Académique Documents
Professionnel Documents
Culture Documents
The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://circ.ahajournals.org/content/123/24/2870
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published
in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial
Office. Once the online version of the published article for which permission is being requested is located,
click Request Permissions in the middle column of the Web page under Services. Further information about
this process is available in the Permissions and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Circulation is online at:
http://circ.ahajournals.org//subscriptions/
Methods
Evidence for effects of dietary factors on cardiometabolic health was
reviewed, often derived from recent comprehensive reviews performed for policy-making or similar activities, including those of the
American Heart Association (AHA) 2020 Impact Goals Committee
(D.M., L.J.A.),7 the AHA Nutrition Committee (D.M., L.J.A.,
L.V.H.),8,9 the US Dietary Guidelines Advisory Committee (L.J.A.,
L.V.H.),10 the World Health Organization Expert Consultation on
Fats and Fatty Acids in Human Nutrition (D.M.),11 the World Health
Organization Global Burden of Diseases, Risk Factors, and Injuries
Foods
Randomized, controlled trials (RCTs) of cardiometabolic risk
factors and prospective cohort studies of disease end points
provide strong concordant evidence for cardiovascular effects
of several specific foods. In contrast with individual nutrients
in isolation, health effects of foods likely represent the
synergy of composite effects and interactions of multiple
factors, including carbohydrate quality, fiber content, specific
fatty acids and proteins, preparation methods, food structure,
and bioavailability of inherent micronutrients and phytochemicals.6,16,17 Dietary patterns based on particular foods/
components (Table 1) have established cardiometabolic benefits and are higher in dietary fiber, healthy fatty acids,
vitamins, antioxidants, potassium, other minerals, and phytochemicals and lower in refined carbohydrates, sugars, salt,
saturated fatty acid (SFA), dietary cholesterol, and trans fat.
From the Division of Cardiovascular Medicine and Channing Laboratory, Brigham and Womens Hospital and Harvard Medical School, and
Departments of Epidemiology and Nutrition, Harvard School of Public Health; Boston, MA (D.M.); Welch Center for Prevention, Epidemiology and
Clinical Research, Johns Hopkins University, Baltimore, MD (L.J.A.); and Department of Preventive Medicine, Feinberg School of Medicine,
Northwestern University, Chicago, IL (L.V.H.).
Correspondence to D. Mozaffarian, 665 Huntington Ave, Bldg 2-319, Boston, MA 02115. E-mail dmozaffa@hsph.harvard.edu
(Circulation. 2011;123:2870-2891.)
2011 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org
DOI: 10.1161/CIRCULATIONAHA.110.968735
Mozaffarian et al
Table 1.
2871
Serving Sizes
Nutrient Benefits
Fruits
Vegetables
Dairy products
Vegetable oils
Consume more:
Whole grains
Nuts
Consume less:
Fats, oils, or foods containing
or made with partially
hydrogenated vegetable oils
Avoid intake
50 g (1.75 oz)
Sugar-sweetened beverages,
sweets, and grain-based
desserts and bakery foods
Alcohol
Energy balance
*On the basis of the evidence described in this review, and generally consistent with US Department of Agriculture and American Heart Association guidelines and
the American Heart Association 2020 Impact Goals. Food-based recommendations can facilitate communication and translation to both individual patients and
populations. Some specific individual nutrients, such as sodium and industrially produced trans fats, are also highly relevant and can be successfully targeted by policy
measures to reduce their consumption.
Based on a 2000-kcal/d diet. Servings should be adjusted accordingly for higher or lower energy consumption.
Or potentially, whole legumes (beans), although evidence for equivalent effects is limited. Characterization of whole grain content in packaged foods is challenging;
pragmatically, sufficient whole grain content was defined by the American Heart Association 2020 Impact Goals7 as the fiber content of whole wheat, ie, at least 1.1 g
of naturally occurring dietary fiber per 10 g of carbohydrate in the grain product.
Because of alcohol-related accidents, homicides, and suicides, especially among younger adults, alcohol use has an overall net adverse effect on population
mortality.2 Thus, alcohol use is not advisable as a population-based strategy to reduce cardiovascular risk. For adults who already drink alcohol, no more than
moderate use should be encouraged.
Higher levels of physical activity may be needed to promote prolonged negative energy balance, ie, sustained weight loss.
2872
Circulation
Figure 1. Relationships of consumption of different foods with incidence of coronary heart disease (CHD), stroke, and diabetes in metaanalyses of prospective cohort studies (PCs). Adapted with permission from Mozaffarian.29 Dashes indicate not reported; CVD, cardiovascular disease; and RR (95% CI), relative risk (95% confidence interval).
Mozaffarian et al
This evidence suggests that benefits might be derived from
(1) a more complex set of micronutrients, phytochemicals,
and fiber found in fruits and vegetables; (2) potentially
enhanced bioavailability of these nutrients in their natural
state; and/or (3) replacement of less healthful foods in the
diet. In long-term observational studies, greater fruit and
vegetable consumption are each associated with lower incidence of coronary heart disease (CHD), and greater fruit
consumption is associated with lower incidence of stroke
(Figure 1).27,28 The results of RCTs of physiological measures
and prospective cohorts of disease outcomes together provide
strong concordant evidence that fruit and vegetable consumption lowers CVD risk (Table 2). Potential differences in
health effects contributed by specific types of fruits, vegetables, or their juices require further investigation.
Whole Grains
Although no single accepted definition of whole grain
exists, whole grains generally comprise bran, germ, and
endosperm from the natural cereal. Bran contains soluble
and insoluble dietary fiber, B vitamins, minerals, flavonoids, and tocopherols; germ contains numerous fatty
acids, antioxidants, and phytochemicals. Endosperm provides largely starch (carbohydrate polysaccharides) and
storage proteins.30 The type and extent of processing
appear to modify the health effects of grain and carbohydrate consumption (Figure 2). For example, removal of
bran and germ reduces dietary fiber that has important
benefits, including lowering of BP and cholesterol levels31,32; increases bioavailability and rapidity of digestion
of remaining endosperm, which increases glycemic responses33; and eliminates minerals, micronutrients, and
other phytochemicals that may have additional independent health benefits16 (see Carbohydrate Amount and
Quality).
In RCTs, consumption of whole grains improves glucoseinsulin homeostasis and endothelial function and possibly
reduces inflammation and improves weight loss.34 36 Consumption of whole grain oats reduces low-density lipoprotein
(LDL) cholesterol without reducing high-density lipoprotein
cholesterol or raising triglycerides.37 Consistent with physiological benefits, greater whole grain consumption is associated with lower incidence of CHD, DM, and possibly stroke
(Figure 1). The higher dietary fiber in whole grains contributes to these benefits. In RCTs, increased dietary fiber
reduces serum triglycerides, LDL cholesterol, blood glucose,
and BP.31,32 Emerging evidence supports additional independent contributions to health from other characteristics of
whole grains, including slower digestion (lower glycemic
responses) and higher content of minerals, phytochemicals,
and fatty acids.16,17 Thus, similar to fruits and vegetables,
health effects of whole grains may result from synergistic
effects of multiple constituents that are unlikely to be
matched by supplemental fiber alone, added bran, or isolated
micronutrients, as well as from dietary substitution for more
highly refined/processed carbohydrates and starches that may
2873
themselves induce adverse cardiometabolic effects (see Carbohydrate Amount and Quality).
Improved nutritional assessment techniques and databases are needed to further quantify and evaluate potential
contributions to health of each component of whole grains.
Evidence-based yet pragmatic definitions of what constitutes a whole grain food (Figure 2) are also essential to
reduce public confusion and allow consumers to choose
healthy grains wisely. As one example, to help monitor
national progress toward achieving dietary goals, the AHA
2020 Impact Goals developed a pragmatic definition of
whole grains based on the fiber content of whole wheat, ie,
1.1 g of naturally occurring dietary fiber per 10 g of
carbohydrate in the grain product (eg, bread, cracker, etc).7
Fish
Fish and other seafood contain several healthful constituents, including specific proteins, unsaturated fats, vitamin
D, selenium, and long-chain omega-3 polyunsaturated
fatty acids (PUFAs), which include eicosapentaenoic acid
(EPA; 20:5 omega-3) and docosahexaenoic acid (DHA;
22:6 omega-3). In humans, EPA and especially DHA are
synthesized in low amounts (5%) from their plantderived precursor, -linolenic acid (18:3 omega-3).38
Thus, tissue levels of EPA plus DHA are strongly influenced by their direct dietary consumption. Average EPA
plus DHA contents of different seafood species vary by
10-fold. Fatty (oily) fish such as anchovies, herring,
farmed and wild salmon, sardines, trout, and white tuna
tend to have the highest concentrations.39
In vitro and animal experiments suggest that fish oil has
direct antiarrhythmic effects,40 but trials to establish direct
antiarrhythmic effects in patients with preexisting arrhythmias have been inconsistent.41,42 In human trials, fish oil
lowers triglyceride levels,43 systolic and diastolic BP,44
and resting heart rate.45 Observational and RCT evidence
suggests that fish or fish oil consumption may also reduce
inflammation, improve endothelial function, normalize
heart rate variability, improve myocardial relaxation and
efficiency, and, at high doses, limit platelet aggregation.46
Consistent with these physiological benefits, habitual
fish consumption is associated with lower incidence of
CHD and ischemic stroke, especially risk of cardiac death
(Figure 1), among generally healthy populations.39,47,48
Compared with no fish consumption, consumption of
250 mg/d EPA plus DHA from fish is associated with
36% lower CHD mortality.39 Fish and fish oil are among
only a handful of dietary factors for which both long-term
observational studies and RCTs of CVD outcomes have
been performed (Table 2). Four of 8 large RCTs of fish or
fish oil, including participants with and without prevalent
heart disease, documented significant reductions in CHD
events.46 Several of these RCTs had relevant limitations.46
In meta-analyses of RCTs, fish oil supplementation significantly reduced cardiac mortality, including fatal CHD and
sudden cardiac death.46,49,50 Overall, these findings are
concordant with long-term observational studies of habitual fish intake in generally healthy populations and with
physiological benefits of fish or fish oil in intervention
2874
Circulation
Table 2.
Evidence From Human Studies Using Different Research Paradigms for Effects of Selected Foods, Nutrients, and Dietary
Patterns on Cardiovascular Diseases
Ecologic Studies of Clinical
End Points*
Randomized Trials of
Risk Factors
Vegetables
Whole grains
Fish
Processed meats
Nuts
Dairy
Sodium
Dietary fiber
Total fat
Trans fat
Saturated fat
Carbohydrate
Saturated fat
72
Carbohydrate
Carbohydrate
1 7
Sugar-sweetened beverages
Alcohol
Nutrients
Vegetarian
Japanese
DASH
Mediterranean
Dashes () indicate too few studies performed to provide meaningful evidence; , conflicting or limited supporting evidence; , some evidence from a relatively
limited number of studies, but with relevant shortcomings (eg, insufficient numbers of studies, limited types of populations, inadequate sample sizes, or insufficient
follow-up) or relevant evidence to the contrary that raises important questions; , fairly consistent evidence from several well-conducted studies, but with some
perceived shortcomings in the available evidence or some evidence to the contrary that precludes a more definite judgment; , consistent evidence from
multiple well-conducted studies, with little or no evidence to the contrary; 2, evidence for benefit (lower risk) from higher intake; 1, evidence for harm (increased
risk) from higher intake; 7, evidence for no appreciable effects (null); and DASH, Dietary Approaches to Stop Hypertension.
*Based on the strongest evidence for effects on any single major clinical end point, including coronary heart disease, stroke, or diabetes.
Based on the strongest evidence for effects on any single major risk factor, including blood pressure, blood lipids, plasma glucose or insulin resistance, heart
rate, or systemic inflammation.
See text and Table 4 for evidence on minerals, vitamins, and other supplements.
Lowering of low-density lipoprotein cholesterol, but also lowering of high-density lipoprotein cholesterol and no change in the ratio of total cholesterol to
high-density lipoprotein cholesterol.
The evidence for effects of consuming saturated fat in place of polyunsaturated fat or monounsaturated fat is summarized above for the reverse exchanges, ie,
polyunsaturated fat in place of saturated fat, and monounsaturated fat in place of saturated fat.
Mozaffarian et al
2875
Figure 2. Types of processing and structure of grains, sugars, and starches. A major research and policy gap is the absence of one
accepted taxonomy to define whole grains or carbohydrate quality that incorporates their various characteristics that can influence cardiometabolic health, including extent of processing, food structure, dietary fiber content, content of bran and germ, and glycemic
response to ingestion. This Figure presents a proposed taxonomy to integrate these various characteristics. Types of foods with evidence for cardiometabolic benefits are shaded green, and those with evidence for adverse cardiometabolic effects are shaded red.
Intact and minimally processed whole grains (darker green; ie, greater benefits) may plausibly have greater benefits than milled whole
grains (lighter green; ie, lesser benefits) because of intact food structure and lower glycemic response; refined sugars in liquid form
(darkest red, ie, greatest harms) may have greater adverse effects than refined grains, starches, and sugars (lighter red; ie, lesser
harms) because of particularly unfavorable effects on satiety and weight gain. Both simple and complex refined carbohydrates induce
similarly high glycemic responses following ingestion and, in amounts typically consumed in Western diets, induce de novo lipogenesis
in the liver, ie, the conversion of carbohydrates to fat. Compared to glucose, fructose produces smaller blood glycemic responses but
more strongly stimulates de novo lipogenesis, Animal-experimental and limited human studies suggest that fructose, which represents
about half of all sugars in refined sugars such as either high frucose corn syrup or sucrose (eg, cane sugar, beet sugar), may have
additional adverse effects on hepatic steatosis and insulin resistance. Corn provides reasonable fiber and modestly lower glycemic
responses than many types of potatoes. Yams and sweet potatoes are not included herein because of higher nutrient contents and
lower glycemic responses to ingestion.
Evidence for possible adverse cardiovascular effects of methylmercury found in a few fish species is limited and conflicting; if present, such effects do not appear to outweigh the net
cardiovascular benefits of fish consumption.10,54a
Nuts
Nuts contain several bioactive constituents that could improve cardiometabolic health, including unsaturated fatty
acids, vegetable proteins (eg, L-arginine, a nitric oxide precursor), fiber, folate, minerals, antioxidants, and phytochemicals.5557 In RCTs, nut consumption reduces total cholesterol,
LDL cholesterol, postprandial hyperglycemia from highcarbohydrate meals, and (variably) oxidative, inflammatory,
and endothelial biomarkers.55,5759 Nut consumption is also
associated with less adiposity in observational studies, and in
RCTs, the addition of nuts to weight loss diets results in either
similar or greater overall weight loss.60 In prospective cohorts, modest nut consumption is associated with lower CHD
incidence (Figure 1).61,62 Epidemiological and clinical studies
have predominantly evaluated tree nuts and peanuts, and
effects of specific types of nuts require further study. Overall,
cardiovascular benefits of modest nut consumption are supported by effects on risk factors in short-term trials and by the
magnitude and consistency of reduced CVD risk observed in
prospective cohort studies (Table 2).
Legumes (eg, peas, beans, lentils, and chickpeas) may
also provide cardiovascular benefits. In a meta-analysis of
RCTs, consumption of soy-containing foods produced
trends toward lowering of systolic (5.8 mm Hg) and
diastolic (4.0 mm Hg) BP, but effects did not achieve
statistical significance.63 Isolated soy protein or isoflavones
(phytoestrogens) appear to have smaller effects, producing
2876
Circulation
Sugar-Sweetened Beverages
Meats
Several constituents of red meats could increase cardiometabolic risk, including SFA, cholesterol, heme iron, and in
processed meats, high levels of salt and other preservatives.
Lower consumption of red meats is consistently part of
overall dietary patterns associated with lower CVD risk (see
Dietary Patterns and Table 2). In meta-analyses of prospective cohort studies, total red meat consumption was associated with overall nonsignificant trends toward higher risk of
CHD and DM (Figure 1).61,65 When different types of meat
were evaluated systematically, consumption of processed
meats but not unprocessed red meats was associated with
higher incidence of CHD and DM.65 These findings suggest
that adverse effects of preservatives (eg, sodium, nitrites, and
phosphates) and/or preparation methods (eg, hightemperature commercial cooking/frying) could influence
health effects of meat consumption.65 In one observational
analysis, both unprocessed and processed meat consumption
were associated with higher CHD risk when such consumption replaced foods with cardiometabolic benefits, such as
low-fat dairy, nuts, and fish.66
Dairy Foods
Some short-term RCTs have evaluated the potential benefits
of dairy consumption for satiety or weight loss, with inconsistent and inconclusive findings.67,68 Multicomponent dietary interventions that included daily intake of low-fat dairy
foods significantly lowered BP, lipid levels, and insulin
resistance and improved endothelial function, independent of
changes in weight.20 22,26 In such multicomponent interventions, the specific benefits of dairy foods cannot be quantified
separately. Nonetheless, consistent with physiological benefits, higher dairy consumption was associated with lower risk
of both stroke and DM in long-term observational cohorts
(Figure 1).69 71
The active constituents for such cardiometabolic benefits
are not established. On the basis of lower content of calories,
SFA, and cholesterol, together with no established nutritional
advantage of whole-fat dairy, most dietary guidelines and
scientific organizations recommend low-fat or nonfat dairy
consumption.10 These guidelines generally recommend dairy
foods as a source of selected nutrients (eg, calcium, vitamin
D, protein, potassium, magnesium, and other vitamins) rather
than based on equally or more relevant evidence for their
effects as a whole food that may reduce cardiometabolic risk.
In long-term observational studies, a lower risk of DM and
metabolic abnormalities has been variably linked to consumption of low-fat dairy, whole-fat dairy, or both.7277
Conjugated linoleic acid and calcium were proposed as
potential mediators, but RCTs have demonstrated very small
benefits or even adverse cardiometabolic effects of these
factors.78 84 Dairy foods contain a complex assortment of
Evidence from ecological comparisons and prospective cohorts supports positive associations of sugar-sweetened beverage intake with adiposity in children and adults.87a,88 In the
United States between 1965 and 2002, when overweight/
obesity was increasing rapidly, the proportion of total dietary
calories consumed from beverages increased from 11.8% to
21.0%, or 222 calories/d per person.89 Most of this increase
was from sugar-sweetened beverages (60%), such as sodas/
colas, sweetened fruit drinks, and sports drinks, followed by
alcohol (31%) and 100% fruit juices (9%); calories from
other beverages (eg, milk) did not increase. The average
American teenage boy drinks 24 oz/d (300 kcal) of sugarsweetened beverages; the average American teenage girl,
16 oz/d (200 kcal).90 Most sugar-sweetened beverage intake
by children occurs at home, not at school.91
Limited short-term trials suggest that compared with solid
foods, calories in liquid form may be less satiating and
thereby increase the total amount of daily calories consumed.92,93 Sugar-sweetened beverage intake can also displace more healthful beverages, such as milk.94 Several RCTs
of small (n15) to moderate (n644) sizes have demonstrated that reduced sugar-sweetened beverage intake improves weight loss or reduces weight gain in both children
and adults.88 In one multicomponent lifestyle intervention,
each 1-serving/d reduction in sugar-sweetened beverages was
associated with 0.65-kg greater weight loss.95 In a meta-analysis of prospective cohorts, higher sugar-sweetened beverage
intake was associated with higher incidence of DM and
metabolic syndrome.96 One cohort observed a positive association between sugar-sweetened beverage intake and incident CHD.97 The combination of highly refined carbohydrate
calories, a liquid form that may minimize satiety, absence of
other beneficial nutrients/constituents, displacement of more
healthful beverages, and very high intake in many population
subgroups renders reduction in sugar-sweetened beverages an
important dietary target for improving individual and population cardiometabolic health.
Alcohol
Alcohol use has been related to both beneficial and adverse
cardiovascular outcomes. Habitual heavy alcohol intake is
cardiotoxic, causing a large portion of nonischemic dilated
cardiomyopathies in many nations.98 The ensuing ventricular
dysfunction is often irreversible, even when alcohol consumption is stopped; continued drinking in such patients is
associated with high mortality. Both acute binges and higher
habitual intake of alcohol have also been associated with
higher risk of atrial fibrillation.99
Conversely, in controlled trials and in the absence of
weight gain, modest alcohol use raises high-density lipoprotein cholesterol, reduces systemic inflammation, and improves insulin resistance.100 102 Consistent with these effects,
Mozaffarian et al
compared with nondrinkers, individuals who drink alcohol
moderately (up to 2 drinks/d for men and 1 drink/d for
women) experience a lower incidence of CHD and DM.61,103
In these observational studies, benefits of moderate alcohol
intake could be overestimated, because the comparison category of nondrinkers often includes former drinkers and other
individuals who avoid alcohol because of poor health,104 and
because individuals burdened by negative effects of alcohol
are generally underrepresented in such long-term studies, for
which participation requirements favor healthier individuals.
Nonetheless, the consistently lower event rates in observational studies and demonstrated physiological benefits in
RCTs provide concordant evidence that moderate alcohol use
confers at least some cardiometabolic benefit.
Experimental studies suggest that some nonalcohol components, such as resveratrol in wine, could have potential
benefits, but evidence from both RCTs of risk factors and
prospective cohort studies of clinical end points are most
consistent with direct effects of alcohol itself.100 102,105 For
example, moderate intakes of wine, beer, and liquor have
each been associated with lower CHD risk in different
populations.106 The pattern of drinking appears quite relevant,
with lowest cardiovascular risk seen among individuals who
drink moderately on several days of the week, rather than
among irregular or binge drinkers.107 Because of alcoholrelated accidents, homicides, and suicides, especially among
younger adults, alcohol use has an overall net adverse effect
on population mortality.2 Thus, alcohol use is not advisable as
a population-based strategy to reduce CVD risk. For adults
who already drink alcohol, no more than moderate use can be
encouraged. Avoidance of weight gain should also be reinforced, because an average serving of alcohol contributes
120 to 200 kcal that, as discussed previously, may be less
satiating than calories from solid foods.
Dietary Patterns
An impressive and expanding body of evidence demonstrates
that overall dietary patterns can improve health and prevent
CVD (Table 2).108 Several healthful dietary patterns have
been identified, often derived by different research approaches but sharing several key characteristics, including
an emphasis on fruits, vegetables, other plant foods such as
beans and nuts, and (in many patterns) whole grains and
fish; with limited or occasional dairy products; and often
with limited red meats or processed meats and fewer
refined carbohydrates and other processed foods (Table 3).
These dietary patterns are each generally consistent with
food-based priorities for CVD health (Table 1). In RCTs,
consumption of such dietary patterns substantially improves multiple cardiovascular risk factors (Figure 3).
2877
Mediterranean
Diverse agricultural patterns, cultures, and countries bordering the Mediterranean Sea preclude defining any single
Mediterranean dietary pattern or simple criteria. Mediterranean
diets have also changed over time: In Crete, a Mediterranean
island with historically low rates of CHD, diets now contain
less fruit and olive oil and more meats than diets of earlier
generations, with associated increases in serum cholesterol
and adiposity among these modern residents.114 Still, many
traditional Mediterranean diets share common characteristics, including an emphasis on vegetables, fruits, breads/
cereal foods usually made from wheat, nuts, and olive oil;
sometimes including fish and (in non-Islamic countries)
wine with meals; and being lower in saturated fat, cholesterol, and meats.110,115 Ecological comparisons and prospective cohort studies consistently demonstrate inverse
associations between consumption of traditional Mediterranean diets and risk of CHD, stroke, and total mortality.116 In RCTs, traditional Mediterranean diets improve
several physiological risk factors (Figure 3).
Vegetarian
Several types of vegetarian diets are consumed around the
world, including those consumed by pesco-vegetarians (who
consume fish); lacto-ovo-vegetarians (who consume milk and
eggs); and strict vegans (who consume no animal products).
Potentially different cardiometabolic effects of these different
vegetarian diets are not established. Few RCTs of vegetarian
diets have been performed (Table 2). Two small trials (n58
and n20 subjects, respectively) demonstrated reductions in
BP with vegetarian diets versus typical Western diets.117,118
Three other trials found no differences between lactovegetarian or vegan diets versus conventional dietary recommendations for improving weight loss, BP, blood lipids, or
insulin resistance.119 122 In several observational studies,
vegetarians experienced improved health outcomes compared
with nonvegetarians.10,110a,110b,123,124 Several characteristics of
vegetarian diets could account for these relationships, including greater inclusion of plant-based foods and fewer meats,
processed meats, and other processed and fast foods.110c
Because vegetarians are often generally more health conscious, other lifestyle characteristics, in addition to diet, could
contribute to observed lower rates of CVD. Overall, vegetarian diets have been studied less extensively than DASH or
Mediterranean patterns, and although the foods that are not
27
13
Saturated fat, %
energy
Monounsaturated
fat, % energy
Polyunsaturated fat,
% energy
29
4450
1181
473
2190
Dietary fiber, g
Potassium, mg
Calcium, mg
Magnesium, mg
Sodium, mg
150
15
Protein, % energy
Cholesterol, mg
2000
Processed meats
Carbohydrates, %
energy
Calories, kcal
Nutrients/day
Lean meat
2190
473
1181
4450
29
150
10
21
37
15
48
2000
Processed meats
Lean meat
Nutrient-dense
vegetables, fruits,
whole grains, fish,
and low-fat dairy
products
2190
473
1181
4450
29
150
13
27
25
48
2000
Processed
meats
Lean meat
Nutrient-dense
vegetables,
fruits, whole
grains, fish,
and low-fat
dairy products
Swain et al,
2008109
DASH (Higher
Protein)
DASH (Higher
Monounsaturated Fat)
ND
ND
ND
ND
ND
ND
6.9
22.7
13.3
42.9
ND
ND
2000
Meats, dairy
Vegetables, beans,
fruits, nuts and
seeds, fish and
seafood, cereals,
olive oil
Trichopoulou et al,
2003110
Traditional
Mediterranean
(Greece)*
2532
396
1028
4589
29
ND
5.1
15
10
33
18
47
2000
Red meats,
sweets
Cheese, yogurt,
red wine
Plant foods,
vegetables, fruits,
breads, other
cereals potatoes,
beans, nuts and
seeds, olive oil,
and fish
Nunez-Cordoba
et al, 2009110a
Traditional
Mediterranean
(Spain)
Dietary Pattern
ND
ND
ND
ND
20
ND
ND
9.5
10 (Including
trans)
ND
15.1
39.1
2000
Potatoes
Lean meat
Plant foods,
vegetables,
fruits, whole
grains,
legumes, fish
Fung et al,
2009110b
Mediterranean
(US)
110c
2000
Fish (pesco
vegetarians); dairy
and eggs
(lacto-ovovegetarians)
Vegetarian
2370
317
315
2623
22
ND
3.5
2.3
2.0
13
79
2000
Milk products
Willcox et al,
2007111 and
2009111a
Traditional
Japanese
(Continued)
1269
444
566
5826
26
ND
2.4
1.8
1.9
85
2000
Traditional Okinawan
Circulation
Includes
Nutrient-dense
vegetables, fruits,
whole grains, fish,
and low-fat dairy
products
Emphasizes
109
DASH (Higher
Carbohydrate)
Citation
Table 3.
2878
June 21, 2011
1.9
0.9
1.6
0.4
1.3
1.8
1.1
0.2
Meat
Poultry
Eggs
Fish/seafood
Legumes
Soy products
Other protein
sources, oz
0.1
Whole-fat
2.0
Low-fat
3.9
Whole grains, oz
5.3
0.2
Starchy
Grains, total, oz
ND
Other
6.6
ND
Red orange
ND
Dark green
DASH (Higher
Carbohydrate)
4.4
Continued
Vegetables, total,
servings
Foods/day
Table 3.
1.1
1.0
1.3
0.2
1.8
1.0
1.8
0.1
1.9
ND
4.3
4.8
0.4
ND
ND
ND
6.3
DASH (Higher
Monounsaturated Fat)
1.2
1.1
3.0
1.5
1.9
2.6
1.1
2.1
0.2
2.3
ND
5.0
3.8
0.3
ND
ND
ND
5.4
DASH (Higher
Protein)
ND
2.4
0.4
0.8
1.9
ND
3.6
0.1
0.6
ND
3.5
0.8
1.3
1.0
2.1
ND
2.5
ND
ND
ND
ND
2.8
Traditional
Mediterranean
(Spain)
0.1
1.0
ND
5.3
0.9
ND
ND
ND
7.5
Traditional
Mediterranean
(Greece)*
Dietary Pattern
ND
0.5
0.3
1.5
ND
ND
2.4
ND
ND
ND
1.6
ND
3.2
No potatoes
ND
ND
ND
4.4
Mediterranean
(US)
Vegetarian
0.1 (seaweed)
0.1
(Continued)
See legumes
1 g
See legumes
0.6
0.1
ND
0.1
2.1
0.3
ND
0.4
ND
0.1
0.1
ND
ND
ND
0.1
0.1 (other
potatoes)
0.9 (pickled
vegetables)
ND
ND
0.2
0.3 (other
potatoes)
0.1 (seaweed)
0.5 (Asian sweet
potatoes)
ND
Traditional Okinawan
ND
Traditional
Japanese
Mozaffarian et al
Cardioprotective Diet: New Insights
2879
ND
25
10
ND
20
17
31
DASH (Higher
Protein)
7.9
24.3
40.3
ND
ND
ND
ND
Traditional
Mediterranean
(Greece)*
ND
19.0
ND
ND
ND
ND
Traditional
Mediterranean
(Spain)
Dietary Pattern
7.3
ND
ND
ND
ND
ND
ND
Mediterranean
(US)
ND
Vegetarian
7.7
ND
ND
ND
ND
ND
Traditional
Japanese
3.4
ND
ND
ND
ND
ND
Traditional Okinawan
This table was adapted, with several additions and modifications, from the 2010 Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, US Department of Agriculture, Agricultural Research
Service, available at http://www.cnpp.usda.gov/DGAs2010-DGACReport.htm.10 DASH indicates Dietary Approaches to Stop Hypertension; ND, not described.
*Values are based on the average (mean) consumption levels in the population, not on the optimal consumption levels for a traditional Mediterranean diet.
Adjusted to an average 2000 kcal/d diet.
Vegetarian diets are defined only by what is not consumed (ie, meats and, variably, dairy, eggs, and/or fish). Thus, although many vegetarians tend to be health-conscious and may consume higher amounts of fruits,
vegetables, nuts, and legumes, what actually is consumed can vary considerably and no typical vegetarian diet can be reliably defined.
ND
Alcohol, g
25
19
Olive oil
11
Cooking oils,
except olive oil
Added sugar,
candy, g
13
20
Salad dressing,
mayonnaise
22
Margarines and
spreads
70
DASH (Higher
Monounsaturated Fat)
46
DASH (Higher
Carbohydrate)
Continued
Circulation
Table 3.
2880
June 21, 2011
Mozaffarian et al
2881
Figure 3. Effects of dietary patterns on cardiovascular risk factors in randomized controlled trials. Effects of the DASH (Dietary
Approaches to Stop Hypertension) low-fat, high-protein, and
high-monounsaturated-fat (MUFA) diets compared with baseline
among 162 participants in a 6-week feeding trial; and of the
Mediterranean diet compared with a low-fat diet among 180
participants in a 2-year dietary advice trial.19,22,112 All differences
were statistically significant at P0.05, except for changes in
high-density lipoprotein cholesterol (HDL-C) with the DASH
high-MUFA diet and in triglycerides with the DASH low-fat diet.
Where no results are shown (eg, DASH diets and glucoseinsulin measures), findings were not reported. Across diets,
blood pressure and low-density lipoprotein cholesterol (LDL-C)
were generally improved to a greater extent with DASH dietary
patterns, whereas atherogenic dyslipidemia and glucose-insulin
measures were generally improved to a greater extent with
Mediterranean dietary patterns. Overall risk factor changes with
any of these dietary patterns would predict substantial reductions in cardiovascular risk. SBP indicates systolic blood pressure; DBP, diastolic blood pressure; CRP, C-reactive protein.
Japanese
Japanese diets have been of considerable interest, particularly
from Okinawa, which until recently experienced among the
lowest rates of CHD in the world.111 Traditional Japanese
diets emphasize soybean products, fish, seaweeds, vegetables, fruits, and green tea and are low in meats.126 Conversely,
Japanese diets often contain high sodium from soy sauce and
added salt at home, likely contributing to the relatively high
incidence of stroke and some cancers. Very low-fat Japanese
diets have also been linked to higher observed stroke risk,
including hemorrhagic stroke.127 Food staples of traditional
Okinawan diets include orange-yellow root vegetables and
green leafy vegetables, which are antioxidant rich and relatively low in calories; wide varieties of seaweeds; tofu; and
herbaceous plants.111a Appropriate energy balance and little
age-related weight gain are also important features of the
Okinawan diet pattern.111 Japanese dietary patterns appear
promising for CHD prevention, but the reasons for relatively
high rates of stroke and some cancers require further investigation, and epidemiological and clinical trial evidence for
benefits remains more limited than evidence supporting the
DASH and Mediterranean diets.
2882
Circulation
Mozaffarian et al
other RCTs,146 148 and was related to lower CVD risk (when
consumed from vegetable oils) in ecological studies.149 However, because consumption of monounsaturated fatty acids
has been shown to increase atherosclerosis in nonhuman
primates150 and has mixed relations with clinical CVD events
in long-term cohort studies, some caution is needed.61,142
Also, because monounsaturated fat is derived from both
animal (eg, meats and dairy) and vegetable (eg, olive oil, and
canola) sources, health effects may plausibly vary depending
on the types of foods consumed. For example, potential
adverse effects of saturated fat, cholesterol, heme iron, or
preservatives in meats could counter cardiometabolic benefits,65 whereas potential effects of phenolic compounds in
olive oil could augment benefits.151 Thus, consumption of
vegetable oils, including those that contain PUFA, plantderived omega-3 fats, and MUFA, is an important feature of
dietary patterns that reduce CVD risk (Table 1).
Sodium
Animal experiments, migration studies, ecological studies,
longitudinal observational studies, RCTs, and meta-analyses
confirm that higher salt (sodium chloride) consumption raises
BP.152 Elevated BP is estimated to account for nearly two
thirds of strokes and half of all CHD events.153 Individual
large-scale trials and meta-analyses of trials have documented
conclusively that several different BP-reduction therapies
prevent stroke and CHD.154 This compelling body of evidence has led numerous organizations to conclude that salt
reduction, through its effects on BP, should likewise prevent
stroke and CHD.10,13 A meta-analysis of prospective observational studies supports a direct relationship between increased salt intake and CVD events.155 Limited evidence
from trials, including long-term follow-up of salt-reduction
trials, is also consistent with lower CVD event rates after salt
reduction.156,157
In North America and Europe, 75% of sodium intake is
derived from packaged, preprepared, or restaurant foods, with
the rest being naturally occurring or added at home.158 In
Asian countries, most sodium is from soy sauce or is added at
home.158 Given ubiquitous sources of sodium in American
and similar diets (Figure 4),159 policy-level approaches are
well-suited for reduction efforts. Projected benefits are enormous. A national effort that reduced US salt intake by 3 g/d
(1.2 g/d less sodium) could annually prevent between
60 000 and 120 000 CHD events and 32 000 to 66 000
strokes, saving 194 000 to 392 000 quality-adjusted life-years
and $10 to $24 billion in healthcare costs.160 Smaller reductions in salt intake are also estimated to produce large
population benefits.160,161 Overall, the totality of evidence
supports aggressive policy-level approaches to lower sodium
intake as a means to prevent the CVD consequences of
elevated BP. Optimal BP reduction occurs when sodium
reduction is combined with a healthier food based dietary
pattern such as the DASH-type diet (Table 1).
Dietary Supplements
Use of dietary supplements, often at high or pharmacological
doses, is commonplace, despite the absence of convincing
evidence that supplements have health benefits. Several
2883
Table 4.
Summary of Evidence of the Effects of Vitamin
Supplements on Cardiovascular Disease
Beta-carotene
Calcium
Vitamin D
Vitamin E
Folic acid,
vitamin B6,
vitamin B12
Fish oils
Multivitamins
2884
Table 5.
Circulation
Evidence-Based Strategies for Promoting Individual-Level Dietary Change to Reduce Cardiovascular Disease Risk
Cognitive-behavioral
strategies
Class I
Class IB
Long-Term Support: Provide direct or peer-based long-term support and follow-up, such as referral to ongoing
community-based programs, to offset the common occurrence of declining adherence over time.
Class IIB
Individual Sessions: Use individual-oriented sessions to assess where the individual is in relation to behavior
change, to jointly identify the goals for risk reduction or improved cardiovascular health, and to develop a
personalized plan to achieve it.
Group Sessions: Use group sessions with cognitive-behavioral strategies to teach skills to modify the diet to
provide role modeling and positive observational learning, and to maximize the benefits of peer support and
group problem solving.
Class IB
E-Programs: For appropriate target populations, use Internet- and computer-based programs to target behavior
change, preferably including E-counseling and feedback.
Class IIA
Individualized Print/Media: For print- or media-only strategies, use individualized (rather than nonindividualized)
approaches.
Multicomponent: Use a multiple-component delivery strategy that includes both individual and group
components.
Cultural Adaptation: Use culturally adapted strategies, including use of peer or lay health advisors to increase
trust, as well as tailored health messages and counseling strategies sensitive to cultural beliefs, values,
language, literacy, and customs of the individual.
Class IIB
Settings: Use work, community, church, or clinic settings for delivery of interventions.
Problem Solving: Use problem-solving strategies to address barriers such as lack of access to healthier foods,
lack of knowledge related to cooking or food preparation, or transportation barriers.
Energy Balance
Energy balance (calories consumed versus expended) is the
principal determinant of weight gain and adiposity. Basal and
activity-related energy expenditure are determined by physical activity, body size, muscle mass, age, and sex. Appropriate energy consumption (total dietary calories per day) is
determined by energy expenditure and goals for weight loss,
gain, or stability. Some people may consume relatively high
calories but have neutral or negative energy balance because
of high expenditure, whereas others may consume relatively
few calories but have positive energy balance because of low
expenditure. Thus, change in weight (supplemented with
waist circumference), rather than direct measurement of
energy expenditure or consumption, is the most practical
metric to assess energy balance.
Mozaffarian et al
appear to have a greater influence on body weight.87a,88,136,176 181
Thus, these features of dietary quality appear to impact dietary
quantity.
Other individual, social, and environmental factors are also
linked to energy imbalance.87a,182184 These include television
watching and lower average sleep duration, especially among
children/adolescents; socioeconomic status and race/ethnicity; local environments, such as the presence of fast food
restaurants, grocery stores, crime safety, parks or open
spaces, and walking or biking paths; and influences of
advertising, social norms, and work and home dynamics.
Ultimately, these influences act through changes in diet or
activity to influence weight change. For example, effects of
television watching and poor sleep may be mediated predominantly by dietary changes.185190 Although the quality of
available time-trend data is suboptimal, the recent obesity
pandemic appears temporally related to increased energy
consumption in developed nations90 and to both increased
consumption and decreased expenditure in some developing
nations.3
A sustained energy imbalance of 50 to 100 extra kcal/d
may be enough to produce the weight gain observed in many
individuals.191,192 The often small size of this energy gap
makes unintentional gradual weight gain easy, but also means
that small improvements in energy balance, sustained over
the long term, could prevent or even reverse adiposity in
many individuals and populations.87a,193
Changing Behavior
A growing body of literature supports several effective
strategies for successful behavior change.194 197 Evidence for
individual-level approaches was reviewed recently (Table
5).197 Targeted goals are most effective for individuals.196,197
Clinical providers can help patients prioritize the most relevant foods and dietary patterns (Table 1) and perform simple
office-based assessments to inquire about and help set dietary
goals.198 Clinic-based strategies are facilitated by healthcare
systems changes, including scheduled visits for individual/
group education; sustained in-person, telephone, or electronic
feedback; and quality and reimbursement guidelines that
support behavior-change efforts.199,200
Although individual-based strategies can successfully improve an individuals diet quality, public health strategies at
community, state, and national levels are essential to produce
a substantial and sustained population impact.196,201 Several
approaches are effective (Table 6).152,196,202214 Given the
scope of prevailing adverse dietary patterns, population
approaches are critical to achieving the AHAs 2020 Strategic
Goals.7 Overall, although more research on the best translational strategies is needed, sufficient evidence presently exists
to implement several individual- and population-level approaches to improving diet.
Conclusions
High-quality evidence is now available from multiple complementary research paradigms on the cardiometabolic effects of specific dietary factors, offering new and expanded
insights into dietary priorities for preventing CVD and DM.
Consumption of specific foods and dietary patterns appear
2885
Table 6.
Evidence-Based Strategies for Promoting
Population-Level Dietary Change to Reduce Cardiovascular
Disease Risk*
Policies directly targeting selected nutrients to increase or reduce levels in
foods152,202
Direct mandates or bans
Coordinated, multicomponent media, education, and labeling
Changes in the food environment196,203209
Increasing availability of healthier foods, eg, in cafeterias, grocery stores,
or neighborhoods
Changes in food pricing by means of subsidies or taxation
Point-of-purchase prompts and education
Media and other educational strategies196,210 212
Intensive mass media campaigns promoting one simple message
National logos or simple branding to identify healthier foods
Provision of focused, targeted messages as part of a larger
multicomponent strategy
Regulation of advertising to particular at-risk groups
Posting of information on food labels or menu boards
Social and community supports196
Coordinated educational and environmental efforts in schools, workplaces,
community centers, and religious centers
Group sessions and self-monitoring strategies
Multicomponent strategies196,211,213
Combinations of upstream policy measures, midstream environmental
approaches and media campaigns, and downstream community
approaches
*Such interventions experience greatest success when multiple stakeholders
(community members, local organizations, policy makers) are involved
throughout planning, implementation, and sustainability.196,214
Evidence that this strategy alters consumer behavior is still relatively
limited, but this strategy appears to at least contribute to food industry choices
in terms of what is offered.
2886
Circulation
Acknowledgments
Supported by the National Heart, Lung, and Blood Institute, with
cofunding from the Office of Dietary Supplements (R01-HL085710), National Institutes of Health. We thank Dr Frank Sacks for
his critical reading of and comments on an earlier version of this
report.
Disclosures
Dr Mozaffarian reports receiving research grants from GlaxoSmithKline, Sigma Tau, Pronova, and the National Institutes
of Health for an investigator-initiated, not-for-profit clinical
trial of fish oil; travel reimbursement, honoraria, or consulting fees from the International Life Sciences Institute, Unilever, SPRIM, Nutrition Impact, and Foodminds; and royalties from UpToDate for an online scientific chapter. Harvard
University has filed a provisional patent application, assigned
to Harvard University, listing Dr. Mozaffarian as a coinventor to the US Patent and Trademark Office for use of
trans-palmitoleic acid to prevent and treat insulin resistance,
type 2 diabetes, and related conditions. The other authors
report no conflicts.
References
1. Mathers CD, Loncar D. Projections of global mortality and burden of
disease from 2002 to 2030. PLoS Med. 2006;3:e442.
2. Danaei G, Ding EL, Mozaffarian D, Taylor B, Rehm J, Murray CJ,
Ezzati M. The preventable causes of death in the United States: comparative risk assessment of dietary, lifestyle, and metabolic risk factors.
PLoS Med. 2009;6:e1000058.
3. Popkin BM. Global nutrition dynamics: the world is shifting rapidly
toward a diet linked with noncommunicable diseases. Am J Clin Nutr.
2006;84:289 298.
4. Stampfer MJ, Hu FB, Manson JE, Rimm EB, Willett WC. Primary
prevention of coronary heart disease in women through diet and
lifestyle. N Engl J Med. 2000;343:16 22.
5. Mozaffarian D, Kamineni A, Carnethon M, Djousse L, Mukamal KJ,
Siscovick DS. Lifestyle risk factors and new-onset diabetes mellitus in
older adults: the Cardiovascular Health Study. Arch Intern Med. 2009;
169:798 807.
6. Mozaffarian D, Ludwig DS. Dietary guidelines in the 21st century: a
time for food. JAMA. 2010;304:681 682.
7. Lloyd-Jones DM, Hong Y, Labarthe D, Mozaffarian D, Appel LJ, Van
Horn L, Greenlund K, Daniels S, Nichol G, Tomaselli GF, Arnett DK,
Fonarow GC, Ho PM, Lauer MS, Masoudi FA, Robertson RM, Roger V,
Schwamm LH, Sorlie P, Yancy CW, Rosamond WD. Defining and
setting national goals for cardiovascular health promotion and disease
reduction: the American Heart Associations strategic Impact Goal
through 2020 and beyond. Circulation. 2010;121:586 613.
8. Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, Franch
HA, Franklin B, Kris-Etherton P, Harris WS, Howard B, Karanja N,
Lefevre M, Rudel L, Sacks F, Van Horn L, Winston M, Wylie-Rosett J.
Diet and lifestyle recommendations revision 2006: a scientific statement
from the American Heart Association Nutrition Committee. Circulation.
2006;114:8296.
9. Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH,
Sacks F, Steffen LM, Wylie-Rosett J. Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation. 2009;120:10111020.
10. Dietary Guidelines Advisory Committee. 2010 Report of the Dietary
Guidelines Advisory Committee on the Dietary Guidelines for
Americans. US Department of Agriculture, Agricultural Research
Service. http://www.cnpp.usda.gov/DGAs2010-DGACReport.htm.
Accessed September 26, 2010.
11. Joint FAO/WHO expert consultation on fats and fatty acids in human
nutrition: interim summary. Food and Agriculture Organization of the
United Nations, World Health Organization. http://www.who.int/
nutrition/topics/FFA_summary_rec_conclusion.pdf. Accessed September 22, 2010.
12. World Health Organization. Global Burden of Disease (GBD) 2010
study. http://www.who.int/healthinfo/global_burden_disease/
GBD_2005_study/en/index.html. Accessed September 1, 2010.
13. Food and Nutrition Board, Institute of Medicine. Strategies to reduce
sodium intake in the United States. http://www.iom.edu/Reports/2010/
Strategies-to-Reduce-Sodium-Intake-in-the-United-States.aspx.
Accessed October 11, 2010.
14. Hill AB. The environment and disease: association or causation? Proc R
Soc Med. 1965;58:295300.
15. World Health Organization. Diet, Nutrition and the Prevention of
Chronic Diseases: Report of a Joint WHO/FAO Expert Consultation.
Geneva, Switzerland: World Health Organization; 2003:916:iviii.
16. Jacobs DR Jr, Steffen LM. Nutrients, foods, and dietary patterns as
exposures in research: a framework for food synergy. Am J Clin Nutr.
2003;78:508S513S.
17. Jacobs DR Jr, Tapsell LC. Food, not nutrients, is the fundamental unit in
nutrition. Nutr Rev. 2007;65:439 450.
18. Ainsworth BE, Haskell WL, Whitt MC, Irwin ML, Swartz AM, Strath
SJ, OBrien WL, Bassett DR Jr, Schmitz KH, Emplaincourt PO, Jacobs
DR Jr, Leon AS. Compendium of physical activities: an update of
activity codes and MET intensities. Med Sci Sports Exerc. 2000;32:
S498 S504.
19. Esposito K, Marfella R, Ciotola M, Di Palo C, Giugliano F, Giugliano
G, DArmiento M, DAndrea F, Giugliano D. Effect of a
Mediterranean-style diet on endothelial dysfunction and markers of
vascular inflammation in the metabolic syndrome: a randomized trial.
JAMA. 2004;292:1440 1446.
20. Ard JD, Grambow SC, Liu D, Slentz CA, Kraus WE, Svetkey LP. The
effect of the PREMIER interventions on insulin sensitivity. Diabetes
Care. 2004;27:340 347.
21. Elmer PJ, Obarzanek E, Vollmer WM, Simons-Morton D, Stevens VJ,
Young DR, Lin PH, Champagne C, Harsha DW, Svetkey LP, Ard J,
Brantley PJ, Proschan MA, Erlinger TP, Appel LJ. Effects of comprehensive lifestyle modification on diet, weight, physical fitness, and
blood pressure control: 18-month results of a randomized trial. Ann
Intern Med. 2006;144:485 495.
22. Miller ER 3rd, Erlinger TP, Appel LJ. The effects of macronutrients on
blood pressure and lipids: an overview of the DASH and OmniHeart
trials. Curr Atheroscler Rep. 2006;8:460 465.
23. Svendsen M, Blomhoff R, Holme I, Tonstad S. The effect of an
increased intake of vegetables and fruit on weight loss, blood pressure
and antioxidant defense in subjects with sleep related breathing disorders. Eur J Clin Nutr. 2007;61:13011311.
24. McCall DO, McGartland CP, McKinley MC, Patterson CC, Sharpe P,
McCance DR, Young IS, Woodside JV. Dietary intake of fruits and
vegetables improves microvascular function in hypertensive subjects in
a dose-dependent manner. Circulation. 2009;119:21532160.
25. Jenkins DJ, Wong JM, Kendall CW, Esfahani A, Ng VW, Leong TC,
Faulkner DA, Vidgen E, Greaves KA, Paul G, Singer W. The effect of
a plant-based low-carbohydrate (Eco-Atkins) diet on body weight and
blood lipid concentrations in hyperlipidemic subjects. Arch Intern Med.
2009;169:1046 1054.
26. Al-Solaiman Y, Jesri A, Mountford WK, Lackland DT, Zhao Y, Egan
BM. DASH lowers blood pressure in obese hypertensives beyond
potassium, magnesium and fibre. J Hum Hypertens. 2009;24:237246.
27. Dauchet L, Amouyel P, Hercberg S, Dallongeville J. Fruit and vegetable
consumption and risk of coronary heart disease: a meta-analysis of
cohort studies. J Nutr. 2006;136:2588 2593.
28. Dauchet L, Amouyel P, Dallongeville J. Fruit and vegetable consumption and risk of stroke: a meta-analysis of cohort studies. Neurology. 2005;65:11931197.
Mozaffarian et al
29. Mozaffarian D. Nutrition and cardiovascular disease. In: Bonow RO,
Mann DL, Zipes DP, Libby P, eds. Braunwalds Heart Disease: A
Textbook of Cardiovascular Medicine. 9th ed. Chapter 48. Philadelphia,
PA: Elsevier/Saunders; 2011.
30. Sabelli PA, Larkins BA. The development of endosperm in grasses.
Plant Physiol. 2009;149:14 26.
31. Anderson JW, Randles KM, Kendall CW, Jenkins DJ. Carbohydrate and
fiber recommendations for individuals with diabetes: a quantitative
assessment and meta-analysis of the evidence. J Am Coll Nutr. 2004;
23:517.
32. Whelton SP, Hyre AD, Pedersen B, Yi Y, Whelton PK, He J. Effect of
dietary fiber intake on blood pressure: a meta-analysis of randomized,
controlled clinical trials. J Hypertens. 2005;23:475 481.
33. Ludwig DS. The glycemic index: physiological mechanisms relating to
obesity, diabetes, and cardiovascular disease. JAMA. 2002;287:
2414 2423.
34. de Munter JS, Hu FB, Spiegelman D, Franz M, van Dam RM. Whole
grain, bran, and germ intake and risk of type 2 diabetes: a prospective
cohort study and systematic review. PLoS Med. 2007;4:e261.
35. Mellen PB, Walsh TF, Herrington DM. Whole grain intake and cardiovascular disease: a meta-analysis. Nutr Metab Cardiovasc Dis. 2008;18:
283290.
36. Katcher HI, Legro RS, Kunselman AR, Gillies PJ, Demers LM,
Bagshaw DM, Kris-Etherton PM. The effects of a whole grain-enriched
hypocaloric diet on cardiovascular disease risk factors in men and
women with metabolic syndrome. Am J Clin Nutr. 2008;87:79 90.
37. Kelly SA, Summerbell CD, Brynes A, Whittaker V, Frost G. Wholegrain cereals for coronary heart disease. Cochrane Database Syst Rev.
2007;(2):CD005051.
38. Williams CM, Burdge G. Long-chain n-3 PUFA: plant v. marine
sources. Proc Nutr Soc. 2006;65:4250.
39. Mozaffarian D, Rimm EB. Fish intake, contaminants, and human health:
evaluating the risks and the benefits. JAMA. 2006;296:18851899.
40. Leaf A, Kang JX, Xiao YF, Billman GE. Clinical prevention of sudden
cardiac death by n-3 polyunsaturated fatty acids and mechanism of
prevention of arrhythmias by n-3 fish oils. Circulation. 2003;107:
2646 2652.
41. Brouwer IA, Raitt MH, Dullemeijer C, Kraemer DF, Zock PL, Morris C,
Katan MB, Connor WE, Camm JA, Schouten EG, McAnulty J. Effect of
fish oil on ventricular tachyarrhythmia in three studies in patients with
implantable cardioverter defibrillators. Eur Heart J. 2009;30:820 826.
42. Kowey PR, Reiffel JA, Ellenbogen KA, Naccarelli GV, Pratt CM.
Efficacy and safety of prescription omega-3 fatty acids for the prevention of recurrent symptomatic atrial fibrillation: a randomized controlled trial. JAMA. 2010;304:23632372.
43. Eslick GD, Howe PR, Smith C, Priest R, Bensoussan A. Benefits of fish
oil supplementation in hyperlipidemia: a systematic review and metaanalysis. Int J Cardiol. 2009;136:4 16.
44. Geleijnse JM, Giltay EJ, Grobbee DE, Donders AR, Kok FJ. Blood
pressure response to fish oil supplementation: metaregression analysis of
randomized trials. J Hypertens. 2002;20:14931499.
45. Mozaffarian D, Geelen A, Brouwer IA, Geleijnse JM, Zock PL, Katan
MB. Effect of fish oil on heart rate in humans: a meta-analysis of
randomized controlled trials. Circulation. 2005;112:19451952.
46. Mozaffarian D, Wu JHY. Omega-3 fatty acids and cardiovascular disease effects on risk factors, molecular pathways, and clinical events.
J Am Coll Cardiol. In press.
47. He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR, Goldbourt
U, Greenland P. Fish consumption and incidence of stroke: a meta-analysis of cohort studies. Stroke. 2004;35:1538 1542.
48. Wang C, Harris WS, Chung M, Lichtenstein AH, Balk EM, Kupelnick
B, Jordan HS, Lau J. n-3 Fatty acids from fish or fish-oil supplements,
but not -linolenic acid, benefit cardiovascular disease outcomes in
primary- and secondary-prevention studies: a systematic review. Am J
Clin Nutr. 2006;84:517.
49. Leon H, Shibata MC, Sivakumaran S, Dorgan M, Chatterley T, Tsuyuki
RT. Effect of fish oil on arrhythmias and mortality: systematic review.
BMJ. 2008;337:a2931.
50. Marik PE, Varon J. Omega-3 dietary supplements and the risk of
cardiovascular events: a systematic review. Clin Cardiol. 2009;32:
365372.
51. Mozaffarian D, Gottdiener JS, Siscovick DS. Intake of tuna or other
broiled or baked fish versus fried fish and cardiac structure, function,
and hemodynamics. Am J Cardiol. 2006;97:216 222.
2887
52. Chung H, Nettleton JA, Lemaitre RN, Barr RG, Tsai MY, Tracy RP,
Siscovick DS. Frequency and type of seafood consumed influence
plasma (n-3) fatty acid concentrations. J Nutr. 2008;138:24222427.
53. He K, Liu K, Daviglus ML, Mayer-Davis E, Jenny NS, Jiang R, Ouyang
P, Steffen LM, Siscovick D, Wu C, Barr RG, Tsai M, Burke GL. Intakes
of long-chain n-3 polyunsaturated fatty acids and fish in relation to
measurements of subclinical atherosclerosis. Am J Clin Nutr. 2008;88:
11111118.
54. Patel PS, Sharp SJ, Luben RN, Khaw KT, Bingham SA, Wareham NJ,
Forouhi NG. The association between type of dietary fish and seafood
intake and the risk of incident type 2 diabetes: the EPIC-Norfolk cohort
study. Diabetes Care. 2009;32:18571863.
54a. Mozaffarian D, Shi P, Morris JS, Spiegelman D, Grandjean P, Siscovick
DS, Willett WC, Rimm EB. Mercury exposure and risk of cardiovascular disease in two US cohorts. New Engl J Med. 2011;364:
1116 1125.
55. Kris-Etherton PM, Hu FB, Ros E, Sabate J. The role of tree nuts and
peanuts in the prevention of coronary heart disease: multiple potential
mechanisms. J Nutr. 2008;138:1746S1751S.
56. King JC, Blumberg J, Ingwersen L, Jenab M, Tucker KL. Tree nuts and
peanuts as components of a healthy diet. J Nutr. 2008;138:
1736S1740S.
57. Ros E. Nuts and novel biomarkers of cardiovascular disease. Am J Clin
Nutr. 2009;89:1649S1656S.
58. Banel DK, Hu FB. Effects of walnut consumption on blood lipids and
other cardiovascular risk factors: a meta-analysis and systematic review.
Am J Clin Nutr. 2009;90:56 63.
59. Kendall CW, Josse AR, Esfahani A, Jenkins DJ. Nuts, metabolic
syndrome and diabetes. Br J Nutr. 2010;104:465 473.
60. Mattes RD, Kris-Etherton PM, Foster GD. Impact of peanuts and tree
nuts on body weight and healthy weight loss in adults. J Nutr. 2008;
138:1741S1745S.
61. Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of
the evidence supporting a causal link between dietary factors and
coronary heart disease. Arch Intern Med. 2009;169:659 669.
62. Kelly JH Jr, Sabate J. Nuts and coronary heart disease: an epidemiological perspective. Br J Nutr. 2006;96(suppl 2):S61S67.
63. Hooper L, Kroon PA, Rimm EB, Cohn JS, Harvey I, Le Cornu KA,
Ryder JJ, Hall WL, Cassidy A. Flavonoids, flavonoid-rich foods, and
cardiovascular risk: a meta-analysis of randomized controlled trials.
Am J Clin Nutr. 2008;88:38 50.
64. Sacks FM, Lichtenstein A, Van Horn L, Harris W, Kris-Etherton P,
Winston M. Soy protein, isoflavones, and cardiovascular health: an
American Heart Association Science Advisory for professionals from
the Nutrition Committee. Circulation. 2006;113:1034 1044.
65. Micha R, Wallace S, Mozaffarian D. Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes: a systematic review and meta-analysis. Circulation. 2010;121:
22712283.
66. Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC.
Major dietary protein sources and risk of coronary heart disease in
women. Circulation. 2010;122:876 883.
67. Lanou AJ, Barnard ND. Dairy and weight loss hypothesis: an evaluation
of the clinical trials. Nutr Rev. 2008;66:272279.
68. Christensen R, Lorenzen JK, Svith CR, Bartels EM, Melanson EL, Saris
WH, Tremblay A, Astrup A. Effect of calcium from dairy and dietary
supplements on faecal fat excretion: a meta-analysis of randomized
controlled trials. Obes Rev. 2009;10:475 486.
69. Elwood PC, Givens DI, Beswick AD, Fehily AM, Pickering JE, Gallacher J. The survival advantage of milk and dairy consumption: an
overview of evidence from cohort studies of vascular diseases, diabetes
and cancer. J Am Coll Nutr. 2008;27:723S734S.
70. Tremblay A, Gilbert JA. Milk products, insulin resistance syndrome and
type 2 diabetes. J Am Coll Nutr. 2009;28(suppl 1):91S102S.
71. Soedamah-Muthu SS, Ding EL, Al-Delaimy WK, Hu FB, Engberink
MF, Willett WC, Geleijnse JM. Milk and dairy consumption and
incidence of cardiovascular diseases and all-cause mortality: doseresponse meta-analysis of prospective cohort studies. Am J Clin Nutr.
2010;93:158 171.
72. Choi HK, Willett WC, Stampfer MJ, Rimm E, Hu FB. Dairy consumption and risk of type 2 diabetes mellitus in men: a prospective
study. Arch Intern Med. 2005;165:9971003.
73. Liu S, Choi HK, Ford E, Song Y, Klevak A, Buring JE, Manson JE. A
prospective study of dairy intake and the risk of type 2 diabetes in
women. Diabetes Care. 2006;29:1579 1584.
2888
Circulation
74. Pereira MA, Jacobs DR Jr, Van Horn L, Slattery ML, Kartashov AI,
Ludwig DS. Dairy consumption, obesity, and the insulin resistance
syndrome in young adults: the CARDIA Study. JAMA. 2002;287:
20812089.
75. Rosell M, Hakansson NN, Wolk A. Association between dairy food
consumption and weight change over 9 y in 19,352 perimenopausal
women. Am J Clin Nutr. 2006;84:14811488.
76. Beydoun MA, Gary TL, Caballero BH, Lawrence RS, Cheskin LJ,
Wang Y. Ethnic differences in dairy and related nutrient consumption
among US adults and their association with obesity, central obesity, and
the metabolic syndrome. Am J Clin Nutr. 2008;87:1914 1925.
77. Mozaffarian D, Cao H, King IB, Lemaitre RN, Song X, Siscovick DS,
Hotamisligil GS. Trans-palmitoleic acid, metabolic risk factors, and
new-onset diabetes in U.S. adults: a cohort study. Ann Intern Med.
2010;153:790 799.
78. Chardigny J-M, Destaillats F, Malpuech-Bruge`re C, Moulin J, Bauman
DE, Lock AL, Barbano DM, Mensink RP, Bezelgues JB, Chaumont P,
Combe N, Cristiani I, Joffre F, German JB, Dionisi F, Boirie Y, Sebedio
JL. Do industrially-produced and natural trans fatty acid sources have
the same impact on cardiovascular diseases risk factors in healthy
subjects? Results of the TRANSFACT Study. Am J Clin Nutr. 2008;87:
515516.
79. Motard-Belanger A, Charest A, Grenier G, Paquin P, Chouinard Y,
Lemieux S, Couture P, Lamarche B. Study of the effect of trans fatty
acids from ruminants on blood lipids and other risk factors for cardiovascular disease. Am J Clin Nutr. 2008;87:593599.
80. Riserus U, Smedman A, Basu S, Vessby B. Metabolic effects of conjugated linoleic acid in humans: the Swedish experience. Am J Clin
Nutr. 2004;79:1146S1148S.
81. Moloney F, Yeow TP, Mullen A, Nolan JJ, Roche HM. Conjugated
linoleic acid supplementation, insulin sensitivity, and lipoprotein metabolism in patients with type 2 diabetes mellitus. Am J Clin Nutr.
2004;80:887 895.
82. Zemel MB, Thompson W, Milstead A, Morris K, Campbell P. Calcium
and dairy acceleration of weight and fat loss during energy restriction in
obese adults. Obes Res. 2004;12:582590.
83. Harvey-Berino J, Gold BC, Lauber R, Starinski A. The impact of
calcium and dairy product consumption on weight loss. Obes Res.
2005;13:1720 1726.
84. Bolland MJ, Avenell A, Baron JA, Grey A, MacLennan GS, Gamble
GD, Reid IR. Effect of calcium supplements on risk of myocardial
infarction and cardiovascular events: meta-analysis. BMJ. 2010;341:
c3691.
85. Tholstrup T, Hoy CE, Andersen LN, Christensen RD, Sandstrom B.
Does fat in milk, butter and cheese affect blood lipids and cholesterol
differently? J Am Coll Nutr. 2004;23:169 176.
86. Biong AS, Muller H, Seljeflot I, Veierod MB, Pedersen JI. A comparison of the effects of cheese and butter on serum lipids, haemostatic
variables and homocysteine. Br J Nutr. 2004;92:791797.
87. Nestel PJ, Chronopulos A, Cehun M. Dairy fat in cheese raises LDL
cholesterol less than that in butter in mildly hypercholesterolaemic
subjects. Eur J Clin Nutr. 2005;59:1059 1063.
87a. Mozaffarian D, Hao T, Rimm EB, Willett WC, Hu FB. Changes in diet
and lifestyle and long-term weight gain in women and men. New Engl
J Med. In press.
88. Wolff E, Dansinger ML. Soft drinks and weight gain: how strong is the
link? Medscape J Med. 2008;10:189.
89. Duffey KJ, Popkin BM. Shifts in patterns and consumption of beverages
between 1965 and 2002. Obesity (Silver Spring). 2007;15:2739 2747.
90. Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB,
Flegal K, Ford E, Furie K, Go A, Greenlund K, Haase N, Hailpern S, Ho
M, Howard V, Kissela B, Kittner S, Lackland D, Lisabeth L, Marelli A,
McDermott M, Meigs J, Mozaffarian D, Nichol G, ODonnell C, Roger
V, Rosamond W, Sacco R, Sorlie P, Stafford R, Steinberger J, Thom T,
Wasserthiel-Smoller S, Wong N, Wylie-Rosett J, Hong Y. Heart disease
and stroke statistics2009 update: a report from the American Heart
Association Statistics Committee and Stroke Statistics Subcommittee.
Circulation. 2009;119:e21 e181.
91. Wang YC, Bleich SN, Gortmaker SL. Increasing caloric contribution
from sugar-sweetened beverages and 100% fruit juices among US children
and adolescents, 19882004. Pediatrics. 2008;121:e1604e1614.
92. Stull AJ, Apolzan JW, Thalacker-Mercer AE, Iglay HB, Campbell WW.
Liquid and solid meal replacement products differentially affect postprandial appetite and food intake in older adults. J Am Diet Assoc.
2008;108:1226 1230.
Mozaffarian et al
112. Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF, Miller ER 3rd,
Conlin PR, Erlinger TP, Rosner BA, Laranjo NM, Charleston J,
McCarron P, Bishop LM. Effects of protein, monounsaturated fat, and
carbohydrate intake on blood pressure and serum lipids: results of the
OmniHeart randomized trial. JAMA. 2005;294:24552464.
113. Mellen PB, Gao SK, Vitolins MZ, Goff DC Jr. Deteriorating dietary
habits among adults with hypertension: DASH dietary accordance,
NHANES 1988 1994 and 1999 2004. Arch Intern Med. 2008;168:
308 314.
114. Vardavas CI, Linardakis MK, Hatzis CM, Saris WH, Kafatos AG.
Cardiovascular disease risk factors and dietary habits of farmers from
Crete 45 years after the first description of the Mediterranean diet. Eur
J Cardiovasc Prev Rehabil. 2010;17:440 446.
115. Kris-Etherton P, Eckel RH, Howard BV, St Jeor S, Bazzarre TL. AHA
Science Advisory: Lyon Diet Heart Study: benefits of a Mediterraneanstyle, National Cholesterol Education Program/American Heart Association step I dietary pattern on cardiovascular disease. Circulation.
2001;103:18231825.
116. Sofi F, Abbate R, Gensini GF, Casini A. Accruing evidence about
benefits of adherence to the Mediterranean diet on health: an updated
systematic review and meta-analysis. Am J Clin Nutr. 2010;92:
1189 1196.
117. Margetts BM, Beilin LJ, Vandongen R, Armstrong BK. Vegetarian diet
in mild hypertension: a randomised controlled trial. BMJ (Clin Res Ed).
1986;293:1468 1471.
118. Sciarrone SE, Strahan MT, Beilin LJ, Burke V, Rogers P, Rouse IR.
Ambulatory blood pressure and heart rate responses to vegetarian meals.
J Hypertens. 1993;11:277285.
119. Hakala P, Karvetti RL. Weight reduction on lactovegetarian and mixed
diets: changes in weight, nutrient intake, skinfold thicknesses and blood
pressure. Eur J Clin Nutr. 1989;43:421 430.
120. Barnard ND, Cohen J, Jenkins DJ, Turner-McGrievy G, Gloede L,
Green A, Ferdowsian H. A low-fat vegan diet and a conventional
diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial. Am J Clin Nutr. 2009;89:1588S1596S.
121. Burke LE, Styn MA, Steenkiste AR, Music E, Warziski M, Choo J. A
randomized clinical trial testing treatment preference and two dietary
options in behavioral weight management: preliminary results of the
impact of diet at 6 months: PREFER study. Obesity (Silver Spring).
2006;14:20072017.
122. Burke LE, Hudson AG, Warziski MT, Styn MA, Music E, Elci OU,
Sereika SM. Effects of a vegetarian diet and treatment preference on
biochemical and dietary variables in overweight and obese adults: a
randomized clinical trial. Am J Clin Nutr. 2007;86:588 596.
123. Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V, Reeves G,
Burr ML, Chang-Claude J, Frentzel-Beyme R, Kuzma JW, Mann J,
McPherson K. Mortality in vegetarians and non-vegetarians: a collaborative analysis of 8300 deaths among 76,000 men and women in five
prospective studies. Public Health Nutr. 1998;1:33 41.
124. Fraser GE. Associations between diet and cancer, ischemic heart
disease, and all-cause mortality in non-Hispanic white California
Seventh-day Adventists. Am J Clin Nutr. 1999;70:532S538S.
125. Deleted in proof.
126. Shimazu T, Kuriyama S, Hozawa A, Ohmori K, Sato Y, Nakaya N,
Nishino Y, Tsubono Y, Tsuji I. Dietary patterns and cardiovascular
disease mortality in Japan: a prospective cohort study. Int J Epidemiol.
2007;36:600 609.
127. Ding EL, Mozaffarian D. Optimal dietary habits for the prevention of
stroke. Semin Neurol. 2006;26:1123.
128. Deleted in proof.
129. Livesey G, Taylor R, Hulshof T, Howlett J. Glycemic response and
health: a systematic review and meta-analysis: relations between dietary
glycemic properties and health outcomes. Am J Clin Nutr. 2008;87:
258S268S.
130. Riccardi G, Rivellese AA, Giacco R. Role of glycemic index and
glycemic load in the healthy state, in prediabetes, and in diabetes. Am J
Clin Nutr. 2008;87:269S274S.
131. Thomas D, Elliott EJ. Low glycaemic index, or low glycaemic load,
diets for diabetes mellitus. Cochrane Database Syst Rev. 2009;(1):
CD006296.
132. OKeefe JH, Gheewala NM, OKeefe JO. Dietary strategies for
improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol. 2008;51:249 255.
132a.Tappy L, Le KA. Metabolic effects of fructose and the worldwide
increase in obesity. Physiol Rev. 2010;90:23 46.
2889
133. Howard BV, Van Horn L, Hsia J, Manson JE, Stefanick ML,
Wassertheil-Smoller S, Kuller LH, LaCroix AZ, Langer RD, Lasser NL,
Lewis CE, Limacher MC, Margolis KL, Mysiw WJ, Ockene JK, Parker
LM, Perri MG, Phillips L, Prentice RL, Robbins J, Rossouw JE, Sarto
GE, Schatz IJ, Snetselaar LG, Stevens VJ, Tinker LF, Trevisan M,
Vitolins MZ, Anderson GL, Assaf AR, Bassford T, Beresford SA, Black
HR, Brunner RL, Brzyski RG, Caan B, Chlebowski RT, Gass M, Granek
I, Greenland P, Hays J, Heber D, Heiss G, Hendrix SL, Hubbell FA,
Johnson KC, Kotchen JM. Low-fat dietary pattern and risk of cardiovascular disease: the Womens Health Initiative Randomized Controlled
Dietary Modification Trial. JAMA. 2006;295:655 666.
134. Halton TL, Liu S, Manson JE, Hu FB. Low-carbohydrate-diet score and
risk of type 2 diabetes in women. Am J Clin Nutr. 2008;87:339 346.
135. Tinker LF, Bonds DE, Margolis KL, Manson JE, Howard BV, Larson J,
Perri MG, Beresford SA, Robinson JG, Rodriguez B, Safford MM,
Wenger NK, Stevens VJ, Parker LM. Low-fat dietary pattern and risk of
treated diabetes mellitus in postmenopausal women: the Womens
Health Initiative randomized controlled dietary modification trial. Arch
Intern Med. 2008;168:1500 1511.
136. Micha R, Mozaffarian D. Trans fatty acids: effects on metabolic
syndrome, heart disease and diabetes. Nat Rev Endocrinol. 2009;5:
335344.
137. Mozaffarian D. Does alpha-linolenic acid intake reduce the risk of
coronary heart disease? A review of the evidence. Altern Ther Health
Med. 2005;11:24 30.
138. Kromhout D, Giltay EJ, Geleijnse JM; Alpha Omega Trial Group. n-3
Fatty acids and cardiovascular events after myocardial infarction. N Engl
J Med. 2010;363:20152026.
139. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty
acids and carbohydrates on the ratio of serum total to HDL cholesterol
and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003;77:1146 1155.
140. Skeaff CM, Miller J. Dietary fat and coronary heart disease: summary of
evidence from prospective cohort and randomised controlled trials. Ann
Nutr Metab. 2009;55:173201.
141. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with
cardiovascular disease. Am J Clin Nutr. 2010;91:502509.
142. Jakobsen MU, OReilly EJ, Heitmann BL, Pereira MA, Balter K, Fraser
GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman
D, Stevens J, Virtamo J, Willett WC, Ascherio A. Major types of dietary
fat and risk of coronary heart disease: a pooled analysis of 11 cohort
studies. Am J Clin Nutr. 2009;89:14251432.
143. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease
of increasing polyunsaturated fat in place of saturated fat: a systematic
review and meta-analysis of randomized controlled trials. PLoS Med.
2010;7:e1000252.
144. Micha R, Mozaffarian D. Saturated fat consumption and effects on
cardiometabolic risk factors and coronary heart disease, stroke, and
diabetes mellitus: a fresh look at the evidence. Lipids. 2010;45:893905.
145. Jakobsen MU, Dethlefsen C, Joensen AM, Stegger J, Tjonneland A,
Schmidt EB, Overvad K. Intake of carbohydrates compared with intake
of saturated fatty acids and risk of myocardial infarction: importance of
the glycemic index. Am J Clin Nutr. 2010;91:1764 1768.
146. Galgani JE, Uauy RD, Aguirre CA, Diaz EO. Effect of the dietary fat
quality on insulin sensitivity. Br J Nutr. 2008;100:471 479.
147. Riserus U, Willett WC, Hu FB. Dietary fats and prevention of type 2
diabetes. Prog Lipid Res. 2009;48:44 51.
148. Jebb SA, Lovegrove JA, Griffin BA, Frost GS, Moore CS, Chatfield
MD, Bluck LJ, Williams CM, Sanders TA. Effect of changing the
amount and type of fat and carbohydrate on insulin sensitivity and
cardiovascular risk: the RISCK (Reading, Imperial, Surrey, Cambridge,
and Kings) trial. Am J Clin Nutr. 2010;92:748 758.
149. Keys A, Menotti A, Karvonen MJ, Aravanis C, Blackburn H, Buzina R,
Djordjevic BS, Dontas AS, Fidanza F, Keys MH, Kromhout D,
Nedeljkovic S, Punsar S, Seccareccia F, Toshima H. The diet and
15-year death rate in the seven countries study. Am J Epidemiol. 1986;
124:903915.
150. Degirolamo C, Shelness GS, Rudel LL. LDL cholesteryl oleate as a
predictor for atherosclerosis: evidence from human and animal studies
on dietary fat. J Lipid Res. 2009;50(suppl):S434 S439.
151. Beauchamp GK, Keast RS, Morel D, Lin J, Pika J, Han Q, Lee CH,
Smith AB, Breslin PA. Phytochemistry: ibuprofen-like activity in extravirgin olive oil. Nature. 2005;437:45 46.
2890
Circulation
152. He FJ, MacGregor GA. A comprehensive review on salt and health and
current experience of worldwide salt reduction programmes. J Hum
Hypertens. 2009;23:363384.
153. World Health Organization. World Health Report 2002: Reducing Risks,
Promoting Healthy Life. Geneva, Switzerland: World Health Organization; 2002.
154. Law MR, Morris JK, Wald NJ. Use of blood pressure lowering drugs in
the prevention of cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies. BMJ. 2009;338:b1665.
155. Strazzullo P, DElia L, Kandala NB, Cappuccio FP. Salt intake, stroke,
and cardiovascular disease: meta-analysis of prospective studies. BMJ.
2009;339:b4567.
156. Cook NR, Cutler JA, Obarzanek E, Buring JE, Rexrode KM,
Kumanyika SK, Appel LJ, Whelton PK. Long term effects of dietary
sodium reduction on cardiovascular disease outcomes: observational
follow-up of the Trials Of Hypertension Prevention (TOHP). BMJ.
2007;334:885 888.
157. Appel LJ. At the tipping point: accomplishing population-wide sodium
reduction in the United States. J Clin Hypertens (Greenwich). 2008;
10:711.
158. Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes around the
world: implications for public health. Int J Epidemiol. 2009;38:
791 813.
159. Risk Factor Monitoring and Methods Branch Web site, Applied
Research Program, National Cancer Institute. Sources of sodium among
the US population, 2005 06. http://riskfactor.cancer.gov/diet/
foodsources/sodium/. Accessed May 6, 2010.
160. Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood
JM, Pletcher MJ, Goldman L. Projected effect of dietary salt reductions
on future cardiovascular disease. N Engl J Med. 2010;362:590 599.
161. Smith-Spangler CM, Juusola JL, Enns EA, Owens DK, Garber AM.
Population strategies to decrease sodium intake and the burden of
cardiovascular disease: a cost-effectiveness analysis. Ann Intern Med.
2010;152:481 487, W170 W483.
162. Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Mortality
in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA. 2007;
297:842 857.
163. Autier P, Gandini S. Vitamin D supplementation and total mortality: a
meta-analysis of randomized controlled trials. Arch Intern Med. 2007;
167:1730 1737.
164. Miller ER 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ,
Guallar E. Meta-analysis: high-dosage vitamin E supplementation may
increase all-cause mortality. Ann Intern Med. 2005;142:37 46.
165. Miller ER 3rd, Juraschek S, Pastor-Barriuso R, Bazzano LA, Appel LJ,
Guallar E. Meta-analysis of folic acid supplementation trials on risk of
cardiovascular disease and risk interaction with baseline homocysteine
levels. Am J Cardiol. 2010;106:517527.
166. Huang HY, Caballero B, Chang S, Alberg AJ, Semba RD, Schneyer CR,
Wilson RF, Cheng TY, Vassy J, Prokopowicz G, Barnes GJ 2nd, Bass
EB. The efficacy and safety of multivitamin and mineral supplement use
to prevent cancer and chronic disease in adults: a systematic review for
a National Institutes of Health state-of-the-science conference. Ann
Intern Med. 2006;145:372385.
167. Astrup A, Grunwald GK, Melanson EL, Saris WH, Hill JO. The role of
low-fat diets in body weight control: a meta-analysis of ad libitum
dietary intervention studies. Int J Obes Relat Metab Disord. 2000;24:
15451552.
168. Howard BV, Manson JE, Stefanick ML, Beresford SA, Frank G, Jones
B, Rodabough RJ, Snetselaar L, Thomson C, Tinker L, Vitolins M,
Prentice R. Low-fat dietary pattern and weight change over 7 years: the
Womens Health Initiative Dietary Modification Trial. JAMA. 2006;295:
39 49.
169. Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy WS Jr, Brehm
BJ, Bucher HC. Effects of low-carbohydrate vs low-fat diets on weight
loss and cardiovascular risk factors: a meta-analysis of randomized
controlled trials. Arch Intern Med. 2006;166:285293.
170. Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR,
Kraemer HC, King AC. Comparison of the Atkins, Zone, Ornish, and
LEARN diets for change in weight and related risk factors among
overweight premenopausal women: the A TO Z Weight Loss Study: a
randomized trial. JAMA. 2007;297:969 977.
171. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I,
Golan R, Fraser D, Bolotin A, Vardi H, Tangi-Rozental O, Zuk-Ramot
172.
173.
174.
175.
176.
177.
178.
179.
180.
181.
182.
183.
184.
185.
186.
187.
188.
189.
190.
191.
Mozaffarian et al
192. Zhai F, Wang H, Wang Z, Popkin BM, Chen C. Closing the energy gap
to prevent weight gain in China. Obes Rev. 2008;9(suppl 1):107112.
193. Hill JO. Can a small-changes approach help address the obesity
epidemic? A report of the Joint Task Force of the American Society for
Nutrition, Institute of Food Technologists, and International Food Information Council. Am J Clin Nutr. 2009;89:477 484.
194. Norman GJ, Zabinski MF, Adams MA, Rosenberg DE, Yaroch AL,
Atienza AA. A review of eHealth interventions for physical activity and
dietary behavior change. Am J Prev Med. 2007;33:336 345.
195. Baird J, Cooper C, Margetts BM, Barker M, Inskip HM. Changing
health behaviour of young women from disadvantaged backgrounds:
evidence from systematic reviews. Proc Nutr Soc. 2009;68:195204.
196. World Health Organization. Interventions on Diet and Physical Activity:
What Works. Geneva, Switzerland: WHO Press; 2009.
197. Artinian NT, Fletcher GF, Mozaffarian D, Kris-Etherton P, Van Horn L,
Lichtenstein AH, Kumanyika S, Kraus WE, Fleg JL, Redeker NS,
Meininger JC, Banks J, Stuart-Shor EM, Fletcher BJ, Miller TD, Hughes
S, Braun LT, Kopin LA, Berra K, Hayman LL, Ewing LJ, Ades PA,
Durstine JL, Houston-Miller N, Burke LE. Interventions to promote
physical activity and dietary lifestyle changes for cardiovascular risk
factor reduction in adults: a scientific statement from the American
Heart Association. Circulation. 2010;122:406 441.
198. Barlow SE. Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight
and obesity: summary report. Pediatrics. 2007;120(suppl
4):S164 S192.
199. Bodenheimer T. Helping patients improve their health-related behaviors:
what system changes do we need? Dis Manag. 2005;8:319 330.
200. Simpson LA, Cooper J. Paying for obesity: a changing landscape.
Pediatrics. 2009;123(suppl 5):S301S307.
201. Kumanyika SK, Obarzanek E, Stettler N, Bell R, Field AE, Fortmann
SP, Franklin BA, Gillman MW, Lewis CE, Poston WC II, Stevens J,
Hong Y. Population-based prevention of obesity: the need for comprehensive promotion of healthful eating, physical activity, and energy
balance: a scientific statement from American Heart Association
Council on Epidemiology and Prevention, Interdisciplinary Committee
for Prevention (formerly the Expert Panel on Population and Prevention
Science). Circulation. 2008;118:428 464.
2891
202. Angell SY, Silver LD, Goldstein GP, Johnson CM, Deitcher DR,
Frieden TR, Bassett MT. Cholesterol control beyond the clinic: New
York Citys trans fat restriction. Ann Intern Med. 2009;151:129 134.
203. Matson-Koffman DM, Brownstein JN, Neiner JA, Greaney ML. A
site-specific literature review of policy and environmental interventions
that promote physical activity and nutrition for cardiovascular health:
what works? Am J Health Promot. 2005;19:167193.
204. Dietz WH, Benken DE, Hunter AS. Public health law and the prevention
and control of obesity. Milbank Q. 2009;87:215227.
205. Lytle LA. Measuring the food environment: state of the science. Am J
Prev Med. 2009;36:S134 S144.
206. Sallis JF, Glanz K. Physical activity and food environments: solutions to
the obesity epidemic. Milbank Q. 2009;87:123154.
207. Story M, Giles-Corti B, Yaroch AL, Cummins S, Frank LD, Huang TT,
Lewis LB. Work group IV: future directions for measures of the food
and physical activity environments. Am J Prev Med. 2009;36:
S182S188.
208. Larson NI, Story MT, Nelson MC. Neighborhood environments: disparities in access to healthy foods in the U.S. Am J Prev Med. 2009;36:
74 81.
209. Powell LM, Chaloupka FJ. Food prices and obesity: evidence and policy
implications for taxes and subsidies. Milbank Q. 2009;87:229 257.
210. Harnack LJ, French SA. Effect of point-of-purchase calorie labeling on
restaurant and cafeteria food choices: a review of the literature. Int J
Behav Nutr Phys Act. 2008;5:51.
211. Swinburn B. Obesity prevention in children and adolescents. Child
Adolesc Psychiatr Clin N Am. 2009;18:209 223.
212. Magnus A, Haby MM, Carter R, Swinburn B. The cost-effectiveness of
removing television advertising of high-fat and/or high-sugar food and
beverages to Australian children. Int J Obes (Lond). 2009;33:
1094 1102.
213. Papadakis S, Moroz I. Population-level interventions for coronary heart
disease prevention: what have we learned since the North Karelia project? Curr Opin Cardiol. 2008;23:452 461.
214 Horowitz CR, Robinson M, Seifer S. Community-based participatory
research from the margin to the mainstream: are researchers prepared?
Circulation. 2009;119:26332642.
KEY WORDS: diet
nutrition
prevention
behavior
policy