Convincing associations for reduced risk of CVD include consumption of fruits (including berries) and vegetables, fish and fish oils (eicosapentae-noic 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, p-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 (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 high-density 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 anti-platelet 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 long-term effects remain to be seen.
NSP (dietary fibre)
Dietary fibre is a heterogeneous mixture of polysaccharides and lignin that cannot be degraded by the endogenous enzymes of vertebrate animals. Water-soluble fibres include pectins, gums, mucilages and some hemicelluloses. Insoluble fibres include cellulose and other hemicellu-loses. Most fibres reduce plasma total and LDL cholesterol, as reported by several trials (19). Several large cohort studies carried out in different countries have reported that a high fibre diet as well as a diet high in wholegrain cereals lowers the risk of coronary heart disease (20-23).
Antioxidants, folate, and flavonoids
Even though antioxidants could, in theory, be protective against CVD and there is observational data supporting this theory, controlled trials employing supplements have been disappointing. The Heart Outcomes Prevention Evaluation trial (HOPE), a definitive clinical trial relating vitamin E supplementation to CVD outcomes, revealed no effect of vitamin E supplementation on myocardial infarction, stroke or death from cardiovascular causes in men or women (24). Also, the results of the Heart Protection Study indicated that no significant benefits of daily supplementation of vitamin E, vitamin C and b-carotene were observed among the high-risk individuals that were the subject of the study (25). In several studies where dietary vitamin C reduced the risk of coronary heart disease, supplemental vitamin C had little effect. Clinical trial evidence is lacking at present. Observational cohort studies have suggested a protective role for carotenoids but a meta-analysis of four randomized trials, in contrast, reported an increased risk of cardiovascular death (26).
The relationship of folate to CVD has been mostly explored through its effect on homocysteine, which may itself be an independent risk factor for coronary heart disease and probably also for stroke. Folic acid is required for the methylation of homocysteine to methionine. Reduced plasma folate has been strongly associated with elevated plasma homocysteine levels and folate supplementation has been demonstrated to decrease those levels (27). However, the role of homocysteine as an independent risk factor for CVD has been subject to much debate, since several prospective studies have not found this association to be independent of other risk factors (28, 29). It has also been suggested that elevation of plasma homocysteine is a consequence and not a cause of atherosclerosis, wherein impaired renal function resulting from atherosclerosis raises plasma homocysteine levels (30, 31). Data from the Nurses' Health Study showed that folate and vitamin B6, from diet and supplements, conferred protection against coronary heart disease (32). A recently published metaanalysis concluded that a higher intake of folate (0.8 mg folic acid) would reduce the risk of ischaemic heart disease by 16% and stroke by 24% (33).
Flavonoids are polyphenolic compounds that occur in a variety of foods of vegetable origin, such as tea, onions and apples. Data from several prospective studies indicate an inverse association of dietary flavonoids with coronary heart disease (34,35). However, confounding may be a major problem and may explain the conflicting results of observational studies.
High blood pressure is a major risk factor for coronary heart disease and both forms of stroke (ischaemic and haemorrhagic). Of the many risk factors associated with high blood pressure, the dietary exposure that has been most investigated is daily sodium intake. It has been studied extensively in animal experimental models, in epidemiological studies, controlled clinical trials and in population studies on restricted sodium intake (36, 37).
All these data show convincingly that sodium intake is directly associated with blood pressure. An overview of observational data obtained from population studies suggested that a difference in sodium intake of 100 mmol per day was associated with average differences in systolic blood pressure of 5 mmHg at age 15--19 years and 10 mmHg at age 60--69 years (37). Diastolic blood pressures are reduced by about half as much, but the association increases with age and magnitude of the initial blood pressure. It was estimated that a universal reduction in dietary intake of sodium by 50 mmol per day would lead to a 50% reduction in the number of people requiring antihypertensive therapy, a 22% reduction in the number of deaths resulting from strokes and a 16% reduction in the number of deaths from coronary heart disease. The first prospective study using 24-hour urine collections for measuring sodium intake, which is the only reliable measure, demonstrated a positive relationship between an increased risk of acute coronary events, but not stroke events, and increased sodium excretion (38). The association was strongest among overweight men.
Several clinical intervention trials, conducted to evaluate the effects of dietary salt reduction on blood pressure levels, have been systematically reviewed (39, 40). Based on an overview of 32 methodologically adequate trials, Cutler, Follmann & Allender (39) concluded that a daily reduction of sodium intake by 70-80 mmol was associated with a lowering of blood pressure both in hypertensive and normotensive individuals, with systolic and diastolic blood pressure reductions of 4.8/1.9 mmHg in the former and 2.5/1.1 mmHg in the latter. Clinical trials have also demonstrated the sustainable blood pressure lowering effects of sodium restriction in infancy (41, 42), as well as in the elderly in whom it provides a useful non-pharmacological therapy (43). The results of a low-sodium diet trial (44) showed that low-sodium diets, with 24-hour sodium excretion levels around 70 mmol, are effective and safe. Two population studies, in China and in Portugal, have also revealed significant reductions in blood pressure in the intervention groups (45, 46).
A meta-analysis of randomized controlled trials showed that potassium supplements reduced mean blood pressures (systolic/diastolic) by 1.8/1.0 mmHg in normotensive subjects and 4.4/2.5 mmHg in hypertensive subjects (47). Several large cohort studies have found an inverse association between potassium intake and risk of stroke (48, 49). While potassium supplements have been shown to have protective effects on blood pressure and cardiovascular diseases, there is no evidence to suggest that long-term potassium supplements should be administered to reduce the risk for CVD. The recommended levels of fruit and vegetable consumption assure an adequate intake of potassium.
While the consumption of fruits and vegetables has been widely believed to promote good health, evidence related to their protective effect against CVD has only been presented in recent years (50). Numerous ecological and prospective studies have reported a significant protective association for coronary heart disease and stroke with consumption of fruits and vegetables (50-53). The effects of increased fruit and vegetable consumption on blood pressure alone and in combination with a low-fat diet, were assessed in the Dietary Approaches to Stop Hypertension (DASH) trial (54). While the combination diet was more effective in lowering blood pressure, the fruit and vegetable diet also lowered blood pressure (by 2.8 mmHg systolic and 1.1 mmHg diastolic) in comparison to the control diet. Such reductions, while seeming modest at the individual level, would result in a substantial reduction in population-wide risk of CVD by shifting the blood pressure distribution.
Most, but not all, population studies have shown that fish consumption is associated with a reduced risk of coronary heart disease. A systematic review concluded that the discrepancy in the findings may be a result of differences in the populations studied, with only high-risk individuals benefiting from increasing their fish consumption (55). It was estimated that in high-risk populations, an optimum fish consumption of40-60 g per day would lead to approximately a 50% reduction in death from coronary heart disease. In a diet and reinfarction trial, 2-year mortality was reduced by 29% in survivors of a first myocardial infarction in persons receiving advice to consume fatty fish at least twice a week (56). A recent study based on data from 36 countries, reported that fish consumption is associated with a reduced risk of death from all causes as well as CVD mortality (57).
Several large epidemiological studies have demonstrated that frequent consumption of nuts was associated with decreased risk of coronary heart disease (58, 59). Most of these studies considered nuts as a group, combining many different types of nuts. Nuts are high in unsaturated fatty acids and low in saturated fats, and contribute to cholesterol lowering by altering the fatty acid profile of the diet as a whole. However, because of the high energy content of nuts, advice to include them in the diet must be tempered in accordance with the desired energy balance.
Several trials indicate that soy has a beneficial effect on plasma lipids (60, 61). A composite analysis of 38 clinical trials found that an average consumption of 47 g of soy protein a day led to a 9% decline in total cholesterol and a 13% decline in LDL cholesterol in subjects free of coronary heart disease (62). Soy is rich in isoflavones, compounds that are structurally and functionally similar to estrogen. Several animal experiments suggest that the intake of these isoflavones may provide protection against coronary heart disease, but human data on efficacy and safety are still awaited.
There is convincing evidence that low to moderate alcohol consumption lowers the risk of coronary heart disease. In a systematic review of ecological, case--control and cohort studies in which specific associations were available between risk of coronary heart-disease and consumption of beer, wine and spirits, it was found that all alcoholic drinks are linked with lower risk (63). However, other cardiovascular and health risks associated with alcohol do not favour a general recommendation for its use.
Boiled, unfiltered coffee raises total and LDL cholesterol because coffee beans contain a terpenoid lipid called cafestol. The amount of cafestol in the cup depends on the brewing method: it is zero for paper-filtered drip coffee, and high in the unfiltered coffee still widely drunk in, for example, in Greece, the Middle East and Turkey. Intake of large amounts of unfiltered coffee markedly raises serum cholesterol and has been associated with coronary heart disease in Norway (64). A shift from unfiltered, boiled coffee to filtered coffee has contributed significantly to the decline in serum cholesterol in Finland (65).
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