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5. Population nutrient intake goals for preventing diet-related chronic diseases: Previous page | 1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27

5.4 Recommendations for preventing cardiovascular diseases

5.4.1 Background

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

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

5.4.2 Trends

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

5.4.3 Diet, physical activity andcardiovascular disease

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

5.4.4 Strength of evidence

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

Fatty acids and dietary cholesterol

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

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

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

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

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

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

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

5. Population nutrient intake goals for preventing diet-related chronic diseases: 1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27 | Next page

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