Context Coronary heart disease (CHD) remains the leading cause of mortality
in industrialized countries and is rapidly becoming a primary cause of death
worldwide. Thus, identification of the dietary changes that most effectively
prevent CHD is critical.
Objective To review metabolic, epidemiologic, and clinical trial evidence regarding
diet and CHD prevention.
Data Sources and Study Selection We searched MEDLINE through May 2002 for epidemiologic and clinical
investigations of major dietary factors (fat, cholesterol, omega-3 fatty acids, trans-fatty acids, carbohydrates, glycemic index, fiber,
folate, specific foods, and dietary patterns) and CHD. We selected 147 original
investigations and reviews of metabolic studies, epidemiologic studies, and
dietary intervention trials of diet and CHD.
Data Extraction Data were examined for relevance and quality and extracted by 1 of the
authors.
Data Synthesis Compelling evidence from metabolic studies, prospective cohort studies,
and clinical trials in the past several decades indicates that at least 3
dietary strategies are effective in preventing CHD: substitute nonhydrogenated
unsaturated fats for saturated and trans-fats; increase
consumption of omega-3 fatty acids from fish, fish oil supplements, or plant
sources; and consume a diet high in fruits, vegetables, nuts, and whole grains
and low in refined grain products. However, simply lowering the percentage
of energy from total fat in the diet is unlikely to improve lipid profile
or reduce CHD incidence. Many issues remain unsettled, including the optimal
amounts of monounsaturated and polyunsaturated fats, the optimal balance between
omega-3 and omega-6 polyunsaturated fats, the amount and sources of protein,
and the effects of individual phytochemicals, antioxidant vitamins, and minerals.
Conclusions Substantial evidence indicates that diets using nonhydrogenated unsaturated
fats as the predominant form of dietary fat, whole grains as the main form
of carbohydrates, an abundance of fruits and vegetables, and adequate omega-3
fatty acids can offer significant protection against CHD. Such diets, together
with regular physical activity, avoidance of smoking, and maintenance of a
healthy body weight, may prevent the majority of cardiovascular disease in
Western populations.
The relationship between diet and coronary heart disease (CHD) has been
studied intensively for nearly a century. In 1908, Ignatowski produced atherosclerosis
in rabbits with a diet high in cholesterol and saturated fat1;
feeding the rabbits cholesterol alone produced identical lesions. In the early
1950s, controlled feeding studies demonstrated that saturated fatty acids
and, to a lesser extent, cholesterol increased serum cholesterol concentration
in humans.2 Meanwhile, epidemiologic studies
found that increased serum cholesterol predicted risk of CHD in human populations.
These discoveries led to the classic diet-heart hypothesis, which postulated
a primary role of dietary saturated fat and cholesterol in the cause of atherosclerosis
and CHD in humans.3 The diet-heart hypothesis
gained further support from ecological correlations relating saturated fat
intake to rates of CHD in cohorts from different countries4 and
from studies of migrants from low- to high-risk countries.5
Until recently, most epidemiologic and clinical investigations of diet
and CHD have been dominated by the diet-heart hypothesis. However, the original
hypothesis was overly simplistic because the effects of diet on CHD can be
mediated through multiple biological pathways other than serum total cholesterol
or low-density lipoprotein cholesterol (LDL-C) (Figure 1).6 The existence of these
multiple pathways heightens the need to study clinical outcomes because the
use of a single intermediate end point as a surrogate of CHD risk could be
misleading. In the past 2 decades, understanding of the nutrients and foods
likely to promote cardiac health has grown substantially owing to studies
of the molecular mechanisms of atherosclerosis and the metabolic effects of
various nutrients and foods, large and carefully conducted prospective cohort
investigations, and dietary intervention trials. Although the search for the
optimal diet for prevention of CHD is far from over, more specific and firmer
evidence on diet and CHD is now available.
For this review, we searched MEDLINE through May 2002 for epidemiologic
and clinical investigations of various dietary factors (fat, cholesterol,
omega-3 fatty acids, trans-fatty acids, carbohydrates,
glycemic index, fiber, folate, specific foods, and dietary patterns) and CHD.
We selected 147 original investigations and reviews of metabolic studies,
epidemiologic studies, and dietary intervention trials relating to diet and
CHD. Data were examined for relevance and quality and extracted by 1 of the
authors. Although we emphasized controlled trials with clinical end points,
few such trials exist. Thus, we gave substantial weight to large prospective
cohort studies that reported disease outcomes and metabolic studies with established
intermediate end points. The evidence is considered strongest when results
from different types of studies are consistent.
Metabolic Effects of Dietary Fatty Acids
Numerous controlled feeding studies of the effects of different dietary
fatty acids on serum cholesterol levels have been summarized in several meta-analyses
from which predictive equations have been developed.7-11 All
such analyses confirm early reports by Keys7 and
Hegsted8 that saturated fatty acids increase
and polyunsaturated fatty acids decrease total and LDL cholesterol. All 3
classes of fatty acids (saturated, monounsaturated, and polyunsaturated) elevate
high-density lipoprotein cholesterol (HDL-C) when they replace carbohydrates
in the diet, and this effect is slightly greater with saturated fatty acids
(Figure 2). Also, triglyceride levels
increase when dietary fatty acids are replaced by carbohydrates. Because replacement
of saturated fat with carbohydrates proportionally reduces both LDL-C and
HDL-C, and, thus, has little effect on the LDL-HDL ratio and increases triglycerides,
this change in diet would be expected to have minimal benefit on CHD risk.
However, when monounsaturated or polyunsaturated fats replace saturated fat,
LDL-C decreases and HDL-C changes only slightly. Moreover, substituting polyunsaturated
fat for saturated fat may have beneficial effects on insulin sensitivity12,13 and type 2 diabetes.14,15
In numerous controlled metabolic studies, trans-fatty
acids (found in stick margarine, vegetable shortenings, and commercial bakery
and deep-fried foods) have been shown to raise LDL-C levels and lower HDL-C
relative to cis-unsaturated fatty acids,16-24 and
the increase in the ratio of total to HDL cholesterol for trans-fat is approximately twice that for saturated fat (Figure 3).25Trans-fat increases plasma levels of lipoprotein a18,23 and
triglycerides26 and may reduce endothelial
function by impairing flow-mediated dilation.27 In
addition, trans-fatty acids adversely affect essential
fatty acid metabolism and prostaglandin balance by inhibiting the enzyme delta-6
desaturase.28,29 Finally, high
intake of trans-fat may promote insulin resistance30 and increase risk of type 2 diabetes.15
Geographic and migration studies showed strong positive correlations
between saturated fat intake and rates of CHD.4,5,31 Although
these data provide evidence for the importance of environmental factors in
the cause of CHD, they are seriously confounded by other aspects of diet,
other lifestyle factors, and economic development. Prospective cohort studies
of individuals can better control for potential confounding factors. Despite
long-standing interest in the diet-heart hypothesis, prospective studies of
diet and CHD are surprisingly few32-40;
only 2 found a significant positive association between saturated fat intake
and risk of CHD.35,36 However,
most earlier studies were limited by small study size, inadequate dietary
assessment, or incomplete adjustment for confounding.41
The largest and most detailed analysis included 4 repeated measures
of diet over 14 years among 80 082 women in the Nurses' Health Study
cohort.40 Higher intakes of trans-fat and, to a smaller extent, saturated fat were associated with
increased risk, whereas higher intakes of nonhydrogenated polyunsaturated
and monounsaturated fats were associated with decreased risk. Because of opposing
effects of different types of fat, total fat as percentage of energy was not
appreciably associated with CHD risk. Dietary cholesterol and modest egg consumption
(1 egg per day) were not significantly associated with either CHD or stroke.42
In addition to the Nurses' Health Study, 3 other large prospective studies
have consistently found elevated risk of CHD with higher trans-fat intake.38,39,43 Combining
the results of the 4 prospective studies, the pooled relative risk of CHD
associated with a difference of 2% energy in trans-fatty
acid intake (assessed at baseline) was 1.25 (95% confidence interval, 1.11-1.40).43 Results from case-control studies using biochemical
markers of trans-fat intake have been less consistent.25 In a recent population-based case-control study of
179 cardiac arrest patients and 285 community controls, higher red-cell membrane
levels of trans-fatty acids, especially trans-isomers frompartially hydrogenated vegetable oils, were associated
with significantly increased risk of primary cardiac arrest.44 No
association was seen in a small UK study of sudden death.45
Trials of Change in Dietary Fat
Only a handful of dietary trials with CHD end points have been conducted
and most were among patients with CHD (Table 1). Two dietary approaches were tested in earlier trials;
one replaced saturated fat with polyunsaturated fat, leaving total fat unchanged;
the other lowered total fat. In all the high-polyunsaturated-fat trials,46-51 serum
cholesterol was significantly reduced. In the Finnish Mental Hospital Study,47 soft margarine replaced stick margarine, so the reduction
in CHD was probably in part due to reduction in trans-fat
intake. In the Minnesota Coronary Survey,51 cardiovascular
events were not significantly reduced by a high-polyunsaturated-fat diet despite
a decrease in serum cholesterol, but the mean duration of dietary intervention
was only about 1 year. Two secondary prevention trials testing the approach
of total fat reduction did not find a significant reduction in serum cholesterol
or CHD events.52,53
Omega-3 fatty acids may reduce risk of CHD by preventing cardiac arrhythmia,
lowering serum triglyceride levels, decreasing thrombotic tendency, and improving
endothelial dysfunction.54,55 An
inverse association between fish intake and coronary mortality was first reported
in a Dutch population,56 and more than 15 prospective
studies have followed. A systematic review of the 11 studies published before
2000 concluded that the inverse association was stronger for fatal CHD than
for nonfatal myocardial infarction (MI), and the benefit was most evident
in populations with higher-than-average risk of CHD.57 Since
that review, 4 additional prospective cohort studies58-61 and
1 case-control study62 have provided further
support for the protective effects of marine omega-3 fatty acids against CHD
in diverse populations. Notably, 2 recent studies have shown that consuming
2 or more servings of fish per week was associated with 30% lower risk of
CHD in women60 and that blood levels of eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA) were strongly associated with decreased
risk of sudden cardiac death in men.61
α-Linolenic acid (ALA), an omega-3 fatty acid high in flaxseed,
canola, and soybean oils, can be converted to EPA and DHA in humans and, thus,
may have a role in prevention of CHD. An inverse association between intake
of ALA and risk of fatal CHD was observed in most prospective cohort studies,38,39,63,64 but
not in 1 smaller study.65 In a cohort of women,
frequent consumption of oil-and-vinegar salad dressing (a major source of
ALA in US diets) was associated with a significantly lower risk of fatal CHD.63
Three clinical trials have examined the effects of omega-3 fatty acids
in secondary prevention of CHD (Table 1). In the Diet and Reinfarction Trial,53 patients
advised to eat fish twice weekly or to take fish oil (1.5 g/d) had a 29% lower
mortality after 2 years. In the GISSI-Prevenzione trial,66 daily
supplementation with EPA plus DHA (1 g/d) reduced the main end point (composite
of death, nonfatal MI, and stroke) by 15%, primarily because of a 45% reduction
in sudden death after 3 months of treatment.67 A
trial from India suggested benefits of both fish oil and mustard oil in the
treatment of MI patients.68 In the Lyon Diet
Heart Study, higher ALA consumption in the context of a Mediterranean diet
dramatically reduced total and cardiovascular mortality as well as nonfatal
MI.69,70 These trials strongly
support the protective effects of omega-3 fatty acids, including both ALA
and fish oil, in secondary prevention of CHD. The role of fish oil supplements
in primary prevention of CHD has not been tested.
Prevailing dietary recommendations have emphasized high intake of complex
carbohydrates, mainly starch, and avoidance of simple sugars.71,72 However,
many starchy foods, such as baked potatoes and white bread, are rapidly digested
to glucose and produce even higher glycemic and insulinemic responses than
sucrose (half glucose and half fructose). The glycemic index (GI) ranks foods
based on rise in blood glucose (the incremental area under the curve for blood
glucose levels) after ingestion compared with glucose or white bread, standardizing
the carbohydrate content to 50 g.73,74 Foods
with a low degree of starch gelatinization (more compact granules), such as
spaghetti and oatmeal, and a high level of viscose soluble fiber, such as
barley, oats, and rye, tend to have a slower rate of digestion and, thus,
lower GI values. In several controlled clinical studies,75 feeding
low-GI meals to diabetic patients led to significant improvement in glycemic
control and lipid profile, but larger studies are needed.
Glycemic load (GL; the product of the GI value of a food and its carbohydrate
content) has been used to represent both the quality and quantity of the carbohydrates
consumed.76,77 Dietary GL is more
strongly associated with higher fasting triglycerides and lower HDL-C levels
compared with GI.78 A strong positive association
between GL and risk of CHD was observed among 75 521 women during 10
years of follow-up.79 The increased risk was
more pronounced among overweight and obese women, consistent with metabolic
studies that the adverse effects of a high GL diet are exacerbated by underlying
insulin resistance.80 Thus, carbohydrate-containing
foods should not be judged simply by their GI values; the amount of carbohydrates,
fiber, and other nutrients are also important.
Another way to classify dietary carbohydrates is to subdivide cereal
grains—staple foods in most societies—into whole and refined grains.
Most cereal grains are highly processed before they are consumed. Refined
grain products contain more starch but substantially lower amounts of dietary
fiber, essential fatty acids, and phytochemicals, although these products
are typically enriched with some vitamins and minerals. In several epidemiologic
studies, higher consumption of whole grains was associated with lower risk
of CHD. Also, prospective cohort studies have consistently found an inverse
association between fiber intake and risk of CHD.81 Several
studies have found a stronger association for cereal fiber than for fruit
or vegetable fiber.82-84 The
inverse association for fiber observed in epidemiologic studies cannot be
fully explained by its cholesterol-lowering effects; the low GI of foods with
a high level of fiber and numerous micronutrients in whole grains may also
contribute to the benefits.85
Much evidence suggests that adequate folate consumption is important
for the prevention of CHD. Epidemiologic studies have found an inverse association
between folate intake measured by dietary questionnaire or serum folate level
and risk of CHD,86-90 which
is likely to be mediated through homocysteine-lowering effects of folic acid.
Two randomized placebo-controlled trials evaluated effects of folic acid supplementation
on the development and progression of atherosclerosis. Vermeulen et al91 found that supplementation with folic acid and vitamin
B6 for 2 years significantly decreased subclinical atherosclerosis
indicated by abnormal exercise electrocardiography tests among siblings of
patients with existing cardiovascular disease. In the Swiss Heart Study, treatment
with a combination of folic acid and vitamins B6 and B12 significantly
decreased restenosis and revascularization after coronary angioplasty at 6
months92 and a combined cardiovascular end
point at 11 months.93 Ongoing clinical trials
should provide more definitive data on the role of folic acid supplementation
in CHD prevention, but the interpretation of the findings from trials conducted
in the United States could be complicated by the fortification of flour with
folic acid.94
Specific foods and dietary patterns
The relationship between consumption of specific foods or overall dietary
patterns and risk of CHD has been examined in recent studies. Such analyses
are valuable in evaluating additional diet-heart hypotheses and in making
practical dietary recommendations. For example, replacement of red meat with
chicken and fish has been associated with reduced risk of CHD.95 An
inverse association between nut consumption and risk of CHD has been seen
consistently in prospective studies.96-101 (Figure 4), which further underscores the
importance of distinguishing different types of fat. Although nuts are high
in fat and, thus, routinely proscribed in dietary recommendations, the predominant
types of fat in nuts are monounsaturated and polyunsaturated, which lower
LDL-C level.102
Although beneficial effects of fruits and vegetables are widely assumed,
only in recent years has solid epidemiologic evidence begun to emerge103-110 (Figure 4). In the largest study, including
84 251 women and 42 148 men,107 Joshipura
et al reported a significant inverse association between consumption of fruits
and vegetables, particularly green leafy vegetables and vitamin C–rich
fruits and vegetables, and risk of CHD. Increased consumption of potatoes,
however, was not associated with benefits. In several prospective studies,
a higher consumption of whole grains as opposed to refined grains was associated
with a lower risk of cardiovascular disease (Figure 4).96,111-113
Recently, several studies have reported the role of overall dietary
patterns in predicting long-term risk of CHD.114 In
these analyses, a "prudent" pattern characterized by higher intakes of fruits,
vegetables, legumes, whole grains, poultry, and fish was associated with lower
risk of CHD, whereas a "Western" pattern characterized by higher intakes of
red and processed meats, sweets and desserts, potatoes, french fries, and
refined grains was associated with a higher risk, independent of lifestyle
factors.115,116
Two randomized trials tested the whole-diet approach in secondary prevention
of CHD (Table 1). In the Indian
Heart Study,117 a semivegetarian diet enriched
with fruits, vegetables, whole grains, and nuts reduced coronary death by
41% and nonfatal MI by 38%. In the Lyon Diet Heart Study,69,70 a
Mediterranean diet enriched with ALA reduced CHD death by more than 70%. These
findings, together with the results from prospective cohort studies and the
Dietary Approaches to Stop Hypertension trials,118,119 support
the clinical utility of a whole-diet approach in the prevention of cardiovascular
disease.
Combined effects of diet and lifestyle
The combination of multiple dietary factors is more powerful than a
single factor alone. In the Nurses' Health Study cohort, a diet high in cereal
fiber, marine omega-3 fatty acids, and folate and low in trans-fat and GL, with a high ratio of polyunsaturated fat to saturated
fat, strongly predicted decreased risk of CHD (relative risk comparing highest
with lowest quintiles of the composite score = 0.40; 95% confidence interval,
0.31-0.53).120 Also, improvement in these dietary
factors explained much of the decline in the incidence of CHD during 14 years
of follow-up of the cohort.121
Besides diet, several other behavioral factors strongly influence CHD
risk. Analyses from the Nurses' Health Study estimated that 82% of CHD events
in the study cohort could be potentially prevented by moderate diet and lifestyle
modifications.120 Among nonsmokers, 74% of
coronary events might have been prevented by eating a healthy diet, maintaining
a healthy body weight, exercising regularly for half an hour or more daily,
and consuming a moderate amount of alcohol (≥5 g/d).
Results from several multifactorial primary prevention trials using
diet and lifestyle intervention have been largely unimpressive, probably because
of poor compliance and inadequate power.122 The
Oslo Heart Study, however, demonstrated that stopping smoking and increasing
the ratio of polyunsaturated to saturated fats in the diet reduced CHD incidence
by 47% among men with higher-than-average serum cholesterol levels.123 In the Lifestyle Heart Study,124 a
combination of an extremely low-fat diet, exercise, stress management, and
yoga significantly reduced progression of atherosclerosis, but the low-fat
regimen is unnecessarily rigid and difficult for most people to follow.
The optimal amounts of monounsaturated and polyunsaturated fats in the
diet are still unclear. Intake of linoleic acid is usually recommended not
to exceed 10% of energy, in part because of little long-term human experience
with such diets, although benefits from higher intake exist for blood lipids.
There has been some concern that a high-polyunsaturated-fat diet may increase
cancer risk, but this has not been substantiated in large epidemiologic studies.125
The optimal balance between omega-3 and omega-6 polyunsaturated fatty
acids also remains unsettled. Some have proposed reducing the consumption
of linoleic acid to achieve a greater ratio of omega-3 to omega-6 fatty acids
in the diet.126,127 However, there
is little evidence that a higher ratio predicts a lower risk of CHD.128 Both omega-3 and omega-6 fatty acids have important
roles in reducing CHD risk, probably through different mechanisms. Thus, a
good strategy is to substantially increase intake of omega-3 fatty acids from
fish and plant sources (because intake for many people is clearly suboptimal)
without decreasing intake of linoleic acid. This will improve the ratio and
maximize the cardioprotective benefits of both omega-3 and omega-6 fatty acids.
The amount and type of protein in the diet is a matter of debate. Substitution
of soy for animal protein reduces LDL-C,129 and
substituting animal protein for carbohydrates raises HDL-C and lowers triglyceride
levels.130 Consistent with the metabolic studies,
a prospective cohort study found that a moderately high protein intake (24%
vs 15% of energy from protein) was associated with a significantly lower risk
of CHD after adjustment for cardiovascular risk factors and dietary fat intake.131 To avoid an increase in saturated fat intake, the
major source of protein in the diet should come from nuts, soybeans, legumes,
poultry, and fish.
The role of phytochemicals and antioxidants in the prevention of CHD
is promising but unsettled. The cholesterol-lowering effects of plant sterol
or stanol (saturated sterols) have been well documented in clinical trials132 and commercial products made of these compounds
are widely available, but their long-term effects remain to be seen. Six prospective
cohort studies have evaluated the association between flavonoid intake and
risk of CHD. A significant inverse association was observed in some studies133-136 but
not others.137,138 Although a
body of experimental evidence has demonstrated the role of antioxidant vitamins
in reducing oxidative stress and substantial epidemiologic evidence has linked
intake of vitamin E with a lower CHD risk, results from published clinical
trials of vitamin E supplements, primarily among patients with clinical CHD,
have been largely disappointing.139,140 Ongoing
primary prevention trials should provide more insights.
Finally, a large and inconclusive literature has examined the relationship
between dietary minerals such as calcium, magnesium, zinc, and selenium and
risk of CHD.41 Most studies have been based
on ecological correlations or case-control analyses. Additional large prospective
studies or randomized trials with clinical end points are required to resolve
the role of individual minerals from diet or supplements.
Compelling evidence from metabolic studies, epidemiologic investigations,
and clinical trials in the past several decades converges to indicate that
at least 3 dietary strategies are effective in preventing CHD: substitute
unsaturated fats (especially polyunsaturated fat) for saturated and trans-fats; increase consumption of omega-3 fatty acids
from fish oil or plant sources; and consume a diet high in fruits, vegetables,
nuts, and whole grains and low in refined grains. A combination of these approaches
can confer greater benefits than a single approach. However, simply lowering
the percentage of energy from total fat in the diet is unlikely to improve
lipid profile or reduce CHD incidence.
Obesity is an important avenue by which diet can influence risk of CHD.
However, the relationship between diet, especially dietary fat, and obesity
remains controversial. Although reduction in percentage of calories from dietary
fat intake is commonly recommended for weight loss, long-term clinical trials
have provided no good evidence that reducing dietary fat per se can lead to
weight loss.141,142 There is a
growing consensus that excess calories, whether from carbohydrates or fat,
will induce weight gain. A mildly hypocaloric moderate-fat diet, which allows
for a great variety in choosing foods, can have better long-term compliance
than a typical low-fat diet.143 Small short-term
studies have suggested roles of several diets in weight control, including
a low-GI diet,144 a high-protein diet,145,146 and a diet high in dairy products,147 but larger and long-term studies are needed.
Although prevailing dietary guidelines emphasize target intake of specific
macronutrients (eg, not exceeding 30% of energy from fat),71 such
numerical criteria are not based on solid scientific evidence, and the public
finds it difficult to make dietary changes based on such criteria. A variety
of options exist for designing attractive and heart-healthy diets, with varying
amounts of fat and carbohydrates, as long as the diet embraces healthy types
of fat and carbohydrates and provides an appropriate balance in energy intake
and expenditure. Evidence is now clear that diets including nonhydrogenated
unsaturated fats as the predominant form of dietary fat, whole grains as the
main form of carbohydrate, an abundance of fruits and vegetables, and adequate
omega-3 fatty acids can offer significant protection against CHD. Such diets,
together with regular physical activity, avoidance of smoking, and maintaining
a healthy weight, may prevent the majority of cardiovascular disease in Western
populations.
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