text:
The Committee focused attention on fruits and vegetables, whole grains, and
milk products because of the growing body of research linking them to health
and because intake of these food groups by many Americans is far below previous
recommendations. The fruit and vegetable groups are combined because they are
examined together in much of the scientific literature related to health outcomes.
This section addresses three major questions related to food groups and health:
What are the relationships between fruit and vegetable intake and health?
What are the relationships between whole-grain intake and health?
What are the relationships between milk product intake and health?
The other basic food group (meat, poultry, fish and legumes) is covered in Section
1, "Meeting Recommended Nutrient Intakes," and fish also is covered in the
and "Food Safety" sections.
Greater consumption of fruits and vegetables (5-13 servings or 2 ½-
6 ½ cups per day depending on calorie needs ) is associated with a reduced
risk of stroke and perhaps other cardiovascular diseases, with a reduced risk
of cancers in certain sites (oral cavity and pharynx, larynx, lung, esophagus,
stomach, and colon-rectum), and with a reduced risk of type 2 diabetes (vegetables
more than fruit). Moreover, increased consumption of fruits and vegetables may
be a useful component of programs designed to achieve and sustain weight loss.
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Overview. The conclusion related to cardiovascular
disease (CVD) is based on the Committee's review of evidence from an extensive
literature view covering prospective, observational studies; other observational
studies that addressed whole patterns of food consumption; and trials of the
effects of fruit and vegetable consumption on blood pressure. Fruits and vegetables
are associated with a reduction in CVD through a variety of mechanisms. First,
they provide nutrients, such as fiber, folate, potassium, and carotenoids and
other phytochemicals that may directly reduce CVD risk. Second, certain nutrients
may directly improve established, diet-related CVD risk factors, such as blood
pressure, hyperlipidemia, and diabetes. Third, the consumption of fruits and
vegetables may lead to a reduced intake of saturated fat and cholesterol. Therefore,
it is plausible to hypothesize that diets rich in fruits and vegetables should
reduce the risk of CVD.
Several review articles have summarized the evidence from prospective observational
studies (Bazzano et al., 2003; Law and Morris, 1998; Ness and Powles, 1997).
The review by Bazzano included 10 prospective studies. In 7 of the 10 studies,
an increased intake of fruits and vegetables was associated with a significant
reduction in at least one CVD outcome; in pooled analyses of these studies, the
relative risk of CVD (highest to lowest categories of fruit and vegetable intake)
was 0.82 (95 percent CI: 0.76 to 0.89). Since then, four other major studies
were published (Johnsen et al., 2003; Rissanen et al., 2003; Sauvaget et al.,
2003; Steffen et al., 2003). The two studies that examined the relationship of
fruit and vegetable intake with CVD mortality each documented a significant inverse
relationship (Rissanen, 2003; Steffen et al., 2003;). In six of the seven studies
that examined the relationship of fruit and vegetable intake with stroke, there
was a significant inverse relationship (Bazzano et al., 2002; Gillman et al.,
1995; Johnsen et al., 2003; Joshipura et al., 1999; Rissanen et al., 2003; Steffen
et al., 2003; Sauvaget et al., 2003). Only three studies examined the relationship
of fruit and vegetable intake with CHD (Bazzano et al., 2002; Joshipura et al.,
2001; Steffen et al., 2003); an inverse relationship was documented in only one
study (Joshipura et al., 2001). In most studies, the results were attenuated
in models that included CVD risk factors. This pattern of results suggests that
at least part of the beneficial effects of fruit and vegetable intake is mediated
through CVD risk factors. In most studies that documented a significant relationship,
the general pattern of results appeared be a progressive, inverse relationship
rather than a threshold relationship.
Other observational studies have examined the relationship between whole patterns
of food consumption and CVD. Often these studies use factor analysis to identify
clusters of foods that are commonly consumed together. In these studies, those
dietary patterns associated with a reduced risk of CVD (invariably) are rich
in fruits and vegetables (Fung et al., 2001; Hu et al., 2001; Millen et al.,
To date, no trial has tested the effects of increased fruit and vegetable on
clinical CVD outcomes (i.e., coronary heart disease events, stroke). However,
some trials have assessed the effects of fruits and vegetables on CVD risk factors.
Four trials tested the effects of increased fruit and vegetable intake on blood
pressure. Two of these trials documented that increased fruit and vegetable intake
can lower blood pressure (Appel et al., 1997; John et al., 2002). Mean systolic
blood pressure/diastolic blood pressure reductions were 2.7/1.9 mmHg and 4.0/1.5,
respectively. All reductions were significant. In the two other trials, both
of which were smaller or less well controlled, increased fruit and vegetable
intake did not lower blood pressure (Broekmans et al., 2001; Smith-Warner et
al., 2000). Finally, two trials tested the effects of fruits and vegetables in
the context of multifactorial interventions on blood pressure (Appel et al.,
2003; Sacks et al., 2001). In both studies, the multifactorial interventions
significantly lowered blood pressure. Based on extensive research documenting
that increased potassium intake reduces blood pressure (Whelton et al., 1997),
at least part of the beneficial effect of increased fruit and vegetable intake
on blood pressure results from increased potassium consumption. In summary, prospective
observational studies have documented that increased fruit and vegetable intake
is associated with a reduced risk of stroke and perhaps other cardiovascular
diseases. Clinical trials have documented that an increased intake of fruits
and vegetables can lower blood pressure.
Overview. The conclusion pertaining to fruit and vegetable
intake and cancer prevention is based on the Committee's consideration of published
evidence-based reviews focusing on the relationship between consumption of fruits
and vegetables and cancer risks. These reviews were conducted by expert panels
of the World Cancer Research Fund, American Institute for Cancer Research (WCRF/AICR,
1997), the National Cancer Institute (http://cancer.gov/cancerinfo/pdq/prevention/),
and the World Health Organization (WHO) International Agency for Research on
Cancer (IARC, 2003) (IARC Handbook of Cancer Prevention on Fruits and Vegetables).
All expert panels followed a similar process of reviewing international evidence-based
literature, primarily epidemiological studies including case-control and prospective
cohort studies and controlled trials with meta-analyses and pooled analyses to
establish the strength of the evidence.
It has now been established that cancer results from the interaction of human
genes with environmental factors such as tobacco use, dietary factors including
low fruit and vegetable consumption and high red meat and fat intake, and lifestyle
issues such as physical inactivity and obesity (WCRF/AICR 1997). Individuals
who consume diets rich in fruits and vegetables may be at lower risk for certain
cancers, particularly cancers of the gastrointestinal tract. The World Health
Organization International Agency for Research in Cancer (IARC) has estimated
that low fruit and vegetable intake contributes to 5 to 12 percent of all cancers
and up to 20 to 30 percent of upper gastrointestinal cancers that may otherwise
be preventable. Therefore, the consumption of fruits and vegetables can confer
protection against cancer. The phytochemical components in fruits and vegetables
possess anticarcinogenic properties that influence DNA damage and repair, thus
reducing mutations. These phytochemicals include antioxidants such as carotenoids
and vitamin C, flavanoids, isothiocyanates, and organosulfides, as well as minerals
and other bioactive compounds (Liu et al., 2003b). In addition, fruits and vegetables
provide fiber, which helps decrease gut transit time and binds potential carcinogenic
agents, secondary bile acids, and short-chain fatty acids (WCRF/AICR, 1997).
Review of the Evidence. In 1997, the WCRF/AICR expert
panel provided key evidence that dietary protection against cancer is strongest
and most consistent for diets high in vegetables and fruits, particularly in
relation to cancers of the mouth and pharynx, esophagus, stomach, colon-rectum
(vegetables only), and lung (WCRF/AICR 1997). The National Cancer Institute's PDQ® (Physician Data Query at http://cancer.gov/cancerinfo/pdq/prevention/)
subsequently confirmed these findings. This database formed the basis of the
NCI's National 5-A-Day Program (http://www.5aday.gov).
The WHO IARC published the findings of their working group's
extensive review in the IARC Handbook of Cancer Prevention
on Fruit and Vegetables (2003).
The IARC Working Committee evaluated the evidence gathered
on certain cancer sites in relation to intake of total fruits
or total vegetables. Few of the identified
studies had examined the effects of the total combined intake
of fruits and vegetables. The world literature was reviewed
and grouped together based on study design—either
randomized-controlled trials, cohort studies, or case-control
studies. The expert panel also considered the selection
bias, confounding factors, measurement errors,
and other variables. Human studies were included in the IARC
evaluation only if the reports provided estimates of risk
for total fruit or for total vegetable
consumption and 95 percent confidence intervals were available.
Estimates of a weighted mean of the reported relative risks
were calculated. Evidence tables
have been constructed for each cancer site, and meta-analyses
and pooled analyses are presented. The results of this analysis
of cancer sites are published in
the IARC's handbook. The IARC concluded there is evidence
of cancer preventive effects with increased consumption
of fruits and vegetables for cancers of the
mouth, pharynx, esophagus, colon-rectum, larynx, stomach,
and lung. There is inadequate evidence of a cancer-preventive
effect of fruit and vegetable consumption
for all other cancer sites. The number of studies, mean odd
ratios, and the 95 percent confidence intervals on some
of the cancer sites are listed below in
Tables D6-1 and D6-2.
In addition, the preventive effects of fiber on colorectal cancer were recently
demonstrated in a prospective study conducted by EPIC. Results showed that doubling
total fiber intake from the current average level in most populations (about
20g per day) may reduce the risk of colorectal cancer, particularly colon cancer.
About eight portions (rather than just five) of fruits and vegetables would need
to be consumed per day, along with the equivalent of five slices of whole-grain
bread (Riboli and Norat, 2003).
Recommendations from Other Groups. Agencies of the
Federal government, preventive health organizations, and world bodies have recommended
an increased intake of a variety of fruits and vegetables to 5 to 9 servings
per day, or 400 to 800 g of fruits and vegetables per day (NCI website: http://cancer.gov/cancerinfo/pdq/prevention/,
WCRF and AICR, 1997; IARC, 2003). Adherence to the AICR cancer prevention recommendations
investigated in the Iowa Women's Health Study Cohort have substantial
impact on reducing cancer incidence, with population attributable risks (avoidable
risk) of 22 percent (95 percent CI, 12-30) for cancer incidence and 11 percent
(95 percent CI 4-24) for cancer mortality (Cerhan et al., 2004).
The conclusion relating to the relationship of fruit and vegetable intake with
diabetes is based on the Committee's review of cross-sectional and prospective
studies as described below. The roles of fruits and vegetables tend to be associated
with those of fiber in the prevention of type 2 diabetes, making them difficult
to distinguish. Dietary fiber tends to lower postprandial glucose response (Anderson
and Akanji, 1991). Diets high in complex carbohydrates have been shown to protect
against type 2 diabetes, and this has been ascribed in some studies to their
high fiber content (Yang et al., 2003).
Review of the Evidence. Ford et al. (2000) examined
whether fruit and vegetable consumption was associated with type 2 diabetes incidence
in a cohort of U.S. adults age 25 to 74 years who were followed for about 20
years. After adjustment for a large number of variables, the hazard ratio for
participants consuming five or more servings of fruits and vegetables per day
compared with those consuming none was 0.73 for all participants, 0.53 for women,
and 1.14 for men. Thus, these investigators found conflicting results in men
and women. Williams and colleagues (1999) have shown that frequent intakes of
raw and salad vegetables are protective against type 2 diabetes. However, in
the same study, they did not find a significant association between fruits and
diabetes. A subsequent study in the same cohort showed that a higher intake of
both fruits and vegetables is associated with a lower risk for having glucose
intolerance and undiagnosed diabetes (Williams et al., 2000). Gittelsohn et al.
(1998) also reported that a higher intake of fruits and vegetables was associated
with a lower prevalence of diabetes.
In a cross-sectional study of a large population-based cohort not known to have
diabetes, a report from the European Prospective Investigation into Cancer and
Nutrition (EPIC) group (Sargeant et al., 2001) showed that those individuals
who reported never or seldom having both fruit and green leafy vegetables had
higher mean HgbA1c measurements (5.43 percent) than those who reported more frequent
consumption (5.34 percent). These differences were not substantially changed
after controlling for dietary fiber or for vitamin C. This lends support to the
hypothesis that a high intake of fruits and green leafy vegetables may influence
glucose metabolism and may contribute to the prevention of diabetes. These investigators
carefully excluded participants with a diagnosis of diabetes, who may have changed
their diet and lifestyle as a result of their diagnosis.
In a prospective study of middle-aged men, increased consumption of vegetables
and legumes was inversely associated with 2-hour glucose level (Feskens et al.,
1995). In the Nurses' Health Study (Colditz et al., 1992) the risk of
diabetes was inversely related to vegetable but not to fruit consumption. Another
longitudinal observational study of 20-year duration (Snowdon and Phillips, 1985)
also reported a lower incidence of diabetes in those individuals who increased
their intake of fruits and vegetables during the followup period. Some studies,
however, have shown no effect (Lundgren et al., 1989; Salmeron et al., 1997a,
1997b). On the other hand, no study has found a harmful effect of fruit and vegetable
consumption on the development of diabetes. Van Dam et al. (2002) reported on
two major dietary patterns and the risk of type 2 diabetes in the Male Health
Professionals study. They found that a prudent diet, characterized by a
higher consumption of vegetables, fruit, fish, poultry, and whole grains, was
associated with a significantly decreased risk for the development of diabetes
as compared with a western diet characterized by a higher consumption of red
meat, processed meat, French fries, high-fat dairy products, refined grains,
and sweets and desserts.
Recommendations From Other Groups. Consistent with
the above, current nutrition recommendations from the American Diabetes Association
and the WHO for the prevention of type 2 diabetes encourage the consumption of
carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat
milk (Franz et al., 2002; Mann et al., 2002).
Overview. The conclusion relating to the relationship
of fruit and vegetable intake with weight status is based on the Committee's
review of a number of observational studies, including only two prospective studies,
and several different types of trials, as described below. Fruits and vegetables
are high in water and fiber content and therefore low in energy density. These
types of foods also may promote satiety and decrease energy intake. Therefore,
it is plausible to hypothesize that diets rich in fruits and vegetables might
prevent weight gain and facilitate weight loss.
Review of the Evidence. A relatively large number
of observational studies have examined the relationship between fruit and vegetable
consumption and weight (Bazzano et al., 2002; Drapeau et al., 2004; Nicklas,
2003; Flood et al., 2002; Gillman et al.; 1995; Kobayashi et al., 2002; LaForge
et al., 1994; Lahti-Koski et al., 2002; Lin and Morrison, 2002; Liu et al., 2000;
2001; Patterson et al., 1990; Rissanen et al., 2003; Serdula et al., 1996; Terry
et al., 2001; Trudeau et al., 1998; Williams et al., 1999). However, most are
cross-sectional studies, which limit causal inferences. Drapeau et al. (2004)
reported that increases in the consumption of whole fruits in a cohort of 248
volunteers followed for approximately 6 years was associated with a lower increase
in body weight with time. Only two prospective studies examined the relationship
between fruit and/or vegetable consumption and change in BMI. In one study, Kahn
and colleagues (1997) followed 35,156 men and 44,080 women who participated in
the Cancer Prevention Study II of the American Cancer Society. Over
the course of 10 years, those men and women in the highest quintile of vegetable
intake (> 19 servings per week) experienced a significant decrease in BMI
(that is, a decline of 0.11 kg/m2 in men and 0.10 kg/m2 in women). Another prospective
study (Field et al., 2003) assessed the effects of fruit and vegetable intake
on changes in BMI over the course of 3 years of followup in 8,203 girls and 6,715
boys, age 9 to 14 years. In this study, neither fruits nor fruit juices predicted
changes in BMI. Vegetable intake was inversely associated with BMI change in
boys but not girls. This effect in boys was diminished and no longer statistically
significant once total calories were included in the model. These findings suggest
that the protective effect of vegetables was mediated through reduced calorie
intake rather than the vegetables per se.
As reviewed by Rolls and colleagues (2004), several different types of trials
have assessed the effects of increased fruit and vegetable intake on weight.
In two uncontrolled studies, ad libitum provision of a traditional Native
Hawaiian diet, which is rich in fruits and vegetables, led to reduced weight
in overweight Hawaiians. Several small trials that advised persons to increase
fruit and vegetable consumption but did not advise them to lose weight documented
no net effect on weight (see Table 4 from Rolls et al., 2004). Trials that advised
persons to increase fruit and vegetable consumption and also to decrease fat
intake, again without giving advice to lose weight, tended to show weight maintenance
or net weight loss (see Table 4 from Rolls et al., 2004). Of interest is one
trial that specifically tested the effects of fruits and vegetables on weight
over 1 year (Djuric et al., 2002). In this randomized 2 by 2 factorial trial
that tested the effects of (1) increased fruit and vegetable intake and (2) reduced fat intake, alone or
combined, participants were counseled to maintain their energy intake while they
made the dietary changes relevant to their assigned group. The group assigned
to increase their fruit and vegetable group without reducing fat intake increased
fruit and vegetable consumption from about 4 to 11 servings per day and increased
their energy intake by approximately 170 kcal per day. This group increased their
weight by 4 pounds. Those assigned to the reduced fat group alone reduced their
weight by 11 pounds, while those assigned to both increased intake of fruits
and vegetables and reduced fat had no change in weight. In aggregate, these data
indicate that in the absence of advice to lose weight, increased fruit and vegetable
intake by itself does not lead to weight loss.
Most relevant are those trials that attempted weight loss through increased
fruit and vegetable consumption, often combined with reduced calorie intake,
typically with a focus on decreased fat intake. The largest and longest study
to examine this issue documented the effects of a cardiovascular risk reduction
intervention that attempted to improve blood pressure and lipid control (Stamler
and Dolecek, 1997). In this trial, 6,248 men were advised to lose weight. Several
dietary changes predicted sustained weight loss, including greater intakes of
fruit and vegetables.
Another clinical trial, PREMIER (Appel et al., 2003), tested the effects of
two different behavioral intervention programs to lower blood pressure, in part
through weight loss. One intervention emphasized calorie reduction, reduction
in fat intake to < 30 percent energy, and increased physical activity. The
other intervention emphasized the DASH diet, which is rich in fruits and vegetables
and further reduced fat intake (< 25 percent energy). After 6 months of intervention,
mean intake of fruit and vegetable intake was nearly 8 servings per day in the
group that received advice on the DASH diet but only about 5 servings per day
in the other group. Corresponding net weight loss was 12.8 lb and 10.8 lb, respectively,
but the difference between the groups was not statistically significant (p=0.08).
Two uncontrolled studies documented that a low-fat, low-energy density diet that
allowed unlimited intake of fruits and vegetables led to sustained weight loss.
In the first study with an average followup period of 17 months (Weinsier et
al., 1982), 44 percent of individuals continued to lose weight and 92 percent
remained below their baseline weight. A similar pattern was evident in the second
study by this group with 25 months of followup (Fitzwater et al., 1991).
Overall, available data suggest that increased consumption of fruits and vegetables
may be a useful component of programs designed to achieve and sustain weight
loss. However, there are limited data that increased consumption of fruits and
vegetables prevent weight gain in the first place.
Daily servings of fruits and vegetables for individuals
2 years of age and older remained similar from an average
total of 4.5 servings in 1989–1991 to 4.9 servings
in 1994–1996; they decreased slightly to 4.7 servings in
1999–2000 (NCI website:
Daily vegetable intake increased from 3.2 to 3.4 servings,
then decreased to
3.2 servings. On average, total vegetable intake included
0.3 servings of dark green/deep yellow vegetables, 1.4 servings
of starchy vegetables (primarily fried
potatoes) and 1.5 servings of tomatoes and other vegetables.
Fruit intake increased from 1.3 to 1.5 servings over the
same time frame. Neither trend is considered
statistically significant. Vegetable consumption tends to
increase as individuals age, but fruit consumption is highest
among the very young and oldest individuals
in the population. Individuals of lower education and income
levels tend to eat fewer servings of vegetables and fruit
than do those with more education and
higher income. According to national surveys, African Americans
tend to have the lowest intakes of fruits and vegetables
among ethnic and racial groups (USDA,
Consuming at least 3 servings (equivalent to 3 ounces) of whole grains per
day can reduce the risk of diabetes and coronary heart disease (CHD) and helps
with weight maintenance. Thus, daily intake of 3 ounces of whole grains per day
is recommended, preferably by substituting whole grains for refined grains.
Overview. The conclusion is based on the Committee's
review of scientific evidence from 46 published papers pertaining to coronary
heart disease, diabetes, and obesity. The recommended number of whole grain servings
is based on evidence presented in 12 large prospective studies, which are presented
in Appendix G3.
Whole grains and foods made from them consist of the entire grain seed, usually
called the kernel. The kernel is made of three components—the bran, the germ
and the endosperm. If the kernel has been cracked, crushed, or flaked, then it
must retain nearly the same relative proportions of bran, germ, and endosperm
as the original grain to be called whole grain (AACC et al., 2004). In the grain-refining
process, most of the bran and some of the germ is removed, resulting in the loss
of dietary fiber (also known as cereal fiber), vitamins, minerals, lignans, phytoestrogen,
phenolic compounds and phytic acid (Slavin, 2003). Most refined grains are then
enriched with thiamin, riboflavin, iron and niacin to restore these nutrients
to levels found in the grain prior to refining. Enriched refined grains products
are required by law to be fortified with folic acid, but whole-grain foods are
not required to be fortified with folic acid. (ANON, Federal Register, 1996).
However, food manufacturers may fortify whole-grain foods where regulations permit
the addition of folic acid. Currently, a number of ready-to-eat whole-grain breakfast
cereals are fortified with folic acid.
Important grains in the U.S. diet include wheat, rice, maize, and oats. The
average intake of whole grains is less than 1 serving per day; less than 10 percent
of Americans consume 3 servings per day (Cleveland et al., 2000). In a study
of whole-grain consumption by U.S. children and adolescents using data from the
1994–1996 Continuing Survey of Food Intake by Individuals (CSFII), the
average whole-grain intake ranged from 0.8 servings per day for preschool-aged
children to 1.0 servings per day for adolescents (Harnack et al., 2003). Ready-to-eat
cereals, corn or tortilla chips, and yeast breads were the major sources of whole
grains (30.9 percent, 21.7 percent and 18.1 percent respectively).
Whole-grain intake has been found to be consistently associated with a reduction
in the risk of CHD among both men and women (see Appendix G3) (Jacobs et al.,
1998; 1999; Jensen et al., in press 2004; Liu et al., 1999, 2002; Pietinen et
al., 1996; Rimm et al., 1996; Steffen et al., 2003). Collectively, the studies
suggest a 20 to 30 percent reduced risk of CHD with 3 or more servings of whole
grain foods per day. For example, in the Nurses' Health Study, which
documented 761 cases of CHD in 75,521 women, increased whole-grain intake was
associated with decreased risk of CHD. Women in the highest quintile of intake
had a relative risk of 0.51 (P <0.0001) compared to those in the lowest quintile
(Liu et al., 1999). In the Iowa Women's Health Study (Jacobs et al.,
1998), which involved 34,492 postmenopausal women followed for 6 years, a greater
intake of whole grain was associated with a reduced risk of CHD death (RR = 0.67
comparing the highest quintile to the lowest quintile of intake). In the Health
Professionals Study (all men) (Jensen et al., in press 2004), men in the
highest quintile for whole-grain intake had a RR of 0.64 for CHD compared to
those in the lowest quintile of whole-grain intake. Although adjustment for potential
confounders and risk factors for CHD other than BMI attenuated this association
(Hazard Ratio (HR) = 0.82; P for trend = 0.01), each 20 g increment
in whole-grain consumption corresponded to a 6 percent reduction in CHD risk
(Jensen et al., in press 2004).
Certain studies base their evaluation of the strength of the relationship between
whole-grain intake and reduced risk of CHD on the consumption of specific food
groups or foods that are high in whole grains. For example, The Adventist
Health Study (Fraser et al., 1992) reported an inverse association between
intake of whole wheat bread and risk of myocardial infarction in 31,208 Seventh-Day
Adventists (RR=0.56 for nonfatal myocardial infarction in those consuming whole
wheat compared to white bread). Whole-grain bread intake also has been associated
with a reduced incidence of CHD (Jacobs et al., 2001). Similarly, intake of breakfast
cereals with a high whole-grain content also has been associated with a reduced
incidence of CHD (Liu et al., 2003a).
Fiber and the Observed Protective Effect of Whole Grain.
Because dietary fiber is an important component of whole grains, and the fiber
content is greatly reduced when grains are refined, the literature on fiber and
CHD also is applicable to the protective role of whole grains against CHD (See
"Rationale" for Question 1 on fiber and CHD above). In brief, intake of high
fiber foods has been independently associated with reduced incidence of ischemic
heart disease and stroke (Humble et al., 1993; Khaw and Barrett-Connor, 1987;
Pietinen et al., 1996; Rimm et al., 1996; Wolk et al., 1999).
Mozaffarian et al. (2003) determined whether fiber consumption from fruit, vegetable,
and cereal sources (including whole grains and bran) is associated with incident
cardiovascular disease in elderly persons. During 8.6 years of followup in 3,588
men and women age 65 years or older at baseline, cereal fiber consumption was
inversely associated with incident CVD (P = 0.02). The relative risk
was 0.79 in the highest quintile of intake compared with the lowest quintile.
Neither fruit fiber intake nor vegetable fiber intake were associated with CHD
incidence (Mozaffarian et al., 2003). This finding of a protective effect of
fiber from cereals, but not from fruits or vegetables, is consistent with results
from other studies (Pietinen et al., 1996; Rimm et al., 1996; Wolk et al., 1999)
and supports the importance of whole-grain consumption as protective against
CHD risk.
A number of studies assessing the relationship between whole-grain consumption
and risk of CHD have evaluated the relationship of fiber intake and CHD risk
in the same population. For example, the report on the Nurses' Health Study
(Liu et al., 1999) evaluated whether the association of whole-grain intake with
CHD risk could be attributed to its constituents (e.g., dietary fiber, folate,
vitamin B6, and vitamin E) or if something other than the micronutrient and fiber
content of the whole grain was correlated with the protective effect. When the
investigators adjusted for these protective factors, the significant inverse
relationship of whole-grain intake to CHD risk was still evident. They suggest
that this implies either a synergistic effect of the protective factors in whole
grains or an effect from other substances, as yet unidentified, in whole grains.
When the investigators for the Health Professionals Study looked at
bran (a component of whole grain) and CHD risk, they found that the inverse association
of bran and CHD was even stronger than that for whole grain. The HR of CHD among
men with the highest intake of added bran was 0.70 compared to that among men
with no intake of added bran (P= <0.001) (Jensen et al., in press
2004). The authors conclude that their study supports the reported beneficial
association of whole-grain intake and CHD, and it suggests that the bran component
of whole grains could be a key factor in this relationship. However, the inverse
relationship between whole-grain consumption remained after adjusting for bran
In the Cardiovascular Health Study (a population-based, multicenter
study with 3,588 men and women age 65 or older), cereal fiber consumption was
inversely associated with CHD (P= 0.02). Risk was 21 percent lower in
the highest quintile of intake, compared with the lowest quintile. In similar
analyses, neither fruit fiber intake (P= 0.98) nor vegetable fiber intake
(P=0.95) was associated with incidence of CHD (Mozaffarian et al., 2003).
Physiological Basis for a Relationship Between Whole-Grain intake
and Decreased Risk of CHD. Although well-conducted prospective
cohort studies are important and valuable in determining associations between
nutrient intake and risk of disease, there is more confidence in these results
when they are supported by biologically plausible mechanisms for the observed
effect. One potential mechanism by which whole grains may decrease risk of CHD
is through their antioxidant content (Decker et al., 2002). Vitamin E is present
in whole grains but removed in the refining process and not added back in the
enriching process. Similarly, selenium is present in whole grains but not enriched
grains (Miller et al., 2001). Other bioactive compounds in whole grains include
lignans, phytoestrogens, phytosterols, and digestive enzyme inhibitors. Although
it is difficult to sort out the beneficial effects of whole grains independent
of some of their constitutents such as fiber and antioxidants, Slavin makes a
case that whole-grain consumption is protective beyond what would be predicted
if the protection found with the individual compounds were simply additive (Slavin
et al., 2001; Slavin, 2003).
Possible Confounders With Respect to Whole-Grain Intake and
CHD Incidence. Compared with low consumers of whole-grain foods,
high consumers may smoke less, exercise more, and be more likely to use supplements
of multivitamins. Thus, whole-grain intake may be just a proxy for a healthy
lifestyle. However, when any of these known confounders have been evaluated,
the inverse relationship between whole-grain consumption and risk of CHD (although
attenuated) still remains statistically significant (Jensen et al., in press
2004; Liu et al., 1999). Moreover, in the studies that have evaluated fiber as
a confounder, whole-grain intake has still remained protective against CHD (Liu
et al., 2000). In fact, an argument could be made that the beneficial effects
observed with cereal fiber are really due to whole grains rather than to the
fiber per se, since it is probable that the cereal fiber intake is closely reflective
of the whole-grain intake. Studies that focus on whole grain or on cereal fiber
as the exposure measurements are, therefore, often measuring approximately the
same entity (Mozaffarian et al., 2003). In addition, problems specific to measuring
whole-grain intake may hinder accurate interpretation of results. For example,
often participants are asked how much dark bread they ate; but the whole grain
content of many dark breads is very low.
As with whole grains and CHD, major prospective epidemiological studies show
an inverse relationship between whole-grain consumption and the risk of type
2 diabetes. Three prospective studies in large numbers of men and women examined
the relationship of whole-grain or cereal-fiber intake with the risk of type
2 diabetes. Each study used a mailed food frequency questionnaire as well as
self-reported diabetes diagnosis. Risk of incident diabetes was 21 to 27 percent
lower for those in the highest quintile of whole-grain intake and 30 to 36 percent
lower in the highest quintile of cereal-fiber intake, each compared to the lowest
quintile (Liu et al., 2000; Salmeron et al., 1997a, 1997b,). Risk reduction persisted
after adjustment for the healthier lifestyle found among habitual whole-grain
Similarly, in the Iowa Women's Health Study, approximately 100,000
post-menopausal women were sampled and followed for 6 years. Meyer et al. (2000)
examined the relationship of baseline intake of carbohydrate, fiber, and grains
on the incidence of diabetes in this large cohort of women. Total grain, whole
grain, total fiber, cereal fiber, and dietary magnesium intakes all showed strong
inverse associations with incidence of diabetes after adjustment for potential
nondietary confounding variables. Multivariate-adjusted relative risks of diabetes
were 1.0, 0.99, 0.98, 0.92, and 0.79 (P= 0.0089) for whole grains and
1.0, 0.81, 0.82, 0.81, and 0.67 (P= 0.0003) for total fiber. Women who
consumed the most whole grains (>17.5 servings per week) had a 21 percent
lower risk of diabetes compared with those with the lowest intakes of whole grains
(<3 servings per week) (Meyer et al., 2000). There was no significant effect
of refined grains, or of fruits and vegetables.
Fung et al. (2001) examined prospectively the associations between whole- and
refined-grain intake and the risk of type 2 diabetes among a large cohort of
men in the Health Professionals Follow-UStudy. After adjustment for
age; physical activity; cigarette smoking; alcohol consumption; family history
of diabetes; and fruit, vegetable and energy intakes; the relative risk of diabetes
was 0.58 (P= <0.0001) comparing the highest with the lowest quintile
of whole-grain intake. Intake of refined grains was not significantly associated
with the risk of type 2 diabetes
Whole-grain consumption was associated with a reduced risk of type 2 diabetes
in the Finnish Mobile Clinic Health Examination Survey (Montonen et
al., 2003). This survey consists of a cohort of 2,286 men and 2,030 women during
a 10-year followup. The relative risk between the highest and lowest quartiles
of whole-grain consumption was 0.65; P= 0.02.
In summary, the four prospective studies (Iowa Women's Health, Nurses' Health,
Health Professionals Follow-Up Study and the Finnish Mobile Clinic Health
Examination Survey) all show a risk reduction for type 2 diabetes of 20
to 30 percent. For an excellent review on whole grains and risk of diabetes,
see Murtaugh et al. (2003).
Physiological Basis for a Relationship Between
Whole-Grain Intake and Decreased Risk of Diabetes. The
results of the four epidemiological studies that used
diabetes as the end point are supported by other studies
intermediate markers for diabetes. For example, plasma glucose
and insulin values may supply information on mechanisms
by which whole grains exert their protective
effect. The Committee examined evidence of the relationship
of whole-grain consumption to glucose and insulin levels
included in a recent review (Murtaugh et al., 2003).
Briefly, in one cohort of 3,627 individuals age 18 to 30
(the CARDIA
study) whole-grain consumption was assessed at years 0 and
7 and compared to insulin values at year 10 (Pereira et
al., 1998). Whole-grain consumption was
inversely related to fasting insulin values.
In a feeding study, Pereira et al. (2002) tested whether or not whole-grain
consumption improves insulin sensitivity in overweight and obese adults. When
whole-grain products replaced refined-grain products, fasting insulin decreased
by 10 percent over 6 weeks. In the Framingham Offspring Study (McKeown
et al., 2002), whole-grain consumption in the highest quintile (13 to 64 servings
per week) was associated with a significant decrease in fasting insulin compared
to the lowest whole-grain consumption (0 to 1.5 servings per week) after adjusting
for known confounders (P= 0.01). This relationship was no longer significant
after adjusting for total fiber. Also, whole-grain consumption has been inversely
associated with BMI (McKeown et al., 2002), which is an independent risk factor
for diabetes and CHD (See section below). The American Diabetes Association has
concluded that some evidence supports the role of whole grain or dietary fiber
in reducing the risk of type 2 diabetes (Franz et al., 2002).
Is the Observed Protective Effect of Whole Grain Due to Its Fiber
Content? Some of the published epidemiologic studies have found
an inverse association between fiber intake and the occurrence of type 2 diabetes
(Hu et al., 2001; Meyer et al., 2000; Montonen et al., 2003; Salmeron et al.,
1997a,1997b). For example, in the Nurses' Health Study, Salmeron et
al. reported on fiber intake and its relationship to diabetes. The risk reduction
was similar to that of whole-grain intake in the same cohort (a 28 percent risk
reduction from the highest to the lowest quintile of fiber intake) (Salmeron
et al., 1997a). However, the source of fiber appears to be important, as cereal
fiber but not fruit or vegetable fiber intake has been inversely associated with
risk for diabetes in several studies (Salmeron et al., 1997b).
In the Health Professionals Follow-Up Study (Hu et al., 2001), the
risk of developing diabetes did not decrease with higher total fiber intakes,
but a risk reduction of 30 percent was observed in the highest quintile of cereal-fiber
intake (median 10.2 g per day) compared to the lowest quintile (median intake
1.14 g per day). Again, as in the Nurses' cohort, cereal fiber but not
fruit or vegetable fiber intake was associated with the protective effect. Similarly,
in the Finnish Mobile Clinic Survey (Montonen et al., 2003), cereal
fiber intake also was associated with a reduced risk of type 2 diabetes. The
relative risk between the extreme quartiles of cereal fiber intake was 0.39;
p=0.01. The authors conclude that the similar result for cereal fiber
intake and whole-grain intake suggests that the whole grain association is due
to cereal fiber intake.
Possible Confounders With Whole-Grain Intake and Risk of
Type 2 Diabetes. Salmeron et al. (1997a; 1997b) found that diets
with a high glycemic load and low cereal fiber content were positively associated
with the risk of type 2 diabetes mellitus among both adult males and females
in the United States (Salmeron et al., 1997a, 1997b). This finding suggests that
total glycemic load may be a confounding factor. One study reported a positive
relationship between fiber intake and the incidence of diabetes, but this study
was retrospective and involved 242 individuals with diagnosed diabetes and 460
individuals without a prior diagnosis. More weight is given to the prospective
studies since diet intake is assessed prior to rather than after disease occurrence.
It is possible that individuals change their diets after they have been diagnosed
with a disease (Marshall et al., 1991).
Several studies have investigated the effect of whole-grain consumption on
weight and body mass index (BMI) (often as a secondary analysis in a larger study).
For a recent review of these studies see Koh-Banerjee, 2003. In the Nurses'
Health Study, BMI did not vary appreciably across quintiles of whole-grain
intake (Liu et al., 1999). In a later report on this same cohort, (Liu et al.,
2003b), women who consumed more whole grains consistently weighed less than did
women who consumed less whole grains (P<0.0001). In the Iowa
Women's Health Study, whole-grain intake was inversely correlated with body
weight and fat distribution (Jacobs et al., 1998). In the Health Professionals
Follow-Up Study (Koh-Banerjee, in press 2004), an increase in whole-grain
intake was inversely associated with long-term weight gain (P for trend
<0.0001). A dose-response relation was observed, and for every 40 g increment
in whole grains from all foods, weight gain was reduced by 0.49 kg. Independent
of whole grains, changes in cereal and fruit fiber inversely predicted weight
gain. In the Coronary Artery Risk Development in Young Adults (CARDIA)
study, whole-grain intake was inversely related to BMI at 7-year followup of
the participants (Pereira et al., 1998). In the Framingham Offspring Study,
diets rich in whole grains were inversely associated with BMI and with the waist:hip
ratio (McKeown et al., 2002). BMI values at the lowest whole-grain intake level
averaged 26.9; at the highest whole-grain intake level the average BMI was 26.4
(P= 0.06). Weight was 1 to 2 kg higher among those with the lowest intake
of whole grain than among those in the upper 20 percent of whole-grain intake.
Since whole grains also are high in fiber, the relationship of fiber intake to
BMI is pertinent. In cross-sectional observational studies, fiber has been inversely
associated with body weight (Alfieri et al., 1995) and body fat (Nelson et al.,
1996; Miller et al., 1994). In a longitudinal study (the CARDIA study),
macronutrient and fiber intakes were examined in relation to 10-year weight gain
(Ludwig et al., 1999). Fiber had a strong negative association with weight gain,
whereas fat had no association. Those in the lowest quintile of fiber intake
(<5 g per 1000 kcal per day) gained an average of 8 pounds more than those
in the highest quintile (>12 g per 1000 kcal per day). Fiber was inversely
associated with BMI at all levels of fat intake, and the results were not explained
by dietary fat intake. In the Nurses' Health Study (Liu et al., 1999),
women in the highest quintile of dietary fiber intake had a 49 percent lower
risk of major weight gain. Over a period of 12 years, those with the greatest
increase in intake of dietary fiber gained an average of 1.52 kg less than did
those with the smallest increase in intake of dietary fiber (P= <0.0001).
Again, as shown with whole-grain intake and risk of CHD or diabetes, an important
component of the whole grain appears to be the fiber content.
A meta-analysis of 40 studies on gastrointestinal cancers found a 21 percent
to 43 percent lower cancer risk with high intakes of whole grains compared to
low intakes (Jacobs et al., 1998). In a recently reported case-control study
on the relationship between frequency of consumption of whole-grain foods and
cancer risk in Italy, there was a reduced risk of several cancers. The odds ratios
for the highest intake category of whole-grain cereal consumption compared to
the lowest category were 0.3 to 0.5 for upper digestive tract and respiratory
neoplasms and colon (La Vecchia et al., 2003). A separate case-control study
with 952 incident cases of rectal cancer compared with 1,205 population-based
controls found that whole-grain intake had a reduced risk for rectal cancer (odds
ratio of 0.69) and refined grain intake had a direct association with increased
risk of rectal cancer (1.42) (Slattery et al., 2004). In addition, an inverse
relationship between cereal and cereal fiber intake and colon cancer incidence
was reported in 24 studies although 7 other studies did not see this effect (Jacobs
et al., 1998). The data on dietary fiber intake and colon cancer are inconsistent.
Although between country studies generally show a protective effect of high fiber
intake (Boyle et al., 1985), this is not true for within country studies. For
example, two large prospective cohort studies in the United States, the Nurses'
Health Study (Fuchs et al., 1999) and the Physician's Follow-Up Study
(Giovannucci, 1994) do not show a protective effect of fiber intake against colon
cancer. Most importantly, the three clinical intervention trials with colon polyp
recurrence as an end point also failed to show a protective effect against this
surrogate marker for colon cancer (Alberts et al., 2000; Bonithon-Kopp et al.,
2000); Schatzkin et al., 2000). There are many reasons for the discrepancy among
these different types of studies. Therefore, the overall benefits of whole-grain
intake or any of its constituents (such as cereal fiber or fiber per se)
and the incidence of colon cancer remain an unresolved issue and further research
is needed.
A recent report on the Health Professionals Follow Up Study (Jensen
et al., in press 2004) confirms the results of previous individual studies and
meta-analyses of servings of whole grain foods or products with whole-grain content
above 25 percent (Anderson et al., 2000; Fraser et al., 1992; Jacobs et al.,
1998, 1999; Liu et al., 1999; Steffen et al., 2003). In this report, the beneficial
effects for whole-grain consumption are greatest for a daily whole-grain intake
above approximately 30 g, regardless of the food source. In the Iowa Women's
Health Study the protected quintile for ischemic heart disease was an average
of 3.2 whole-grain servings per day (Jacobs et al., 1998). Taken collectively,
there are strong and consistent data primarily from prospective cohort studies
that whole-grain intake is protective against CHD incidence. The protected quintile
of intake appears to be approximately three servings (equivalent to three ounces)
of whole grains per day (See Appendix G3 Whole Grains and Chronic Disease Risk).
There is good evidence that whole-grain intake may be protective against type
2 diabetes, and this evidence is supported by measurements of intermediate endpoints
such as blood glucose and insulin concentrations. There is suggestive evidence
from a number of secondary analyses, that whole-grain intake may protect against
weight gain and help with weight maintenance although the concept that whole-grain
intake represents a healthy lifestyle cannot be excluded as a confounder. Children
and adolescents should strive to consumer primarily whole grains rather than
refined grains.
Consuming three servings (equivalent to 3 cups) of milk and milk products each
day can reduce the risk of low bone mass and contribute important amounts of
many nutrients. Furthermore, this amount of milk product consumption may have
additional benefits and is not associated with increased body weight. Therefore,
the intake of three cups of milk products per day is recommended.
Overview. The first part of the conclusion is based
on the Committee's review of scientific evidence pertaining to nutrient adequacy,
improving bone health, and reducing the risk of insulin resistance syndrome.
Depending on the study reviewed, milk product intake was assessed by milk (1
serving = 1 cup) and sometimes included other dairy products such as yogurt (1
serving = 1 cup) and cheese (1 serving = 1.5 oz). The conclusion regarding milk
products and weight is supported by the Committee's systematic review of the
scientific evidence including two randomized clinical trials that addressed the
question directly; four randomized controlled trials that addressed other questions;
two longitudinal, case-control studies of milk group consumption and body weight
and fatness; and seven observational studies that reported a secondary analysis
of data collected for another purpose.
Many of the health benefits associated with milk consumption may be attributable
to the component nutrients including calcium, potassium, magnesium, vitamin D,
and vitamin A. The extent to which components unique to milk products play a
role in promoting health such as the nature of milk proteins or conjugated linoleic
acid (see Question 3 in Section 4, "Fats") are not well understood from the current
Milk product consumption has been associated with overall diet quality and
adequacy of intake of many nutrients including calcium, potassium, magnesium,
zinc, iron, riboflavin, vitamin A, folate, and vitamin D for children and younger
and older adults (Ballow et al., 2000; Barger-Lux et al., 1992; Devine et al.,
1996; Foote et al., 2004; Johnson et al., 2002; Weinberg et al., 2004). Increasing
the quartile of milk product intake was associated with increased intakes of
all micronutrients studied except vitamin C among 17,959 participants in CSFII
1994-1996 (Weinberg et al., 2004). One cross-sectional study in young adults
showed that the greatest benefit in intakes of vitamins and minerals was observed
in those consuming three or more servings of milk products compared to those
consuming two servings or less (Ranganathan et al., in press 2004). Choosing
a variety of foods within the dairy food group was strongly associated with improved
nutrient adequacy among 4,969 men and 4,800 women participating in CSFII 1994-1996
(Foote et al., 2004). Milk product and calcium intake in childhood shows a moderate
degree of tracking with age (Whelton et al., 1997; Dwyer et al., 1989; Teegarden
et al., 1999; Skinner et al., 2003). That is, those who consume milk regularly
as children are more likely to do so as adults. Trends in consumption show a
decline in milk intake, suggesting that milk has been displaced by other beverages.
For example, in the Bogalusa Heart Study, (Nicklas et al., 2003b), the
proportion of 10-year-old children consuming milk declined from 1972 to 1994.
During the same period, the children's consumption of sweetened beverages including
soft drinks, sweetened coffee, and fruit-flavored drinks increased. Fluid milk
consumption was negatively related to soft drink consumption in boys and girls
(McGartland et al., 2003; Whiting et al., 2001). Soft drink consumption negatively
affected bone mineral accrual in the adolescent girls in both studies.
Because milk products are the major sources of calcium in the diets of Americans,
low intake of milk products is associated with low calcium intake. The Institute
of Medicine based the Adequate Intakes (AIs) for calcium on maximizing calcium
retention and optimizing bone health (IOM, 1997). Studies relating calcium intake
and bone health were reviewed by the Institute of Medicine (IOM, 1997) and by
Heaney (2000). For dietary guidance, this Committee evaluated studies specifically
on milk and other milk products. All 7 of the randomized, controlled trials and
25 of 34 observational studies showed a positive relationship between the intake
of milk products and bone mineral content or bone mineral density in one or more
skeletal sites (see Appendix G3). Bone mineral density is a strong predictor
of fracture. Therefore, it is a biomarker for the disease of osteoporosis.
In older adults, the strongest outcome measure for bone health is fracture incidence.
Five of the eight observational studies using fracture as an end point found
milk product consumption significantly associated with reduced fracture risk.
Randomized, controlled trials are less confounded, but they are of insufficient
duration to use fracture as an end point.
In studies of all age groups, the magnitude of the effect of milk product consumption
on bone is at least as good as that obtained with calcium supplement trials.
However, calcium supplements and milk products have not been compared in the
same trial to determine if milk products offer more benefits than does calcium
alone. Trials using milk, foods fortified with dairy calcium, or calcium supplements
have demonstrated a comparable and important increase in skeletal mass in younger
subjects and reduction in loss of skeletal mass in older subjects. In trials
using milk or foods fortified with calcium extracted from milk, followup showed
that the increase in skeletal mass was maintained after the intervention ceased
(Bonjour et al., 2001; Ghatge et al., 2001). However, the increase in skeletal
mass was not maintained following the interventions that used calcium supplements
(Lee et al., 1996; Slemenda et al., 1997). This comparison suggests that skeletal
benefits of dairy calcium persist longer than those derived from calcium supplements.
The intake of milk products is especially important to bone health during childhood
and adolescence. Using data from 3251 Caucasian women from NHANES III, low intake
(<1 serving of milk per week compared to >1 serving per day) during childhood
and adolescence was associated with less hip bone mass in adulthood (P<0.04),
and low milk intake during childhood was associated with a two-fold greater risk
of fracture (P<0.05) (Kalkwarf et al., 2003). This association was
not apparent in black women in NHANES III (Opotowsky and Bilezikian, 2003).
In a limited number of studies, the consumption of milk products has been related
to a decreased risk of insulin resistance syndrome (IRS), otherwise known as
syndrome X or the metabolic syndrome. IRS, which is characterized by obesity,
insulin resistance, and hyperinsulinemia, leads to glucose intolerance, dyslipidemia,
hypertension, and impaired fibrinolytic capacity. Thus, IRS leads to an increased
risk for type 2 diabetes and cardiovascular disease (Reaven, 1993). While 22
percent of the U.S. adult population is estimated to have IRS (Ford et al., 2000),
currently there are no standard diagnostic criteria and no treatment (Roth et
al., 2002). In some studies, higher milk product consumption has been associated
with decreased risk of IRS components, including coagulopathy (Mennen et al.,
1999), coronary artery disease (Ness et al., 2001), stroke, and hypertension.
In a cross-sectional analysis of men and women ages 30 to 64 years, Mennen et
al. (2000) demonstrated that greater than 1 serving per day of milk products
was associated with a 40 percent lower risk of IRS only in men.
Perhaps the largest study to examine the relationship of milk and IRS is the
Coronary Artery Risk Development in Adults (CARDIA), a study of 3157
black and white adults age 18 to 30 years. In this prospective observational
study, milk product consumption was inversely associated with the 10-year cumulative
incidence of IRS among those individuals who were overweight (Pereiera, 2002).
Each additional serving of milk products was associated with a 21 percent lower
odds of IRS (odds ratio, 0.79; 95 percent CI, 0.7 to 0.88). Three or more servings
of milk products per day had the most benefit.
Three servings of low-fat milk products were a part of the DASH combination
diet (see Section D1 for a description of this diet), which significantly lowered
blood pressure (one component of IRS) in adults. In two controlled feeding studies
(Appel et al., 1997; Sacks et al., 2001), the DASH diet—which is rich in fruits
and vegetables (8 to 10 servings per day) and low-fat milk products (3 servings
per day) and reduced in saturated and total fat—lowered systolic blood pressure
by 5.5 mmHg and diastolic blood pressure by 3 mmHg in comparison to a typical
American diet. The effect of increased fruits and vegetables alone (without the
milk product component and other aspects of the DASH diet) was approximately
half as large (-2.7 mmHg systolic and -1.9 mmHg diastolic blood pressure). In
the PREMIER trial, there was no significant blood pressure difference between
two lifestyle interventions, one of which emphasized milk products as well as
other features of the DASH diet (Appel et al., 2003). However, participants in
this behavioral intervention study did not fully meet nutrient goals of the DASH
diet; approximately 60 percent of the participants consumed the amount of milk
products prescribed, and only one-third consumed the prescribed amounts of fruits
and vegetables.
An analysis of 10 prospective cohort studies relating milk intake at baseline
to vascular disease events showed a pooled estimate of relative odds of 0.84
(95 percent CI, 0.78-0.90) for any vascular event and 0.87 (0.74 to 1.03) for
ischemic heart disease (Elwood et al., 2004b). Elwood and colleagues (2004a)
followed 2,403 men every 5 years for 20 to 24 years, obtaining data on milk intake
and incidence of ischemic stroke. The hazard ratio for ischemic stroke in those
who consumed 2 or more cups of milk per day, compared to those who did not consume
milk, was 0.64 (0.39 to 1.06). The ratio was 0.37 (0.15 to 0.90) in those who
had experienced a prior vascular event. Blood pressure was slightly (P<0.02)
lower in the men who consumed milk. This emerging role of the relationship between
milk product consumption and IRS and its components is provocative. More research
is warranted to better understand the role of milk products and their constituents.
Randomized Clinical Trials Addressing the Question.
Two randomized clinical trials evaluated the effects of calcium or milk products
on body weight and/or body fat loss (Summerbell et al., 1998; Zemel et al., 2004).
Both of these relatively small trials found a significant negative relationship
between calcium/milk group intake and body weight or fat. Summerbell studied
45 subjects randomized to a control energy-restricted diet, a milk-only diet,
or a milk plus one selected food diet. Only 31 subjects finished the trial, and
it is not clear that the three dietary treatments were eucaloric. Zemel et al.
(2004) randomized 32 subjects to an energy-restricted diet, an energy-restricted
diet plus 800 mg supplemental calcium, or a high-milk products (1,200 to 1,300
mg of calcium per day) energy-restricted diet for 24 weeks. Subjects on the high-milk
products diet lost 70 percent more weight than those on the standard diet.
Secondary Analyses of Data From Other Randomized Controlled Trials.
Four groups evaluated the relationship between milk group or calcium intake and
body weight in randomized controlled trials designed to address other questions.
Energy intakes were not controlled in any of these four trials. Barr and co-workers
(2000) evaluated the impact of milk group consumption on cardiovascular risk
factors and found that subjects in the milk group gained significantly more weight
(0.6 kg) than the control group in the 12-week study. However, the net gain was
less than anticipated from the increased energy intake from milk products (Barr
et al., 2000). To evaluate the relationship between calcium and bone health,
Davies et al. (2000) re-evaluated the data from a randomized trial of 216 women
who received 1,200 mg of supplemental calcium per day for 3.9 years. Both the
calcium-supplemented and control groups lost weight, but the calcium-supplemented
group lost significantly (P <0.025) more (0.346 kg per year) weight
than the placebo group. Stamler and Dolecek (1997) evaluated the relationship
between food intakes and body mass in 6,289 adults participating in the Multiple
Risk Factor Intervention Trial (MRFIT). Greater weight loss was associated
with greater reductions in medium-fat and high-fat milk products. The overall
effect, however, was due to consuming a diet with lower energy density; there
was no specific effect of dietary calcium. Also, in the Trials of Hypertension
Prevention (TOHP) study, Yamamoto and co-workers (1995) found no effect
of supplemental calcium (1 g per day) on BMI in 698 healthy men and women with
high-normal diastolic blood pressure (80 to 89 mm Hg) participating in the trial.
Energy intakes were not controlled in these four trials.
Longitudinal, Case-Control Studies in Children. Two
longitudinal, case-control studies of milk group consumption and body weight
and fatness have been done in children (Carruth and Skinner, 2001; Phillips et
al., 2003). Carruth and Skinner found that the mean longitudinal calcium intake
of preschool children from 24 to 60 months of age was associated with lower body
fat at 70 months. However, Phillips et al (2003) found no evidence that milk
group consumption was associated with the BMI z-score or the percentage of body
fat in 178 nonobese girls followed from premenarche to 4 years postmenarche.
Observational Studies. Observational studies of the
relationship between increased milk group consumption or increased calcium in
the diet and body weight or body fat also have been done. The results of those
studies are mixed (Buchowski et al. 2002; Davies, et al. 2000; Drapeau et al.,
2004; Jacqmain et al., 2003; Lin, et al. 2000; Lovejoy et al., 2001; Melanson
et al., 2003; Pereira et al., 2002). None of the observational studies were designed
with the intention of studying the relationship between milk group intake or
calcium consumption and either body weight or composition. Instead, the papers
report a secondary analysis of data collected for another research question.
Heterogeneity in methodologies used to measure body composition and dietary intake
along with differences in the number and type of variables used as covariates
and the manner in which calcium intake is expressed (i.e., energy-adjusted or
protein-adjusted) may account for the divergent results.
Recommendations from Other Groups. A recommendation
of 3 servings milk products per day (See Table D1-13) is consistent with recommendations
from other authoritative groups (American Academy of Pediatrics, 2001; American
Heart Association, 2004; National Medical Association, 2004). Mean intake of
milk products is much lower than this, and only about 28 percent of men and 15
percent of women consume 2 servings in a day
Milk Products Summary. Taken collectively, there is
strong and consistent evidence that the intake of milk products is protective
against osteoporosis and limited evidence that milk product intake protects against
IRS. The protected quintile of intake appears to be approximately 3 servings
of milk or milk products per day. The possible reduction of the incidence of
IRS with higher milk product consumption may be partially or mostly related to
the calcium content of milk products.
None of the studies show that milk group consumption is
associated with an increase in body weight. Since adults
and children benefit from including milk products
in the amounts suggested in the revised USDA food intake
pattern — both
for bone health and for lowering the risk of several diseases — milk
products are recommended as part of the overall dietary
pattern. There is no evidence that
milk products should be avoided because of concerns that
these foods are fattening. Because of the lack of large-scale,
randomized trials or controlled feeding studies
designed explicitly to test the effect of milk group intake
or calcium consumption on body weight and the limitations
of the studies reported above, at this time
there is insufficient evidence on which to base a more definitive
statement regarding the intake of milk products and management
of body weight.
The main message from these reviews is that an increased intake of fruits and
vegetables (2 ½ to 6 ½ cups; equal to 5 to 13 servings depending
on caloric needs), and the consumption of approximately 3 ounces of whole grains
daily promotes health and reduces the risk of chronic diseases. In addition,
the daily consumption of approximately three cups of nonfat or low-fat milk or
the equivalent from other milk products can reduce the risk of low bone mass.
All these foods make important nutrient contributions. There is no evidence that
the recommended amounts of milk products increases body weight. The DASH diet,
which is consistent with the recommendations made here, has been demonstrated
to have beneficial effects on health (see Section D1).
American Academy of Pediatrics (AAP). Calcium and You: Facts for Teens,
Alberts DS, Martinez ME, Roe DJ, Guillen-Rodriguez JM, Marshall JR, van Leeuwen
JB, Reid ME, Ritenbaugh C, Vargas PA, Bhattacharyya AB, Earnest DL, Sampliner
RE. Lack of effect of a high-fiber cereal supplement on the recurrence of colorectal
adenomas. New England Journal of Medicine 342:1156-62, 2000.
Alfieri M, Pomerleau J, Grace DM. Fiber intake of normal weight, moderately
obese and severely obese subjects. Obesity Research 3:541-547, 1995.
American Association of Cereal Chemists. AACC to create consumer-friendly whole
grain definition, 2004.
American Heart Association, Eating Plan: Milk Products Web Page http://www.americanheart.org/presenter.jhtml?identifier=1080.
Access July 31, 2004.
Anderson JW and Akanji AO. Dietary fiber - an overview. Diabetes Care
14:1126-1131, 1991.
Anderson JW, Hanna TJ, Peng X, Kryscio RJ. Whole grain foods and heart disease
risk. Journal of the American College of Nutrition 19:291S-299S, 2000.
ANON. Food standards: amendment of standards of identity for enriched grain
products to require addition of folic acid. Federal Register 61:8781-8797,
Appel LJ, Champagne CM, Harsha DW, Cooper LS, Obarzanek E, Elmer PJ, Stevens
VJ, Vollmer WM, Lin PH, Svetkey LP, Stedman SW, and Young DR. Effects of comprehensive
lifestyle modification on blood pressure control: main results of the PREMIER
clinical trial. Journal of the American Medical Association 289:2083-93,
Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA,
Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A clinical trial of the
effects of dietary patterns on blood pressure. New England Journal Medicine
336:1117-1124, 1997.
Ballow C, Kuester S, Gillespie C. Beverage choices affect adequacy of children's
nutrient intakes. Archives of Pediatrics and Adolescent Medicine 154;1148-1152,
Barger-Lux, MJ, Heaney RP, Packard PT, Lappe JM, Recker RR. Nutritional correlates
of low calcium intake. Clinics in Applied Nutrition 2:39-44, 1992.
Barr SI, McCarron DA, Heaney RP, Dawson-Hughes B, Berga SL, Stern JS, Oparil
S. Effects of increased consumption of fluid milk on energy and nutrient intake,
body weight, and cardiovascular risk factors in healthy older adults. Journal
of the American Dietetic Association 100(7):810-7, 2000.
Bazzano LA, He J, Ogden LG, Loria CM, Whelton PK. Dietary fiber intake and reduced
risk of coronary heart disease in U.S. men and women. The National Health and
Nutrition Examination Survey I Epidemiologic Follow-up Study. Archives of
Internal Medicine 163:1897-1904, 2003.
Bazzano LA, He J, Ogden LG, Loria CM, Vupputuri S, Myers L, Whelton PK. Fruit
and vegetable intake and risk of cardiovascular disease in US adults: the first
National Health and Nutrition Examination Survey Epidemiologic follow-up study.
American Journal of Clinical Nutrition 76:93-99, 2002.
Bonithon-Kopp C, Kronborg O., Giacosa A., Rath U, Faivre J. Calcium and fibre
supplementation in prevention of colorectal adenoma recurrace: A randomised intervention
trial. Lancet 356:1300-1306, 2000.
Bonjour JP, Chevalley T, Aminan P, Slosman D, Rizzoli R. Gain in bone mineral
mass in prepubertal girls 3.5 years after discontinuation of calcium supplementation:
a follow-up study. Lancet 358:1208-1213, 2001.
Boyle P, Zaridze, DG, and Smans M. Descriptive epidemiology of colorectal cancer.
International Journal of Cancer. 36:9-18, 1985.
Broekmans WMR, Klopping-Ketelaars WAA, Kluft C, van den Berg H, Kok FJ, van
Poppel G. Fruit and vegetable and cardiovascular risk profile: a diet controlled
intervention study. European Journal of Clinical Nutrition 55:636-642,
Buchowski MS, Semenya J, Johnson AO. Dietary calcium intake in lactose maldigesting
intolerant and tolerant African-American women. Journal of the American College
of Nutrition. Feb;21(1):47-54, 2002.
Carruth BR and Skinner JD. The role of dietary calcium and other nutrients in
moderating body fat in preschool children. International Journal of Obesity
and Related Metabolic Disorders 25(4):559-566, 2001.
Cerhan JR, Potter JD, Gilmore JME, Janney CA, Kushi LH, Lazovich D, Anderson
KE, Sellers TA, Folsum, KE. Adherence to the AICR Cancer Prevention Recommendations
and Subsequent Morbidity and Mortality in the Iowa Women's Health Study Cohort.
Cancer Epidemiology, Biomarkers & Prevention 13:1114-1120, 2004.
Cleveland LE, Moshfegh AJ, Albertson AM, Goldman JD. Dietary intake of whole
grains. Journal of the American College of Nutrition 19(3 Suppl):331S-338S,
Colditz GA, Manson JE, Stampfer MJ, Rosner B, Willett WC, Speizer FE. Diet and
risk of clinical diabetes in women. American Journal of Clinical Nutrition
55:1018-1023, 1992.
Davies KM, Heaney RP, Recker RR, Lappe JM, Barger-Lux MJ, Rafferty K, Hinders
S. Calcium intake and body weight. Journal of Clinical Endocrinology and
Metabolism Dec;85(12):4635-8, 2000.
Decker E, Beecher G, Slavin J, Miller HE, Marquart L. Whole grains as a source
of antioxidants. Cereal Foods World 47:370-373, 2002.
Devine A, Prince RL, Bell R. Nutritional effect of calcium supplementation by
skim milk powder or calcium tablets on total nutrient intake in postmenopausal
women. American Journal of Clinical Nutrition 64:731-737, 1996.
Djuric Z, Poore KM, Depper JB, Uhley VE, Lababidi S, Covington C, Klurfeld DM,
Simon MS, Kucuk O, Heilbrun LK. Methods to increase fruit and vegetable intake
with and without a decrease in fat intake: compliance and effects on body weight
in the Nutrition and Breast Health Study. Nutrition and Cancer 43:141-151,
Drapeau V, Despres JP, Bouchard C, Allard L, Fournier G, Leblanc C, Tremblay
A. Modifications in food-group consumption are related to long-term body-weight
changes. American Journal of Clinical Nutrition 80:29-37, 2004.
Dwyer, J.T., Gardner J., Halvorsen K., Krall E.A., Cohen A. and Valadian I.
Memory of food intake in the distant past. American Journal of Epidemiology
130:1033-1046, 1989.
Elwood PC, Pickering JE, Fehily AM, Hughes J, Ness AR. Milk drinking, ischaemic
heart disease and ischaemic stroke. I. Evidence from cohort studies. European
Journal of Clinical Nutrition 58:711-717, 2004a.
Elwood PC, Pickering JE, Hughes J, Fehily AM, Ness AR. Milk drinking ischaemic
heart disease and ischaemic stroke. II. Evidence from cohort studies. European
Journal of Clinical Nutrition 58:718-724, 2004b.
Feskens EJM, Virtanen SM, Rasanen L, Tuomilehto J, Stengard J, Pekkanen J, Nissinen
A, Kromhout D. Dietary factors determining diabetes and impaired glucose tolerance.
A 20-year follow-up of the Finnish and Dutch cohorts of the Seven Countries Study.
Diabetes Care 18:1104-1112, 1995.
Field AE, Gillman MW, Rosner B, Rockett HR, Colditz G.A. Associations between
fruit and vegetable intake and change in body mass index among a large sample
of children and adolescents in the United States. International Journal of
Obesity 27: 821-826, 2003.
Fitzwater, SL, Weinsier RL, Wooldridge NH, Birch R, Liu C, and Bartolucci AA.
Evaluation of long-term weight changes after a multidisciplinary weight control
program. Journal of the American Dietetic Association 4:421-426, 429,
Flood A, Velie EM, Chaterjee N, Subar AF, Thompson FE, Lacey JV, Schairer C,
Troisi R, Schatzkin A. Fruit and vegetable intakes and the risk of colorectal
cancer in the Breast Cancer Detection Demonstration Project follow-up cohort.
American Journal of Clinical Nutrition 75:936-943, 2002.
Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults:
findings from the Third National Health and Nutrition Examination Survey. Journal
of the American Medical Association 287:356-359, 2000.
Foote JA, Murphy SP, Wilkens LR, Basiotis PP, Carlson A. Dietary variant increases
the probability of nutrient adequacy among adults. Journal of Nutrition
134, 2004.
Franz MJ, Bantle JP, Beebe CA, Brunzell JD, Chiasson J, Garg A, Holzmeister
LA, Hoogwerf B, Mayer-Davis E, Mooradian AD, Purnell JQ, Wheeler M. Evidence-based
nutrition principles and recommendations for the treatment and prevention of
diabetes and related complications. Diabetes Care 25:148-198, 2002.
Fraser GE, Sabate J, Beeson WL, Strahan TM. A possible protective effect of
nut consumption on risk of coronary heart disease: the Adventist Health Study.
Archives of Internal Medicine 152:1416-24, 1992.
Fuchs CS, Giovannucci EL, Colditz GA, Hunter DJ, Stampfer MJ, Rosner B, Speizer
FE, Willett WC. Dietary fiber and the risk of colorectal cancer and adenoma in
women. New England Journal of Medicine 340:169-76, 1999.
Fung TT, Rimm EB, Spiegelman D, Rifai N, Tofler GH, Willett WC, Hu FB. Association
between dietary patterns and plasma biomarkers of obesity and cardiovascular
disease risk. American Journal of Clinical Nutrition 73:61-7, 2001.
Ghatge KD, Lambert HL, Barker ME, Eastell R. Bone mineral gain following calcium
supplementation in teenage girls is reserved two years after withdrawl of the
supplement. Journal of Bone and Mineral Research 16(S1):S173. A#1149,
Gillman MW, Cupples A, Gagnon D, Posner BM, Ellison RC, Castelli WP, Wolf PA.
Protective effect of fruits and vegetables on development of stroke in men. Journal
of the American Medical Association 273:1113-1117, 1995.
Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Ascherio A, Willett WC. Intake
of fat, meat, and fiber in relation to risk of colon cancer in men. Cancer
Research 54:2390-7, 1994.
Gittelsohn J, Wolever TMS, Harris SB, Farris-Giraldo R, Hanley AJG, Zinman B.
Specific patterns of food consumption and preparation are associated with diabetes
and obesity in a Native Canadian community. Journal of Nutrition 128:541-547,
Harnack L, Walters SA, Jacobs DRJ. Dietary intake and food sources of whole
grains among US children and adolescents: data from the 1994-1996 Continuing
Survey of Food Intakes by Individuals. Journal of the American Dietetic Association
103:1015-9, 2003.
Heaney RP. Calcium, dairy products and osteoporosis. Journal of the American
College of Nutrition 19:83S-99S, 2000.
Hu FB, Manson JE, Stampfer MJ. Diet, lifestyle, and the risk of type 2 diabetes
mellitus in women. New England Journal of Medicine 345:790-7, 2001.
Humble CG, Malarcher AM, Tyroler H.A. Dietary fiber and coronary heart disease
in middle-aged hypercholesterolemic men. American Journal of Preventative
Medicine 9:197-202, 1993.
Institute of Medicine (IOM). Dietary Reference Intakes for Calcium, Phosphorus,
Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academies Press,
Institute of Medicine (IOM). Dietary carbohydrates: sugars and starches,
Dietary Reference Intakes for Energy, Carbohydraate, Fiber, Fat, Fatty Acids,
Cholesterol, Protein, and Amino Acids. Washington, DC: National Academies
Press, 2002.
IARC Handbooks of Cancer Prevention. International agency for Research on Cancer
World Health Organization. Fruits and Vegetables. Lyon, France. 2003.
Jacobs DRJ, Meyer HE, Solvoll K. Reduced mortality among whole grain bread eaters
in men and women in the Norwegian County Study. European Journal of Clinical
Nutrition 55:137-43, 2001.
Jacobs DRJ, Meyer KA, Kushi LH, Folsom AR. Is whole grain intake associated
with reduced total and cause-specific death rates in older women? The Iowa Women's
Health Study. American Journal of Public Health 89:322, 1999.
Jacobs DRJ, Meyer KA, Kushi LH, Folsom AR. Whole-grain intake may reduce the
risk of ischemic heart disease death in postmenopausal women: the Iowa women's
health study. American Journal of Clinical Nutrition 68:248-257, 1998.
Jacqmain M, Doucet E, Despres J, Bouchard C, Tremblay A. Calcium intake, body
composition, and lipoprotein-lipid concentrations in adults. American Journal
of Clinical Nutrition 77:1448-1452, 2003.
Jensen MK, Koh-Banerjee P, Hu FB, Franz MJ, Sampson L, Gronbaek M, Rimm EB.
Intake of whole grains, bran and germ and risk of coronary heart disease among
men. American Journal of Clinical Nutrition, In press, 2004.
John JH, Ziebland S, Yudkin P, Roe LS, and Neil HA. Effects of fruit and vegetable
consumption on plasma anti-oxidant concentrations and blood pressure: a randomized
controlled trial. Lancet 359:1969-74, 2002.
Johnsen SP, Overvad K, Stripp C, Tjonneland A, Husted SE, Sorensen HT. Intake
of fruit and vegetables and the risk of ischemic stroke in a cohort of Danish
men and women. American Journal of Clinical Nutrition 78:57-64, 2003.
Johnson RK, Frary C, Wang MQ. The nutritional consequences of flavored-milk
consumption by school-aged children and adolescents in the United States. Journal
of the American Dietetic Association 102:853-856, 2002.
Joshipura JH, Hu FB, Manson JE, Stampfer MJ, Rimm EB, Speizer, FE, Colditz G,
Ascherio A, Rosner B, Spiegelman D, and Walter WC. The effect of fruit and vegetable
intake on risk for coronary heart disease. Annals of Internal Medicine
134:1106-1114, 2001.
Joshipura KJ, Ascherio A, Manson JE, Stampfer MJ, Rimm EB, Speizer FE, Hennekens
CH, Spiegelman D, Willett WC. Fruit and vegetable intake in relation to risk
of ischemic stroke. Journal of the American Medical Association 282(13):1233-9,
Kahn HS, Tatham LM, Rodriguez C, Calle EE, Thun MJ, Health CW. Stable behaviors
associated with adults 10-year change in body mass index and likelihood of gain
at the waist. American Journal of Public Health 87:747-754, 1997.
Kalkwarf HJ, Khoury JC, Lanphear BP. Milk intake during childhood and adolescence,
adult bone density, and osteoporotic fractures in US women. American Journal
of Clinical Nutrition 77:257-265, 2003.
Khaw K, Barrett-Connor E. Dietary fiber and reduced ischemic heart disease mortality
rates in men and women: a 12-year prospective study. American Journal of
Epidemiology 126:1093-1102, 1987.
Kobayashi M, Tsubono Y, Sasazuki S, Sasaki S, Tsugane S. Vegetables, fruit and
risk of gastric cancer in Japan: a 10-year follow-up of the JPHC Study Cohort
. International Journal of Cancer 102: 39-44, 2002.
Koh-Banerjee, P. and Rimm E.B. Whole grain consumption and weight gain: a review
of the epidemiological evidence, potential mechanisms and opportunities for future
research. Proceedings of the Nutrition Society 62: 25-29, 2003.
Koh-Banerjee P, Franz M, Sampson L, Liu S, Jacobs D, Spiegelman D,Willett WC,
Rimm E.B. Changes in whole grain, bran, and cereal fiber consumption in relation
to 8-year weight gain among men. Journal of the American Medical Association,
2004. In press .
LaForge RG, Greene GW, Prochaska JO. Psychosocial factors influencing low fruit
and vegetable consumption. Journal of Behavioral Medicine 17:361-374,
Lahti-Koski M, Pietinen P, Heliovaara M, Vartianen E. Assocations of body mass
index and obesity with physical activity, food choices, alcohol intake, and smoking
in the 1982-1997 FINRISK Studies. American Journal of Clinical Nutrition
75:809-817, 2002.
La Vecchia, C., Chatenoud L., Negri E. and Franceschi S. Whole cereal grains,
fibre and human cancer wholegrain cereals and cancer in Italy. Proceedings
Nutrition Society 62(1):45-9, 2003.
Law MR, Morris JK. By how much does fruit and vegetable consumption reduce the
risk of ischaemic heart disease. European Journal of Clinical Nutrition
52:549-556, 1998.
Lee WTK, Leung SSF, Leung DMY, Cheng JCY. Bone mineral acquisition in low calcium
intake children following the withdrawl of calcium supplement. American Journal
of Clinical Nutrition 64:71-77, 1996.
Lin B, Morrison RM. Higher fruit consumption linked with lower body mass index.
Food Review 25(3), 2002.
Lin YC, Lyle RM, McCabe LD, McCabe GP, Weaver CM, Teegarden D. Dairy calcium
is related to changes in body composition during a two-year exercise intervention
in young women. Journal of the American College of Nutrition. Nov-Dec;19(6):754-60,
Liu S, Buring JE, Sesso HD, Rimm EB, Willett WC, Manson JE. A prospective study
of dietary fiber intake and risk of cardiovascular disease among women. Journal
of the American College of Cardiology 39:49-56, 2002.
Liu S, Lee IM, Ajani U, Cole SR, Buring JE, Manson JE. Intake of vegetables
rich in carotenoids and risk of coronary heart disease in men: The Physicians'
Health Study. International Journal of Epidemiology 30:130-135, 2001.
Liu S, Manson JE, Lee IM, Cole SR, Hennekens CH, Willett WC, Buring JE. Fruit
and vegetable intake and risk of cardiovascular disease: the Women's Health Study.
American Journal of Clinical Nutrition 72:922-928, 2000.
Liu S, Sesso HD, Manson JE, Willett WC, Buring JE. Is intake of breakfast cereals
related to total and cause-specific mortality in men? American Journal of
Clinical Nutrition 77:594-99, 2003a.
Liu S, Willett WC, Manson JE, Hu FB, Rosner B, Colditz GA. Relation between
changes in intakes of dietary fiber and grain products and changes in weight
and development of obesity among middle-aged women. Journal of the American
College of Nutrition 78:920-7, 2003b.
Liu SM, Stampfer MJ, Hu FB, Giovannucci E, Rimm E, Manson JE, Hennekens CH,
Willett WC. Whole-grain consumption and risk of coronary heart disease: results
from the Nurses' Health Study. American Journal of Clinical Nutrition 70:412-419,
Lovejoy JC, Champagne CM, Smith SR, de Jonge L, Xie H. Ethnic differences in
dietary intakes, physical activity, and energy expenditure in middle-aged, premenopausal
women: the Healthy Transitions Study. American Journal of Clinical Nutrition
Jul;74(1):90-5, 2001.
Ludwig DS, Pereira MA, Kroenke CH, Hilner JE, Van Horn L, Slattery ML, Jacobs
DR. Dietary fiber, weight gain, and cardiovascular disease risk factors in young
adults. Journal of the American Medical Association 282, 1539-1546,
Lundgren H, Bengtsson C, Blohme G, Isaakson B, Lapidus L, Lenner RA, Saaek A,
Winther E. Dietary habits and incidence of noninsulin-dependent diabetes melitus
in a population study of women in Gothenburg, Sweden. American Journal of
Clinical Nutrition 49:708-712, 1989.
Mann J, Hermansen K, Vessby B, Toller M. Evidence-based nutrition principles
and recommendations for the treatment and prevention of diabetes and related
complications. Diabetes Care 25:1256-1258, 2002.
Marshall JA, Hamman RF, Baxter J. Highfat, low-carbohydrate diet and the etiology
of non-insulin-dependent diabetes mellitus: the San Luis Valley Diabetes Study.
American Journal of Epidemiology 134:590-603, 1991.
McGartland C, Robson PJ, Murray L, Cran G, Savage MJ, Watkins D, Rooney M, Boreham
C. Carbonated soft drink consumption and bone mineral density in adolescence:
the Northern Ireland Young Hearts project. Journal of Bone and Mineral Research
18:1563-1569, 2003.
McKeown NM, Meigs JB, Liu SM, Wilson PW, Jacques PF. Whole-grain intake is favorably
associated with metabolic risk factors for type 2 diabetes and cardiovascular
disease in the Framingham Offspring Study. American Journal of Clinical Nutrition
76:390-398, 2002.
Melanson EL, Sharo TA, Schneider J, Donahoo, WT, Grunwald GK, Hill JO. Relation
between calcium intake and fat oxidation in adult humans. International Journal
of Obesity and Related Metabolic Disorders 27(10):1290-1, 2003.
Mennen LI, Balkau B, Vol S. Tissue-type plasminogen activator antigen and consumption
of dairy products. The DESIR Study. Thrombosis Research 94:381-388,
Mennen LI, Lafay L, Edith JM, Feskens EJM, Novak M, Lépinay P, Balkau
B. Possible protective effect of bread and dairy products on the risk of the
metabolic syndrome. Nutrition Research 20:335-347, 2000.
Meyer KA, Kushi LH, Jacobs DR Jr, Slavin J, Sellers TA, Folsom AR. Carbohydrates,
dietary fiber, and incident type 2 diabetes in older women. American Journal
of Clinical Nutrition 71: 921-930, 2000.
Millen BE, Quatromoni PA, Nam BH O'Horo CE, Polak JF, Wolf PA, D'Agostino RB.
Dietary patterns, smoking, and subclinical heart disease in women: opportunities
for primary prevention from Farmingham Nutrition Studies. Journal of the
American Dietetic Association 10(2):208-14, 2004.
Miller G. Whole grain, fiber and antioxidants. In Spiller, G. (ed.), CRC Handbook
of Dietary Fiber in Human Nutrition. CRC Press, Boca Raton, FL, pp. 453-460,
Miller WC, Niederpruem MG, Wallace JP, Lindeman AK. Dietary fat, sugar, and
fiber predict body fat content. Journal of the American Dietetic Association
94:612-615, 1994.
Montonen J, Knekt P, Jarvinen R, Aromaa A, Reunanen A. Whole-grain and fiber
intake and the incidence of type 2 diabetes. Journal of the American College
of Nutrition 77:622-9, 2003.
Mozaffarian D, Kumanyika SK, Lemaitre RN, Olson JL, Burke GL, Siscovick DS.
Cereal, fruit, and vegetable fiber intake and the risk of cardiovascular disease
in elderly individuals. Journal of the American Medical Association
289:1659-1666, 2003.
Murtaugh MA, Jacobs DRJ, Jacob B, Steffen LM, Marquart L. Epidemiological support
for the protection of whole grains against diabetes. Proceedings of the Nutrition
Society 62:143-149, 2003.
National Medical Association Consensus Statement: The Case for Calcium in the
African American Diet. Journal of the National Medical Association 2004.
In press.
National Cancer Institute (NCI) Web site: http://cancer.gov/cancerinfo/pdq/prevention/.
Accessed May 27, 2004.
Nelson LH, Tucker LA. Diet composition related to body fat in a multivariate
study of 293 men. Journal of the American Dietetic Association 96:771-777,
Ness AR, Powles JW. Fruit and vegetables, and cardiovascular disease. International
Journal of Epidemiology 26(1):1-13, 1997.
Ness AR, Smith GD, Hart C. Milk, coronary heart disease and mortality. Journal
of Epidemiology and Community Health 55:379-382, 2001.
Nicklas TA. Calcium intake trends and health consequences from childhood through
adulthood. Journal of the American College of Nutrition 22:340-356,
Nicklas TA, Yang SJ, Baranowski T, Zakeri I, Berenson G. Eating patterns and
obesity in children. American Journal of Preventive Medicine 25(1):9-16,
Opotowsky AR, Bilezikian JP. Racial differences in the effect of early milk
consumption on peak and postmenopausal bone mineral density. Journal of Bone
and Mineral Research 18(11):1978-88, 2003.
Patterson BH, Block G, Rosenberger WF, Pee D, Kahle LL. Fruit and vegetables
in the American diet: data from the NHANES II Survey. American Journal of
Public Health 80:1443-1449, 1990.
Pereira MA, Jacobs DRJ, Slattery M, Ruth K, Van Horn L, Hilner J, Kushi LH.
The association of whole grain intake and fasting insulin in a biracial cohort
of young adults: the CARDIA study. Cardiovascular Disease Prevention
1:231-242, 1998.
Pereira MA, Jacobs DR, Van Horn L, Slattery ML, Kartashov AI, Ludwig DS. Dairy
consumption, obesity, and the insulin resistance syndrome in young adults. The
CARDIA Study. Journal of the American Medical Association 287:2081-2089,
Phillips SM, Bandini LG, Cyr H, Colclough-Douglas S, Naumova E, Must A. Dairy
food consumption and body weight and fatness studied longitudinally over the
adolescent period. International Journal of Obesity 27: 1106-1113, 2003.
Pietinen P, Rimm EB, Korhonen P. Intake of dietary fiber and risk of coronary
heart disease in a cohort of Finnish men: The alpha-tocopherol, beta-carotene
cancer prevention study. Circulation 94:2720-2727, 1996.
Ranganathan R, Nicklas TA, Yang S, Berenson GS. The nutritional impact of dairy
product consumption on dietary intakes of young adults (1995-1996): the Bogalusa
Heart Study. Journal of the American Dietetic Association, in press,
Reaven, GM. Role of insulin resistance in human disease (syndrome X): an expanded
definition. Annual Review of Medicine 44:121-131, 1993.
Riboli E, Norat T. Epidemiologic evidence of the protective effect of fruit
and vegetables on cancer risk. American Journal of Clinical Nutrition
78(3 Suppl):559S-569S, 2003.
Rimm EB, Ascherio A, Giovannucci E, Spiegelman D, Stampfer MJ, Willett WC. Vegetable,
fruit, and cereal fiber intake and risk of coronary heart disease among men.
Journal of the American Medical Association 275:447-451, 1996.
Rissanen TH, Voutilainen S, Virtanen JK, Venho B, Vanharanta M, Mursu J, Salonen
J. Low intake of fruits and berries and vegetables is associated with excess
mortality in men; the Kupio Ischaemic Heart Disease Risk Factor (KIHD) Study.
American Society for Nutrition Science 199-204, 2003.
Rolls BJ, Ello-Martin JA, Tohill BC. What can intervention studies tell us about
the relationship between fruit and vegetable consumption and weight. Nutrition
Reviews 62:1-17, 2004.
Roth JL, Mobarhan S, Clohisy M. The Metabolic Syndrome: where are we and where
do we go? Nutrition Reviews 60:335-337, 2002.
Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E,
Conlin PR, Miller ER 3rd, Simons-Morton DG, Karanja N, Lin PH. Effects of blood
pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension
(DASH) diet. New England Journal of Medicine 344:3-10; 2001.
Salmeron J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ, Stampfer
MJ, Wing AL, Willett WC. Dietary fiber, glycemic load, and risk of NIDDM in men.
Diabetes Care 20:545-550, 1997a.
Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC. Dietary
fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in
women. Journal of the American Medical Association 277: 472-477, 1997b.
Sargeant LA, Khaw KT, Bingham S, Day NY, Luben RN, Oakes S, Welch A, Wareham
NJ. Fruit and vegetable intake and populaion glycosylated hemoglobin levels:
the EPIC-Norfold Study. European Journal of Clinical Nutrition 55: 342-348,
Sauvaget C, Nagano J, Allen N, Kodama K. Vegetable and fruit intake and stroke
mortality in the Hiroshima/Nagasaki Life Span Study. Stroke 34(10):2355-60,
Schatzkin A, Lanza E, Corle D, Lance P, Iber F, Caan B, Shike M, Weissfeld J,
Burt R, Cooper MR, Kikendall JW, Cahill J. Lack of effect of a low-fat, high-fiber
diet on the recurrence of colorectal adenomas. New England Journal of Medicine
342: 1149-1155, 2000.
Serdula MK, Byers T, Mokdad AH, Simoes E, Mendlein JM, Coates RJ. The association
between fruit and vegetable intake and chronic disease risk factors. Epidemiology
7:161-165, 1996.
Skinner JD, Bounds W, Carruth BR, Ziegler P. Longitudinal calcium intake is
negatively related to children's body fat indices. Journal of the American
Dietetic Association 103:1026-1031, 2003.
Slattery ML, Curtin KP, Edwards SL, Schaffer DM. Plant foods, fiber, and rectal
cancer. American Journal of Clinical Nutrition Feb;79(2):274-81, 2004.
Slavin J. Why whole grains are protective: biological mechanisms. Proceedings
of the Nutrition Society 62:129-134, 2003.
Slavin JL, Jacobs D, Marquart L. Grain processing and nutrition. Critical
Reviews in Biotechnology 21:49-66, 2001.
Slemenda CW, Peacock M, Hui S, Zhou L, Johnston CC. Reduced rates of skeletal
remodeling are associated with increased bone mineral density during the development
of peak skeletal mass. Journal of Bone and Mineral Research 12:676-682,
Smith-Warner, SA, Elmer PJ, Tharp TM, Fosdick L, Randall B, Gross M, Wood J,
Potter JD. Increasing vegetable and fruit intake: randomized intervention and
monitoring in an at-risk population. Cancer Epidemiology, Biomarkers &
Prevention 9:307-317, 2000.
Snowdon DA, Phillips RL. Does a vegetarian diet reduce the occurrence of diabetes?
American Journal of Public Health 75:507-512, 1985.
Stamler J, Dolecek TA. Chapter 13. Relation of food and nutrient intakes to
body mass in the special intervention and usual care groups in the Multiple Risk
Factor Intervention Trial. American Journal of Clinical Nutrition 65(suppl):366S-373S,
Steffen LM, Jacobs DRJ, Stevens J. Associations of whole-grain, refined-grain,
and fruit and vegetable consumption with risks of all-cause mortality and incident
coronary artery disease and ischemic stroke: the Atherosclerosis Risk in Communities
(ARIC) Study. American Journal of Clinical Nutrition 78:383-90, 2003.
Summerbell CD, Watts C, Higgins JP, Garrow JS. Randomised controlled trial of
novel, simple, and well supervised weight reducing diets in outpatients. British
Medical Journal 317:1487-1489, 1998.
Teegarden D, Lyle RM, Proulx WR, Johnston CC Jr, Weaver CM. Previous milk consumption
is associated with greater bone density in young women. American Journal
of Clinical Nutrition 69:1014-1017, 1999.
Terry P, Giovannuci E, Michels KB, Bergkvist L, Hansen H, Holmberg L, Wolk A.
Fruit, vegetables, dietary fiber, and risk of colorectal cancer. Journal
of the National Cancer Institute 93:525-33, 2001.
Trudeau E, Kristal AR, Li S, Patterson RE. Demographic and psychosocial predictors
of fruit and vegetable intakes differ: implications for dietary interventions.
Journal of the American Dietetic Association 98: 1412-1417, 1998.
U.S. Department of Agriculture (USDA). Continuing Survey of Food Intakes by
Individuals 1994-96, 1998. PB2000-500027. CD-ROM, 2004.
U.S. Department of Health and Human Services (HHS), National Center for Health
Statistics. National Health and Nutrition Examination Survey 1999-2000, 2004.
Van Dam RM, Rimm EB, Willett WC, Stampfer MJ, Hu FB. Dietary patterns and risk
for type 2 diabetes mellitus in U.S. men. Annals of Internal Medicine
136: 201-209, 2002.
Weinberg LG, Berner LA, Groves JE. Nutrient contributions of dairy foods in
the United States food supply. Journal of the American Dietetic Association
104:895-902, 2004.
Weinsier RL, Johnston MH, Doleys DM, Bacon JA. Dietary management of obesity;
evaluation of the time-energy displacement diet in terms of its efficacy and
nutritional adequacy for long-term weight control. British Journal of Nutrition
47:367-379, 1982.
Welton DC, Kemper HC, Post GB, Van Staveren WA, Twisk JW. Longitudinal development
and tracking of calcium and diary intake from teenager to adult. European
Journal of Clinical Nutrition 51:612-618, 1997.
Whelton PK, He J, Cutler JA, Brancati FL, Appel LJ, Follmann D, Klag MJ. Effects
of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical
trials. Journal of the American Medical Association 277:1624-1632; 1997.
Whiting SJ, Healey A, Psiuk S. Mirwald R, Kowalski K, Bailey DA. Relationship
between carbonated and other low nutrient dense beverages and bone mineral content
of adolescents. Nutrition Research 21:1107-1115, 2001.
Williams DE, Prevost AT, Whichelow MJ, Cox BD, Day NE, Wareham NJ. A cross-sectional
study of dietary patterns with glucose intolerance and other features of the
metabolic syndrome. British Journal of Nutrition 83:257-266, 2000.
Williams DE, Wareham NJ, Cox BD, Byrne CD, Hales N, Day NE. Frequent salad vegetable
consumption is associated with a reduction in the risk of diabetes mellitus.
Journal of Clinical Epidemiology 52: 329-335, 1999.
Wolk A, Manson JE, Stampfer MJ, Colditz GA, Hu FB, Speizer FE, Hennekens CH,
Willett WC. Long-term intake of dietary fiber and decreased risk of coronary
heart disease among women. Journal of the American Medical Association
281:1998-2004, 1999.
World Cancer Research Fund and American Institute for Cancer Research. Food,
Nutrition and the Prevention of Cancer: A Global Perspective. Washington, DC:
American Institute for Cancer Research, 1997.
Yamamoto ME, Applegate WB, Klag MJ, Borhani NO, Cohen JD, Kirchner KA, Lakatos
E, Sacks FM, Taylor JO, Hennekens CH. Lack of blood pressure effect with calcium
and magnesium supplementation in adults with high-normal blood pressure results
from phase I of the Trials of Hypertension Prevention (TOHP). Annals of Epidemiology
5:96-107, 1995.
Yang EU, Kerver JM, Park YK, Kayitsinga J, Allison DA, Song WO. Carbohydrate
intake and biomarkers of glycemic control among US adults: the third National
Health and Nutrition Examination Survey (NHANES III). American Journal of
Clinical Nutrition 77:1426-1433, 2003.
Zemel MB, Thompson W, Milstead A, Morris K, Campbell P. Dietary calcium and
dairy products accelerate weight and fat loss during energy restriction in obese
adults. Obesity Research 12(4):582-590, 2004.
Table D6-1. Case-control Studies of Fruit or Vegetable Consumption
and Their Cancer Preventive Effect*
*Taken from the IARC Handbooks
of Cancer Prevention Volume 8: Fruit & Vegetables.
**Data were not pooled for analysis.
***Raw vegetables, Cooked.
Table D6-2. Cohort Studies of Fruit or Vegetable Consumption
and Their Cancer Preventive Effect*
*Taken from the IARC Handbooks
of Cancer Prevention Volume 8: Fruit & Vegetables.
of Contents
A. Executive Summary
B. Introduction
C. Methodology
D. Science Base
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