FGM/C and Its Health Consequences: Implications for Policy, Advocacy, and Investment

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Increased methylation leads to silencing of the gene. With the increasing consumption of green tea worldwide, including by the U. Upon successful completion of the course, students will be able to: There were no differences between fibre type or between fibre consumed in food or as supplements. The Juvenile Justice System.

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The evidence regarding the impact of early nutrition on subsequent obesity is also mixed, with some studies showing relationships for high and low birth weights. The prevention of obesity in infants and young children should be considered of high priority. For infants and young children, the main preventive strategies are:. Additional measures include modifying the environment to enhance physical activity in schools and communities, creating more opportunities for family interaction e.

In developing countries, special attention should be given to avoidance of overfeeding stunted population groups.

Nutrition programmes designed to control or prevent undernutrition need to assess stature in combination with weight to prevent providing excess energy to children of low weight-for-age but normal weight-for-height. In countries in economic transition, as populations become more sedentary and able to access energy-dense foods, there is a need to maintain the healthy components of traditional diets e.

Education provided to mothers and low socioeconomic status communities that are food insecure should stress that overweight and obesity do not represent good health. Low-income groups globally and populations in countries in economic transition often replace traditional micronutrient-rich foods by heavily marketed, sugars-sweetened beverages i.

These trends, coupled with reduced physical activity, are associated with the rising prevalence of obesity. Strategies are needed to improve the quality of diets by increasing consumption of fruits and vegetables, in addition to increasing physical activity, in order to stem the epidemic of obesity and associated diseases. BMI can be used to estimate, albeit crudely, the prevalence of overweight and obesity within a population and the risks associated with it.

It does not, however, account for the wide variations in obesity between different individuals and populations. The classification of overweight and obesity, according to BMI, is shown in Table 8. However, BMI may not correspond to the same degree of fatness in different populations due, in part, to differences in body proportions.

The table shows a simplistic relationship between BMI and the risk of comorbidity, which can be affected by a range of factors, including the nature and the risk of comorbidity, which can be affected by a range of factors, including the nature of the diet, ethnic group and activity level. The interpretation of BMI gradings in relation to risk may differ for different populations. Both BMI and a measure of fat distribution waist circumference or waist: In recent years, different ranges of BMI cut-off points for overweight and obesity have been proposed, in particular for the Asia-Pacific region At present available data on which to base definitive recommendations are sparse.

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

A total of one hour per day of moderate-intensity activity, such as walking on most days of the week, is probably needed to maintain a healthy body weight, particularly for people with sedentary occupations. The fat and water content of foods are the main determinants of the energy density of the diet. A lower consumption of energy-dense i.

Conversely, a higher intake of energy-dilute foods i. Economic costs of obesity and inactivity. Medicine and Science in Sport and Exercise , , 31 Suppl. The world health report Geneva, World Health Organization, Manson JE et al.

Body weight and mortality among women. New England Journal of Medicine , , Fogelholm M, Kukkonen-Harjula K. Does physical activity prevent weight gain - a systematic review.

Obesity Reviews , , 1: Dose-response of physical activity in the treatment of obesity-How much is enough to prevent unhealthy weight gain. Outcome of the First Mike Stock Conference.

International Journal of Obesity , , 26 Suppl. Dietary fiber and body-weight regulation. Pediatric Clinics of North America , , Dietary fiber and weight regulation.

Nutrition Reviews , , Astrup A et al. The role of low-fat diets in body weight control: International Journal of Obesity , , Dietary fat plays a major role in obesity: Obesity Reviews , , 3: Campbell K, Crawford D.

Australian Journal of Nutrition and Dietetics , , Gortmaker S et al. Reducing obesity via a school-based interdisciplinary intervention among youth: Archives of Pediatrics and Adolescent Medicine , , Does television cause childhood obesity? Journal of the American Dietetic Association , , Taras HL, Gage M.

Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrate in fluids. Physiology and Behaviour , , Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight.

Soft drink consumption among US children and adolescents: Peña M, Bacallao J. Patterns and trends in food portion sizes, Journal of the American Medical Association , , Epidemic obesity in the United States: American Journal of Public Health , , Sydney, Health Communications Australia, Type 2 diabetes, formerly known as non-insulin-dependent diabetes NIDDM , accounts for most cases of diabetes worldwide.

Type 2 diabetes develops when the production of insulin is insufficient to overcome the underlying abnormality of increased resistance to its action. The early stages of type 2 diabetes are characterized by overproduction of insulin. As the disease progresses, process insulin levels may fall as a result of partial failure of the insulin producing b cells of the pancreas. Complications of type 2 diabetes include blindness, kidney failure, foot ulceration which may lead to gangrene and subsequent amputation, and appreciably increased risk of infections, coronary heart disease and stroke.

The enormous and escalating economic and social costs of type 2 diabetes make a compelling case for attempts to reduce the risk of developing the condition as well as for energetic management of the established disease 1, 2.

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

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

Although increases in both the prevalence and incidence of type 2 diabetes have occurred globally, they have been especially dramatic in societies in economic transition in much of the newly industrialized world and in developing countries 1, Worldwide, the number of cases of diabetes is currently estimated to be around million.

This number is predicted to double by , with the greatest number of cases being expected in China and India. These numbers may represent an underestimate and there are likely to be many undiagnosed cases. Previously a disease of the middle-aged and elderly, type 2 diabetes has recently escalated in all age groups and is now being identified in younger and younger age groups, including adolescents and children, especially in high-risk populations.

Age-adjusted mortality rates among people with diabetes are 1. In Caucasian populations, much of the excess mortality is attributable to cardiovascular disease, especially coronary heart disease 11, 12 ; amongst Asian and American Indian populations, renal disease is a major contributor 13, 14 , whereas in some developing nations, infections are an important cause of death It is conceivable that the decline in mortality due to coronary heart disease which has occurred in many affluent societies may be halted or even reversed if rates of type 2 diabetes continue to increase.

This may occur if the coronary risk factors associated with diabetes increase to the extent that the risk they mediate outweighs the benefit accrued from improvements in conventional cardiovascular risk factors and the improved care of patients with established cardiovascular disease 3. Type 2 diabetes results from an interaction between genetic and environmental factors. The rapidly changing incidence rates, however, suggest a particularly important role for the latter as well as a potential for stemming the tide of the global epidemic of the disease.

The most dramatic increases in type 2 diabetes are occurring in societies in which there have been major changes in the type of diet consumed, reductions in physical activity, and increases in overweight and obesity. The diets concerned are typically energy-dense, high in saturated fatty acids and depleted in NSP.

In all societies, overweight and obesity are associated with an increased risk of type 2 diabetes, especially when the excess adiposity is centrally distributed. Conventional BMI categories may not be an appropriate means of determining the risk of developing type 2 diabetes in individuals of all population groups because of ethnic differences in body composition and because of the importance of the distribution of excess adiposity.

While all lifestyle-related and environmental factors which contribute to excess weight gain may be regarded as contributing to type 2 diabetes, the evidence that individual dietary factors have an effect which is independent of their obesity promoting effect, is inconclusive.

Evidence that saturated fatty acids increase risk of type 2 diabetes and that NSP are protective is more convincing than the evidence for several other nutrients which have been implicated. The presence of maternal diabetes, including gestational diabetes and intrauterine growth retardation, especially when associated with later rapid catch-up growth, appears to increase the risk of subsequently developing diabetes. The association between excessive weight gain, central adiposity and the development of type 2 diabetes is convincing.

The association has been repeatedly demonstrated in longitudinal studies in different populations, with a striking gradient of risk apparent with increasing levels of BMI, adult weight gain, waist circumference or waist-to-hip ratio. Indeed waist circumference or waist-to-hip ratio reflecting abdominal or visceral adiposity are more powerful determinants of subsequent risk of type 2 diabetes than BMI Central adiposity is also an important determinant of insulin resistance, the underlying abnormality in most cases of type 2 diabetes Voluntary weight loss improves insulin sensitivity 21 and in several randomized controlled trials has been shown to reduce the risk of progression from impaired glucose tolerance to type 2 diabetes 22, Longitudinal studies have clearly indicated that increased physical activity reduces the risk of developing type 2 diabetes regardless of the degree of adiposity The minimum intensity and duration of physical activity required to improve insulin sensitivity has not been established.

Offspring of diabetic pregnancies including gestational diabetes are often large and heavy at birth, tend to develop obesity in childhood and are at high risk of developing type 2 diabetes at an early age Those born to mothers after they have developed diabetes have a three-fold higher risk of developing diabetes than those born before In observational epidemiological studies, a high saturated fat intake has been associated with a higher risk of impaired glucose tolerance, and higher fasting glucose and insulin levels Higher proportions of saturated fatty acids in serum lipid or muscle phospholipid have been associated with higher fasting insulin, lower insulin sensitivity and a higher risk of type 2 diabetes Higher unsaturated fatty acids from vegetable sources and polyunsaturated fatty acids have been associated with a reduced risk of type 2 diabetes 36, 37 and lower fasting and 2-hour glucose concentrations 32, Furthermore, higher proportions of long-chain polyunsaturated fatty acids in skeletal muscle phospholipids have been associated with increased insulin sensitivity In human intervention studies, replacement of saturated by unsaturated fatty acids leads to improved glucose tolerance 40, 41 and enhanced insulin sensitivity Long-chain polyunsaturated fatty acids do not, however, appear to confer additional benefit over monounsaturated fatty acids in intervention studies A high total fat intake has also been associated with higher fasting insulin concentrations and a lower insulin sensitivity index 44, Considered in aggregate these findings are deemed to indicate a probable causal link between saturated fatty acids and type 2 diabetes, and a possible causal association between total fat intake and type 2 diabetes.

The two randomized controlled trials which showed a potential for lifestyle modification to reduce the risk of progression from impaired glucose tolerance to type 2 diabetes included advice to reduce total and saturated fat 22, 23 , but in both trials it is impossible to disentangle the effects of individual dietary manipulation.

Research relating to the association between NSP intake and type 2 diabetes is complicated by ambiguity with regard to the definitions used the term dietary fibre and NSP are often incorrectly used interchangeably , different methods of analysis and, consequently, inconsistencies in food composition tables.

Observations by Trowell in Uganda more than 30 years ago suggested that the infrequency of diabetes in rural Africa may be the result of a protective effect of substantial amounts of NSP in the diet referred to as dietary fibre associated with a high consumption of minimally-processed or unprocessed carbohydrate.

The author also hypothesized that throughout the world, increasing intakes of highly-processed carbohydrate, depleted in NSP, had promoted the development of diabetes In many controlled experimental studies, high intakes of NSP dietary fibre have repeatedly been shown to result in reduced blood glucose and insulin levels in people with type 2 diabetes and impaired glucose tolerance Moreover an increased intake of wholegrain cereals, vegetables and fruits all rich in NSP was a feature of the diets associated with a reduced risk of progression of impaired glucose tolerance to type 2 diabetes in the two randomized controlled trials previously described 22, Thus the evidence for a potential protective effect of NSP dietary fibre appears strong.

Many foods which are rich in NSP especially soluble forms , such as pulses, have a low glycaemic index. Low glycaemic index foods, regardless of their NSP content, are not only associated with a reduced glycaemic response after ingestion when compared with foods of higher glycaemic index, but are also associated with an overall improvement in glycaemic control as measured by haemoglobin A1c in people with diabetes A low glycaemic index does not, however, per se, confer overall health benefits, since a high fat or fructose content of a food may also result in a reduced glycaemic index and such foods may also be energy-dense.

Thus while this property of carbohydrate-containing foods may well influence the risk of developing type 2 diabetes, the evidence is accorded a lower level of strength than the evidence relating to the NSP content. There is insufficient evidence to confirm or refute the suggestions that chromium, magnesium, vitamin E and moderate intakes of alcohol might protect against the development of type 2 diabetes.

A number of studies, mostly in developing countries, have suggested that intrauterine growth retardation and low birth weight are associated with subsequent development of insulin resistance In those countries where there has been chronic undernutrition, insulin resistance may have been selectively advantageous in terms of surviving famine.

In populations where energy intake has increased and lifestyles have become more sedentary, however, insulin resistance and the consequent risk of type 2 diabetes have been enhanced. In particular, rapid postnatal catch-up growth appears to further increase the risk of type 2 diabetes in later life.

Appropriate strategies which may help to reduce type 2 diabetes risk in this situation include improving the nutrition of young children, promoting linear growth and preventing energy excess by limiting intake of energy-dense foods, controlling the quality of fat supply, and facilitating physical activity. At a population level, fetal growth may remain restricted until maternal height improves. This may take several generations to correct. The prevention of type 2 diabetes in infants and young children may be facilitated by the promotion of exclusive breastfeeding, avoiding overweight and obesity, and promoting optimum linear growth.

The strength of evidence on lifestyle factors is summarized in Table 9. Summary of strength of evidence on lifestyle factors and risk of developing type 2 diabetes. Overweight and obesity Abdominal obesity Physical inactivity Maternal diabetes a. Measures aimed at reducing overweight and obesity, and cardiovascular disease are likely to also reduce the risk of developing type 2 diabetes and its complications. Some measures are particularly relevant to reducing the risk for diabetes; these are listed below:.

Maintaining an optimum BMI, i. Voluntary weight reduction in overweight or obese individuals with impaired glucose tolerance although screening for such individuals may not be cost-effective in many countries. Practising an endurance activity at moderate or greater level of intensity e. Achieving adequate intakes of NSP through regular consumption of wholegrain cereals, legumes, fruits and vegetables. A minimum daily intake of 20 g is recommended.

Global burden of diabetes, Diabetes Care , , The rising global burden of diabetes and its complications: Diabetic Medicine , , 14 Suppl. Stemming the tide of diabetes mellitus. Definition, diagnosis and classification of diabetes mellitus and its complications. Diagnosis and classification of diabetes mellitus. Harris MI et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U. Flegal KM et al. Mokdad AH et al. Diabetes trends among American Indians and Alaska natives: The continuing epidemics of obesity and diabetes in the United States.

Kleinman JC et al. Mortality among diabetics in a national sample. American Journal of Epidemiology , , Mortality in adults with and without diabetes in a national cohort of the US population, Roper NA et al.

Excess mortality in a population with diabetes and the impact of material deprivation: British Medical Journal , , Diabetologia , , 44 Suppl.

Sievers ML et al. Diabetes in tropical Africa: Colditz GA et al. Weight as a risk factor for clinical diabetes in women. Després JP et al.

Chan JM et al. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Boyko EJ et al. Visceral adiposity and risk of type 2 diabetes: Health consequences of visceral obesity. Annals of Medicine , , McAuley KA et al. Intensive lifestyle changes are necessary to improve insulin sensitivity.

Tuomilehto J et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. Knowler WC et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention of metformin. A prospective study of exercise and incidence of diabetes among US male physicians. Kriska AM et al. The association of physical activity with obesity, fat distribution and glucose intolerance in Pima Indians.

Diabetologia , , Helmrich SP et al. Physical activity and reduced occurrence of non-insulindependent diabetes mellitus. Pettitt DJ et al. Role of intrauterine environment. Diabetes , , Dabelea D et al. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: Feskens EJM et al. Dietary factors determining diabetes and impaired glucose tolerance.

Bo S et al. Dietary fat and gestational hyperglycaemia. Habitual dietary intake and glucose tolerance in euglycaemic men: International Journal of Epidemiology , , Parker DR et al.

Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: Folsom AR et al. Relation between plasma phospholipid saturated fatty acids and hyperinsulinemia.

Metabolism , , Insulin sensitivity is related to the fatty acid composition of serum lipids and skeletal muscle phospholipids in year-old men. Vessby B et al. Salmeron J et al. Dietary fat intake and risk of type 2 diabetes in women. Meyer KA et al. Dietary fat and incidence of type 2 diabetes in older Iowa women.

Mooy JM et al. Prevalence and determinants of glucose intolerance in a Dutch Caucasian population. Pan DA et al. Skeletal muscle membrane lipid composition is related to adiposity and insulin action. Journal of Clinical Investigation , , Uusitupa M et al. Effects of two high-fat diets with different fatty acid compositions on glucose and lipid metabolism in healthy young women. Substituting polyunsaturated for saturated fat as a single change in a Swedish diet: European Journal of Clinical Investigation , , Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: Marshall JA et al.

Mayer EJ et al. Usual dietary fat intake and insulin concentrations in healthy women twins. Lovejoy J, DiGirolamo M. Habitual dietary intake and insulin sensitivity in lean and obese adults. Dietary-fiber hypothesis of the etiology of diabetes mellitus. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women.

Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. Dietary fibre and diabetes revisited. Simpson HRC et al. A high carbohydrate leguminous fibre diet improves all aspects of diabetic control. Diabetic Medicine , , 1: Chandalia M et al. Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus.

Dietary advice based on the glycaemic index improves dietary profile and metabolic control in type 2 diabetic patients. Diabetic Medicine , , Brand JC et al. Fontvieille AM et al. The use of low glycaemic index foods improves metabolic control of diabetic patients over five weeks.

Diabetic Medicine , , 9: Wolever TMS et al. Beneficial effect of a low glycaemic index diet in type 2 diabetes. Stern MP et al. Birth weight and the metabolic syndrome: Infant and young child nutrition. The second half of the 20th century has witnessed major shifts in the pattern of disease, in addition to marked improvements in life expectancy, this period is characterized by profound changes in diet and lifestyles which in turn have contributed to an epidemic of noncommunicable diseases.

This epidemic is now emerging, and even accelerating, in most developing countries, while infections and nutritional deficiencies are receding as leading contributors to death and disability 1. In developing countries, the effect of the nutrition transition and the concomitant rise in the prevalence of cardiovascular diseases will be to widen the mismatch between health care needs and resources, and already scarce resources will be stretched ever more thinly.

Because unbalanced diets, obesity and physical inactivity all contribute to heart disease, addressing these, along with tobacco use, can help to stem the epidemic. A large measure of success in this area has already been demonstrated in many industrialized countries.

Cardiovascular diseases are the major contributor to the global burden of disease among the noncommunicable diseases. WHO currently attributes one-third of all global deaths In the next two decades the increasing burden of CVD will be borne mostly by developing countries.

Overweight, central obesity, high blood pressure, dyslipidaemia, diabetes and low cardio-respiratory fitness are among the biological factors contributing principally to increased risk. Unhealthy dietary practices include the high consumption of saturated fats, salt and refined carbohydrates, as well as low consumption of fruits and vegetables, and these tend to cluster together. Convincing associations for reduced risk of CVD include consumption of fruits including berries and vegetables, fish and fish oils eicosapentaenoic acid EPA and docosahexaenoic acid DHA , foods high in linoleic acid and potassium, as well as physical activity and low to moderate alcohol intake.

While vitamin E intake appears to have no relationship to risk of CVD, there is convincing evidence that myristic and palmitic acids, trans fatty acids, high sodium intake, overweight and high alcohol intake contribute to an increase in risk. There is a probable increase in risk from dietary cholesterol and unfiltered boiled coffee.

Possible associations for reduced risk include intake of flavonoids and consumption of soy products, while possible associations for increased risk include fats rich in lauric acid, b-carotene supplements and impaired fetal nutrition. The evidence supporting these conclusions is summarized below. The relationship between dietary fats and CVD, especially coronary heart disease, has been extensively investigated, with strong and consistent associations emerging from a wide body of evidence accrued from animal experiments, as well as observational studies, clinical trials and metabolic studies conducted in diverse human populations 2.

Saturated fatty acids raise total and low-density lipoprotein LDL cholesterol, but individual fatty acids within this group, have different effects Myristic and palmitic acids have the greatest effect and are abundant in diets rich in dairy products and meat. Stearic acid has not been shown to elevate blood cholesterol and is rapidly converted to oleic acid in vivo. The most effective replacement for saturated fatty acids in terms of coronary heart disease outcome are polyunsaturated fatty acids, especially linoleic acid.

This finding is supported by the results of several large randomized clinical trials, in which replacement of saturated and trans fatty acids by polyunsaturated vegetable oils lowered coronary heart disease risk 6. Trans fatty acids are geometrical isomers of cis-unsaturated fatty acids that adapt a saturated fatty acid-like configuration.

Partial hydrogenation, the process used to increase shelf-life of polyunsaturated fatty acids PUFAs creates trans fatty acids and also removes the critical double bonds in essential fatty acids necessary for the action. Metabolic studies have demonstrated that trans fatty acids render the plasma lipid profile even more atherogenic than saturated fatty acids, by not only elevating LDL cholesterol to similar levels but also by decreasing highdensity lipoprotein HDL cholesterol 7.

Several large cohort studies have found that intake of trans fatty acids increases the risk of coronary heart disease 8, 9. Most trans fatty acids are contributed by industrially hardened oils. Even though trans fatty acids have been reduced or eliminated from retail fats and spreads in many parts of the world, deep-fried fast foods and baked goods are a major and increasing source 7. When substituted for saturated fatty acids in metabolic studies, both monounsaturated fatty acids and n-6 polyunsaturated fatty acids lower plasma total and LDL cholesterol concentrations 10 ; PUFAs are somewhat more effective than monounsaturates in this respect.

The only nutritionally important monounsaturated fatty acids is oleic acid, which is abundant in olive and canola oils and also in nuts. The most important polyunsaturated fatty acid is linoleic acid, which is abundant especially in soybean and sunflower oils. The most important n-3 PUFAs are eicosapentaenoic acid and docosahexaenoic acid found in fatty fish, and a-linolenic acid found in plant foods.

The biological effects of n-3 PUFAs are wide ranging, involving lipids and lipoproteins, blood pressure, cardiac function, arterial compliance, endothelial function, vascular reactivity and cardiac electrophysiology, as well as potent antiplatelet and anti-inflammatory effects The very long chain n-3 PUFAs eicosapentaenoic acid and docosahexaenoic acid powerfully lower serum triglycerides but they raise serum LDL cholesterol. Therefore, their effect on coronary heart disease is probably mediated through pathways other than serum cholesterol.

Most of the epidemiological evidence related to n-3 PUFAs is derived from studies of fish consumption in populations or interventions involving fish diets in clinical trials evidence on fish consumption is discussed further below. Several prospective studies have found an inverse association between the intake of a-linolenic acid, high in flaxseed, canola and soybean oils , and risk of fatal coronary heart disease 13, Cholesterol in the blood and tissues is derived from two sources: Dairy fat and meat are major dietary sources.

Egg yolk is particularly rich in cholesterol but unlike dairy products and meat does not provide saturated fatty acids. Although dietary cholesterol raises plasma cholesterol levels 15 , observational evidence for an association of dietary cholesterol intake with CVD is contradictory There is no requirement for dietary cholesterol and it is advisable to keep the intake as low as possible 2.

If intake of dairy fat and meat are controlled, there is no need to severely restrict egg yolk intake, although some limitation remains prudent. Dietary plant sterols, especially sitostanol, reduce serum cholesterol by inhibiting cholesterol absorption The cholesterol-lowering effects of plant sterols has also been well documented 18 and commercial products made of these compounds are widely available, but their longterm effects remain to be seen.

Dietary fibre is a heterogeneous mixture of polysaccharides and lignin that cannot be degraded by the endogenous enzymes of vertebrate animals. Water-soluble fibres include pectins, gums, mucilages and some hemicelluloses. Insoluble fibres include cellulose and other hemicelluloses. Most fibres reduce plasma total and LDL cholesterol, as reported by several trials Several large cohort studies carried out in different countries have reported that a high fibre diet as well as a diet high in wholegrain cereals lowers the risk of coronary heart disease Even though antioxidants could, in theory, be protective against CVD and there is observational data supporting this theory, controlled trials employing supplements have been disappointing.

The Heart Outcomes Prevention Evaluation trial HOPE , a definitive clinical trial relating vitamin E supplementation to CVD outcomes, revealed no effect of vitamin E supplementation on myocardial infarction, stroke or death from cardiovascular causes in men or women Also, the results of the Heart Protection Study indicated that no significant benefits of daily supplementation of vitamin E, vitamin C and b-carotene were observed among the high-risk individuals that were the subject of the study In several studies where dietary vitamin C reduced the risk of coronary heart disease, supplemental vitamin C had little effect.

Clinical trial evidence is lacking at present. Observational cohort studies have suggested a protective role for carotenoids but a meta-analysis of four randomized trials, in contrast, reported an increased risk of cardiovascular death The relationship of folate to CVD has been mostly explored through its effect on homocysteine, which may itself be an independent risk factor for coronary heart disease and probably also for stroke.

Folic acid is required for the methylation of homocysteine to methionine. Reduced plasma folate has been strongly associated with elevated plasma homocysteine levels and folate supplementation has been demonstrated to decrease those levels However, the role of homocysteine as an independent risk factor for CVD has been subject to much debate, since several prospective studies have not found this association to be independent of other risk factors 28, It has also been suggested that elevation of plasma homocysteine is a consequence and not a cause of atherosclerosis, wherein impaired renal function resulting from atherosclerosis raises plasma homocysteine levels 30, A recently published metaanalysis concluded that a higher intake of folate 0.

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

High blood pressure is a major risk factor for coronary heart disease and both forms of stroke ischaemic and haemorrhagic. Of the many risk factors associated with high blood pressure, the dietary exposure that has been most investigated is daily sodium intake.

It has been studied extensively in animal experimental models, in epidemiological studies, controlled clinical trials and in population studies on restricted sodium intake 36, All these data show convincingly that sodium intake is directly associated with blood pressure.

An overview of observational data obtained from population studies suggested that a difference in sodium intake of mmol per day was associated with average differences in systolic blood pressure of 5 mmHg at age years and 10 mmHg at age years Diastolic blood pressures are reduced by about half as much, but the association increases with age and magnitude of the initial blood pressure. The first prospective study using hour urine collections for measuring sodium intake, which is the only reliable measure, demonstrated a positive relationship between an increased risk of acute coronary events, but not stroke events, and increased sodium excretion The association was strongest among overweight men.

Several clinical intervention trials, conducted to evaluate the effects of dietary salt reduction on blood pressure levels, have been systematically reviewed 39, Clinical trials have also demonstrated the sustainable blood pressure lowering effects of sodium restriction in infancy 41, 42 , as well as in the elderly in whom it provides a useful nonpharmacological therapy The results of a low-sodium diet trial 44 showed that low-sodium diets, with hour sodium excretion levels around 70 mmol, are effective and safe.

Two population studies, in China and in Portugal, have also revealed significant reductions in blood pressure in the intervention groups 45, Several large cohort studies have found an inverse association between potassium intake and risk of stroke 48, While potassium supplements have been shown to have protective effects on blood pressure and cardiovascular diseases, there is no evidence to suggest that long-term potassium supplements should be administered to reduce the risk for CVD.

The recommended levels of fruit and vegetable consumption assure an adequate intake of potassium. While the consumption of fruits and vegetables has been widely believed to promote good health, evidence related to their protective effect against CVD has only been presented in recent years Numerous ecological and prospective studies have reported a significant protective association for coronary heart disease and stroke with consumption of fruits and vegetables The effects of increased fruit and vegetable consumption on blood pressure alone and in combination with a low-fat diet, were assessed in the Dietary Approaches to Stop Hypertension DASH trial While the combination diet was more effective in lowering blood pressure, the fruit and vegetable diet also lowered blood pressure by 2.

Such reductions, while seeming modest at the individual level, would result in a substantial reduction in population-wide risk of CVD by shifting the blood pressure distribution. Most, but not all, population studies have shown that fish consumption is associated with a reduced risk of coronary heart disease. A systematic review concluded that the discrepancy in the findings may be a result of differences in the populations studied, with only high-risk individuals benefiting from increasing their fish consumption A recent study based on data from 36 countries, reported that fish consumption is associated with a reduced risk of death from all causes as well as CVD mortality Several large epidemiological studies have demonstrated that frequent consumption of nuts was associated with decreased risk of coronary heart disease 58, Most of these studies considered nuts as a group, combining many different types of nuts.

Nuts are high in unsaturated fatty acids and low in saturated fats, and contribute to cholesterol lowering by altering the fatty acid profile of the diet as a whole. However, because of the high energy content of nuts, advice to include them in the diet must be tempered in accordance with the desired energy balance. Several trials indicate that soy has a beneficial effect on plasma lipids 60, Soy is rich in isoflavones, compounds that are structurally and functionally similar to estrogen.

Several animal experiments suggest that the intake of these isoflavones may provide protection against coronary heart disease, but human data on efficacy and safety are still awaited. There is convincing evidence that low to moderate alcohol consumption lowers the risk of coronary heart disease.

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

Boiled, unfiltered coffee raises total and LDL cholesterol because coffee beans contain a terpenoid lipid called cafestol. The amount of cafestol in the cup depends on the brewing method: Intake of large amounts of unfiltered coffee markedly raises serum cholesterol and has been associated with coronary heart disease in Norway A shift from unfiltered, boiled coffee to filtered coffee has contributed significantly to the decline in serum cholesterol in Finland Measures aimed at reducing the risk of CVD are outlined below.

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

Summary of strength of evidence on lifestyle factors and risk of developing cardiovascular diseases. Myristic and palmitic acids Trans fatty acids High sodium intake Overweight High alcohol intake for stroke. Fats rich in lauric acid Impaired fetal nutrition Beta-carotene supplements. The evidence shows that intake of saturated fatty acids is directly related to cardiovascular risk. Within these limits, intake of foods rich in myristic and palmitic acids should be replaced by fats with a lower content of these particular fatty acids.

The amount and quality of fat supply has to be considered keeping in mind the need to meet energy requirements. Specific sources of saturated fat, such as coconut and palm oil, provide low-cost energy and may be an important source of energy for the poor.

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

To promote cardiovascular health, diets should provide a very low intake of trans fatty acids hydrogenated oils and fats. This recommendation is especially relevant in developing countries where low-cost hydrogenated fat is frequently consumed. The potential effect of human consumption of hydrogenated oils of unknown physiological effects e. Diets should provide an adequate intake of PUFAs, i. Recommendations for total fat intake may be based on current levels of population consumption in different regions and modified to take account of age, activity and ideal body weight.

Where obesity is prevalent, for example, an intake in the lower part of the range is preferable in order to achieve a lower energy intake. While there is no evidence to directly link the quantity of daily fat intake to an increased risk of CVD, total fat consumption should be limited to enable the goals of reduced intake of saturated and trans fatty acids to be met easily in most populations and to avoid the potential problems of undesirable weight gain that may arise from unrestricted fat intake.

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

Preference should be given to food preparation practices that employ non-frying methods. Fruits and vegetables contribute to cardiovascular health through the variety of phytonutrients, potassium and fibre that they contain. Daily intake of fresh fruit and vegetables including berries, green leafy and cruciferous vegetables and legumes , in an adequate quantity g per day , is recommended to reduce the risk of coronary heart disease, stroke and high blood pressure.

Dietary intake of sodium, from all sources, influences blood pressure levels in populations and should be limited so as to reduce the risk of coronary heart disease and both forms of stroke. Current evidence suggests that an intake of no more than 70 mmol or 1. The special situation of individuals i. Limitation of dietary sodium intake to meet these goals should be achieved by restricting daily salt sodium chloride intake to less than 5 g per day. This should take into account total sodium intake from all dietary sources, for example additives such as monosodium glutamate and preservatives.

Use of potassium-enriched low-sodium substitutes is one way to reduce sodium intake. Adequate dietary intake of potassium lowers blood pressure and is protective against stroke and cardiac arrythmias. Potassium intake should be at a level which will keep the sodium to potassium ratio close to 1.

This may be achieved through adequate daily consumption of fruits and vegetables. Fibre is protective against coronary heart disease and has also been used in diets to lower blood pressure. Adequate intake may be achieved through fruits, vegetables and wholegrain cereals. Regular fish consumption servings per week is protective against coronary heart disease and ischaemic stroke and is recommended.

The serving should provide an equivalent of mg of eicosapentaenoic and docosahexaenoic acid. People who are vegetarians are recommended to ensure adequate intake of plant sources of a-linolenic acid. Although regular low to moderate consumption of alcohol is protective against coronary heart disease, other cardiovascular and health risks associated with alcohol do not favour a general recommendation for its use.

Physical activity is related to the risk of cardiovascular diseases, especially coronary heart disease, in a consistent inverse dose-response fashion when either volume or intensity are used for assessment.

These relationships apply to both incidence and mortality rates from all cardiovascular diseases and from coronary heart disease. At present, no consistent dose-response relationship can be found between risk of stroke and physical activity. The lower limits of volume or intensity of the protective dose of physical activity have not been defined with certainty, but the current recommendation of at least 30 minutes of at least moderate-intensity physical activity on most days of the week is considered sufficient.

A higher volume or intensity of activity would confer a greater protective effect. The recommended amount of physical activity is sufficient to raise cardiorespiratory fitness to the level that has been shown to be related to decreased risk of cardiovascular disease. Individuals who are unaccustomed to regular exercise or have a high-risk profile for CVD should avoid sudden and high-intensity bursts of physical activity. Cardiovascular diseases in the developing countries: Public Health Nutrition , , 5: Kris-Etherton PM et al.

Summary of the scientific conference on dietary fatty acids and cardiovascular health: Circulation , , Plasma cholesterol responsiveness to saturated fatty acids. Dietary oils, serum lipoproteins and coronary heart disease. American Journal of Clinical Nutrition , , 61 Suppl. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arteriosclerosis and Thrombosis , , Hu FB et al. Dietary fat intake and the risk of coronary heart disease in women.

Trans fatty acids and plasma lipoproteins. Oomen CM et al. Association between trans fatty acid intake and year risk of coronary heart disease in the Zutphen Elderly Study: Willett WC et al. Intake of trans fatty acids and risk of coronary heart disease among women. Monosaturated fatty acids and risk of cardiovascular disease. Long-chain omega 3 fatty acids, blood lipids and cardiovascular risk reduction.

Current Opinion in Lipidology , , Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. Ascherio A et al. Dietary fat and risk of coronary heart disease in men: Effects of dietary cholesterol on serum cholesterol: A prospective study of egg consumption and risk of cardiovascular disease in men and women. Miettinen TA et al. Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population.

Plant sterols and stanol margarines and health. Impact of nondigestible carbohydrates on serum lipoproteins and risk for cardiovascular disease. Journal of Nutrition , , Cereal grains and coronary heart disease. Liu S et al. Whole-grain consumption and risk of coronary heart disease: Pietinen P et al. Intake of dietary fiber and risk of coronary heart disease in a cohort of Finnish men. Rimm EB et al. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men.

Yusuf S et al. Vitamin E supplementation and cardiovascular events in high-risk patients. Heart Protection Study Collaborative Group. Meta-analysis of observational studies. Brouwer IA et al. Low dose folic acid supplementation decreases plasma homocysteine concentrations: Ueland PM et al. The controversy over homocysteine and cardiovascular risk. Nygard O et al. Total plasma homocysteine and cardiovascular risk profile.

The Hordaland Homocysteine Study. Homocysteine and cardiovascular disease: Guttormsen AB et al. Kinetic basis of hyperhomocysteinemia in patients with chronic renal failure. Kidney International , , Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. British Medical Journal, Keli SO et al. Dietary flavonoids, antioxidant vitamins, and incidence of stroke: Archives of Internal Medicine , Hertog MGL et al.

Dietary antioxidant flavonoids and risk of coronary heart disease: Salt and cardiovascular disease: Journal of Cardiovascular Risk , , 7: By how much does salt reduction lower blood pressure? III-Analysis of data from trials of salt reduction. Urinary sodium excretion and cardiovascular mortality in Finland: Randomized trials of sodium reduction: Midgley JP et al. Effect of reduced dietary sodium on blood pressure: Geleijnse JM et al.

Long-term effects of neonatal sodium restriction on blood pressure. Hypertension , , A randomized trial of sodium intake and blood pressure in newborn infants. Whelton PK et al. Sodium reduction and weight loss in the treatment of hypertension in older persons. Sacks FM et al. Forte JG et al. Salt and blood pressure: Journal of Human Hypertension , , 3: Tian HG et al. Changes in sodium intake and blood pressure in a community-based intervention project in China. Journal of Human Hypertension , , 9: Effects of oral potassium on blood pressure.

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