental studies (126, 127), and in human observational studies (67) and intervention studies (128). Cow’s milk contains calcium, phosphorus and casein, all of that are thought to inhibit caries. Several research has shown that this fall in plaque pH following milk consumption is negligible (129, 130). The cariostatic nature of milk has been demonstrated in animal studies (131, 132). Rugg-Gunn et al. (67) found an inverse relationship between the usage of milk and caries increment in a study of adolescents in England. Wholegrain foods have protective properties; they might need more mastication thereby stimulating increased saliva flow. Other foods which might be good gustatory and/or mechanical stimulants to salivary flow include peanuts, hard cheeses and periodontal. Both organic and inorganic phosphates (found in unrefined plant foods) are actually found to be cariostatic in animal studies, but studies in humans have produced inconclusive results (133, 134). Both animal studies and experimental investigations in humans have shown that black tea extract increases plaque fluoride concentration and reduces the cariogenicity of a sugars-rich diet (135, 136).



Breastfeeding and dental caries



In line using the positive health effects of breastfeeding, epidemiological studies have associated breastfeeding with low degrees of dental caries (137, 138). A few specific case studies have linked prolonged ad libitum and nocturnal breastfeeding to early childhood caries. Breastfeeding gets the advantage that it will not necessitate the use of your feeder bottle, which may be associated with early childhood caries. A breastfed infant will likely receive milk of a controlled composition that additional free sugars are not added. There are no benefits to teeth's health of feeding employing a formula feed.



Dental erosion



Dental erosion is the progressive irreversible loss in dental hard tissue that's chemically etched away in the tooth surface by extrinsic and/or intrinsic acids by the process that does not involve bacteria. Extrinsic dietary acids include citric acid, phosphoric acid, vitamin c, malic acid, tartaric acid and carbonic acid found, as an example, in fruits and juices, soft drinks and vinegar. Erosion in severe cases brings about total tooth destruction (139). Human observational reports have shown a connection between dental erosion along with the consumption of a number of acidic foods and drinks, including frequent consumption of fruit juice, carbonated drinks (including sports drinks), pickles (containing vinegar), citrus fruits and berries (140-144). Age-related increases in dental erosion have been shown to get greater in those while using highest intake of sodas (20). Experimental clinical studies have shown that utilization of, or rinsing with, acidic beverages significantly lowers the pH in the oral fluids (121). Enamelis softened within one hour of experience of cola but this could possibly be reversed by experience milk or cheese (145, 146). Animal studies show that fruit and soft drinks cause erosion (124, 147), although fruit drinks are a lot more destructive than whole fruits (148, 149).



5.6.4 Strength of evidence



The strength with the evidence linking dietary sugars to the chance of dental caries is in the multiplicity in the studies rather than the power of the individual study. Strong evidence is provided from the intervention studies (50, 51) however the weakness of these studies is they were conducted inside the pre-fluoride era. More recent studies also show an association between sugars intake and dental caries albeit less strong as within the prefluoride era. However, in several developing countries people are not yet exposed for the benefits of fluoride.



Cross-sectional studies ought to be interpreted with caution because dental caries develop over time and thus simultaneous measurements of disease levels and diet might not give a true reflection of the role of diet in the development in the disease. It is the diet several years earlier that could be responsible for current caries levels. Longitudinal studies (66, 67) who have monitored a alteration of caries experience and related this to dietary factors provide stronger evidence. Such studies have been conducted on populations by having an overall high sugars intake but the lowest interindividual variation; this could account for that weak associations that happen to be reported.



The studies that overcome the problem of low variation in usage of sugars are studies which have monitored dental caries after a marked change in diet, for instance, those conducted on populations in the Second World War and studies of populations before and as soon as the introduction of sugars into the dietary plan. Such studies show clearly that adjustments to dental caries mirror adjustments to economic growth and increased usage of free sugars. Sometimes modifications in sugars consumption were accompanied by an boost in other refined carbohydrates. There are, however, examples where sugars consumption decreased and starch consumption increased yet levels of dental caries declined.



Strong evidence in the relationship between sugar availability and dental caries levels originates from worldwide ecological studies (26, 28). The limitations of such studies are which they use data on sugar availability rather than actual intake, they don't measure frequency of sugars intake, and they also assume that a higher level intake is equal throughout the people. Also, the values are for sucrose, yet many countries get a considerable amount of their total sugars from other sugars. These numerous studies have only considered DMFT of 12-year-olds, not always from your representative sample of people.



Caution needs being applied when extrapolating the results of animal studies to humans because of differences in tooth morphology, plaque bacterial ecology, salivary flow and composition, along with the form in that your diet is provided (usually powdered form in animal experiments). Nonetheless, animal numerous studies have enabled the impact on caries of defined types, frequencies and levels of carbohydrates to become studied.



Plaque pH studies measure plaque acid production, but the acidogenicity of the foodstuff can't be taken as a direct measurement of its cariogenic potential. Plaque pH studies take no account of protective factors in foods, salivary flow and the effects of other components of the diet. Many with the plaque pH studies that demonstrate falls in pH below the critical value of 5.5 with fruits and cooked starchy foods are already conducted using the indwelling electrode technique. This electrode is thought to be being hypersensitive and non-discriminating, tending to present an “all or nothing” reply to all carbohydrates (150).



Research has consistently shown that after annual sugar consumption exceeds 15 kg per person annually (or 40 g per person per day) dental caries increase with increasing sugar intake. When sugar consumption is below 10 kg per person each year (around 27 g per person each day), numbers of dental caries are minimal (26, 28, 29, 51, 151-158). Exposure to fluoride (i.e. where the proportion of fluoride in drinking-water is 0.7-1.0 ppm, or where over 90% of toothpastes available contain fluoride) raises the safe level of sugars consumption.



Tables 14-17 summarize the evidence relating to diet, nutrition and dental diseases.



Table 14. Summary of strength of evidence linking diet to dental caries



Evidence



Fluoride exposure (local and systematic)



Starch intake (cooked and raw starch foods, for example rice, potatoes and bread; excludes cakes, biscuits and snacks with added sugars)



Amount of free sugars



Frequency of free sugars



Dried fruits



Table 15. Summary of strength of evidence linking diet to dental erosion



Evidence



Possible



Whole berry



Table 16. Summary of strength of evidence linking diet to enamel developmental defects



Evidence



Probable



Hypocalcaemia



Table 17. Summary of strength of evidence linking diet to periodontal disease



Evidence



5.6.5 Disease-specific recommendations



It is important to set a recommended maximum level for your consumption of free sugars; the lowest free sugars consumption by a population will result in a low degree of dental caries. Population goals enable the oral health perils associated with populations being assessed and health promotion goals monitored.



The best available evidence indicates how the level of dental caries is lower in countries the place that the consumption of free sugars is below 15-20 kg per person each year. This is equivalent with a daily intake of 40-55 g per person and also the values equate to 6-10% of your energy intake. It is of particular importance that countries which currently have low use of free sugars (<15-20 kg per person each year) usually do not increase consumption levels. For countries with good consumption levels it's recommended that national health authorities and decision-makers formulate countryspecific and community-specific goals for reduction inside amount of free sugars, aiming towards recommended maximum of no greater than 10% of one's intake.



In addition to population targets given in terms of the amount of free sugars, targets to the frequency of free sugars consumption are also important. The frequency of consumption of foods and/or drinks containing free sugars needs to be limited with a maximum of 4 times daily.



Many countries which can be currently undergoing nutrition transition do not have adequate exposure to fluoride. There should be promotion of adequate fluoride exposure via appropriate vehicles, for instance, affordable toothpaste, water, salt and milk. It will be the responsibility of national health authorities to make sure implementation of feasible fluoride programmes for their country. Research in to the outcome of alternative community fluoride programmes should be encouraged.



In order to attenuate the occurrence of dental erosion, the quantity and frequency of intake of soft drinks and juices needs to be limited. Elimination of undernutrition prevents enamel hypoplasia as well as the other potential results of undernutrition on teeth's health (e.g. salivary gland atrophy, periodontal disease, oral infectious diseases).



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5.7 Recommendations for preventing osteoporosis



5.7.1 Background



Osteoporosis can be a disease affecting many millions of individuals around the entire world. It is characterized by low bone mass and micro-architectural deterioration of bone tissue, bringing about bone fragility and a consequent increase in risk of fracture (1, 2).



The incidence of vertebral and hip fractures increases exponentially with advancing age (while those of wrist fractures levels off following your age of 60 years) (3). Osteoporosis fractures are a serious cause of morbidity and disability the aged and, in the case of hip fractures, can cause premature death. Such fractures impose a big economic burden on health services worldwide (4).



5.7.2 Trends



Worldwide variation in the incidence and prevalence of osteoporosis is challenging to determine as a result of problems with definition and diagnosis. The most useful way of comparing osteoporosis prevalence between populations is to use fracture rates the aged. However, because osteoporosis is often not life-threatening, quantitative data from developing countries are scarce. Despite this, the current consensus is the fact that approximately 1.66 million hip fractures occur each and every year worldwide, how the incidence is set to improve four-fold by 2050 because with the increasing numbers of older people, and the age-adjusted incidence rates are many times higher in affluent western world than in sub-Saharan Africa and Asia (5-7).



In countries with a high fracture incidence, rates are greater among women (by three- to four-fold). Thus, although widely regarded of these countries like a disease that affects women, 20% of symptomatic spine fractures and 30% of hip fractures occur in men (8). In countries where fracture rates are low, men and some women are more equally affected (7, 9-11). The incidence of vertebral and hip fractures both in sexes increases exponentially as we grow old. Hip-fracture rates are highest in Caucasian women moving into temperate climates, are somewhat lower in women from Mediterranean and Asian countries, and are lowest in women in Africa (9, 10, 12). Countries in economic transition, such as Hong Kong Special Administrative Region (SAR) of China, have observed significant increases in age-adjusted fracture rates in recent decades, whilst the rates in industrialized countries apparently have reached a plateau (13, 14).



5.7.3 Diet, physical exercise and osteoporosis



Diet appears to have only an average relationship to osteoporosis, but calcium and vitamin D tend to be important, a minimum of in older populations.



Calcium is one in the main bone-forming minerals and an appropriate supply to bone is essential in any respect stages of life. In estimating calcium requirements, most committees manipulate either a factorial approach, where calculations of skeletal accretion and turnover rates are coupled with typical values for calcium absorption and excretion, or possibly a variety of methods determined by experimentally-derived balance data (15, 16). There continues to be considerable debate about whether current recommended intakes are adequate to increase peak bone mass and also to minimize bone loss and fracture risk in later life, and the controversies continue (2, 12, 15-17).



Vitamin D is obtained either from the diet or by synthesis within the skin under the action of sunlight. Overt vitamin D deficiency causes rickets in youngsters and osteomalacia in adults, conditions where the ratio of mineral to osteoid inbone is reduced. Poor vitamin D status inside elderly, at plasma amounts of 25-hydroxyvitamin D above those related to osteomalacia, has been linked to age-related bone loss and osteoporotic fracture, in which the ratio of mineral to osteoid remains normal.



Many other nutrients and dietary factors could possibly be important for long-term bone health and the prevention of osteoporosis. Among the necessary nutrient elements, plausible hypotheses for involvement with skeletal health, determined by biochemical and metabolic evidence, may be made for zinc, copper, manganese, boron, vitamin A, vitamin C, vitamin K, the B vitamins, potassium and sodium (15). Evidence from physiological and clinical studies is essentially lacking, and the data will often be difficult to interpret due to potential size-confounding or bone remodelling transient effects.



5.7.4 Strength of evidence



For seniors, there is certainly convincing evidence for a decline in risk for osteoporosis with plenty intake of vitamin D and calcium together, and for an increase in risk with high usage of alcohol and low weight. Evidence suggesting a probable relationship, again the over 60's, supports a job for calcium and vitamin D separately, but none with fluoride.



Strength of evidence with fracture as outcome



There is considerable geographical variation within the incidence of fractures, and cultural variation within the intakes of nutrients connected with osteoporosis and the clinical upshot of fracture. In Table 18, the place that the evidence on risk factors for osteoporosis is summarized, it's important to note how the level of certainty is given with regards to fracture because the outcome, rather than apparent bone mineral density as measured by dual-energy X-ray absorptiometry or any other indirect methods. Since the Consultation addressed health in terms of burden of disease, fractures were considered the greater relevant end-point.



Table 18. Summary of strength of evidence linking diet to osteoporotic fractures



Evidence



High protein intake



a In populations rich in fracture incidence only. Applies to men and women older than 50-60 years, using a low calcium intake and/or poor vitamin D status.



b At levels employed to fluoridate water supplies. High fluoride intake causes fluorosis and may even also alter bone matrix.



c Several components of vegetables and fruit are associated with a decreased risk at levels of intake inside the normal variety of consumption (e.g. alkalinity, vitamin K, phytoestrogens, potassium, magnesium, boron). Vitamin C deficiency (scurvy) brings about osteopenic bone disease.



5.7.5 Disease-specific recommendations



In countries with a higher fracture incidence, at the least 400-500 mg of calcium intake is needed to prevent osteoporosis. When consumption of dairy products is limited, other causes of calcium include fish with edible bones, tortillas processed with lime, green vegetables full of calcium (e.g. broccoli, kale), legumes and by-products of legumes (e.g. tofu). The interaction between calcium intake and physical exercise, sun exposure, and intake of other dietary components (e.g. vitamin D, vitamin K, sodium, protein) and protective phytonutrients (e.g. soy compounds), needs being considered before recommending increased calcium intake in countries with low fracture incidence in order to get in line with strategies for industrialized countries (18).



With regard to calcium intakes to prevent osteoporosis, the Consultation referred to the recommendations of the Joint FAO/WHO Expert Consultation on Vitamin and Mineral Requirements in Human Nutrition (18) which highlighted the calcium paradox. The paradox (that hip fracture rates are higher in civilized world where calcium intake is greater than in developing countries where calcium intake is leaner) clearly calls with an explanation. To date, the accumulated data indicate the adverse effect of protein, in particular animal (however, not vegetable) protein, might outweigh the positive effect of calcium intake on calcium balance.



The report with the Joint FAO/WHO Expert Consultation on Vitamin and Mineral Requirements in Human Nutrition managed to get clear that the recommendations for calcium intakes were depending on long-term (ninety days) calcium balance data for adults produced by Australia, Canada, the European Union, the United Kingdom and also the United States, and weren't necessarily applicable to all countries worldwide. The report also acknowledged that strong evidence was emerging that this requirements for calcium might differ from culture to culture for dietary, genetic, lifestyle and geographical reasons. Therefore, two teams of allowances were recommended: one for countries with low usage of animal protein, and another based on data from North America and Western Europes (18).



The following conclusions were reached:



There is no case for global, population-based approaches. A case could be made for targeted approaches regarding calcium and vitamin D in high-risk subgroups of populations, i.e. those with an increased fracture incidence.



In countries with good osteoporotic fracture incidence, a decreased calcium intake (i.e. below 400-500 mg per day) (15) among older men and some women is connected with increased fracture risk.



In countries with good fracture incidence, increases in dietary vitamin D and calcium within the older populations can decrease fracture risk. Therefore, an acceptable vitamin D status needs to be ensured. If vitamin D is obtained predominantly from dietary sources, by way of example, when sunshine exposure is fixed, an intake of 5-10 mg each day is recommended.



Although firm evidence is lacking, prudent dietary and several lifestyle recommendations created in respect of other chronic diseases may prove helpful with regards to reducing fracture risk. These include:



- increase exercising;



- reduce sodium intake;



- keep a healthy body mass;



- avoid smoking;



- limit alcohol intake.



Convincing evidence indicates that physical activity, particularly activity that maintains or increases muscle strength, coordination and balance as essential determinants of propensity for falling, works in prevention of osteoporotic fractures. In addition, regular lifetime weight-bearing activities, particularly in modes that include impacts on bones and so are done in vigorous fashion, increase peak bone mass in youth and help to keep up bone mass in later life.



References



1. Consensus Development Conference. Diagnosis, prophylaxis, and treatments for osteoporosis. American Journal of Medicine, 1993, 94:646-650.



2. Prentice A. Is nutrition essential in osteoporosis, Proceedings in the Nutrition Society, 1997, 56:357-367.



3. Compston JE. Osteoporosis. In: Campbell GA, Compston JE, Crisp AJ, eds. The control over common metabolic bone disorders. Cambridge, Cambridge University Press, 1993:29-62.



4. Johnell The socioeconomic burden of fractures: today and inside 21st century. American Journal of Medicine, 1997, 103(Suppl. 2A):S20-S25.



5. Royal College of Physicians. Fractured neck of femur. Prevention and management. Summary and recommendations of the report of the Royal College of Physicians. Journal from the Royal College of Physicians, 1989, 23:8-12.



6. Cooper C, Campion G, Melton LJ. Hip fractures inside the elderly: a world-wide projection. Osteoporosis International, 1992, 2:285-289.



7. Melton LJ III. Epidemiology of fractures. In: Riggs BL, Melton LJ III, eds. Osteoporosis: etiology, diagnosis, and management, 2nd ed. Philadelphia, Lippincott-Raven, 1995:225-247.



8. Eastell R et al. Management of male osteoporosis: report from the UK Consensus Group. Quarterly Journal of Medicine, 1998, 91:71-92.



9. Yan L et al. Epidemiological study of hip fracture in Shenyang, People’s Republic of China. Bone, 1999, 24:151-155.



10. Elffors L et al. The variable incidence of hip fracture in southern Europe: the MEDOS Study. Osteoporosis International, 1994, 4:253-263.



11. Maggi S et al. Incidence of hip fracture in the elderly: a cross-national analysis. Osteoporosis International, 1991, 1:232-241.



12. Osteoporosis: clinical guidelines for prevention and treatment. London, Royal College of Physicians, 1999.



13. Kannus P et al. Epidemiology of hip fractures. Bone, 1996, 18(Suppl.1): 57S-63S.



14. Lau EM, Cooper C. The epidemiology of osteoporosis: the oriental perspective inside a world context. Clinical Orthopaedics and Related Research, 1996, 323:65-74.



15. Department of Health. Nutrition and bone health: with particular experience of calcium and vitamin D. Report in the Subgroup on Bone Health, Working Group around the Nutritional Status of the Population in the Committee on Medical Aspects of Food and Nutrition Policy. London, The Stationery Office, 1998 (Report on Health and Social Subjects, No. 49).



16. Standing Committee around the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington, DC, National Academy Press, 1997.



17. NIH Consensus Development Panel on Optimal Calcium Intake. Optimal calcium intake. NIH Consensus Conference. Journal with the American Medical Association, 1994, 272:1942-1948.



18. Vitamin and mineral requirements in human nutrition. Report with the Joint FAO/WHO Expert Consultation. Geneva, World Health Organization, (in press).



4 A WHO Expert Consultation on Appropriate BMI for Asian Populations and its particular Implications for Policy and Intervention Strategies was kept in Singapore from 8 to 11 July 2002 in order to: (i) look at the scientific evidence about the relationship between BMI, body composition and risk factors in Asian populations; (ii) examine if population specific BMI cut-off points for overweight and obesity are essential for Asian populations; (iii) examine the purpose and foundation of ethnic-specific definitions; and iv) examine further research needs with this area. As one of its recommendations, the Consultation formed a Working Group to look at available data for the relationship between waist circumference and morbidity, and also the interaction between BMI, waist circumference and health risk in order to define future research needs and develop ideas for the utilization of additional waist measurements to help expand define risks.



5 See also reference 5.



6 The glycaemic index is calculated because the glycaemic response with a quantity of food containing a set amount, usually 50 g, of carbohydrate, expressed being a percentage with the glycaemic response following ingestion of a similar volume of glucose or of carbohydrate in white bread.



7 Specific amounts will be based on the analytical methodologies accustomed to measure fibre.



8 One unit is equal to approximately 10 g of alcohol and is provided by one glass of beer, wine or spirits.

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