1. No category

46
REVIEW / SYNTHE`SE
Nutritional strategies in the prevention and
treatment of metabolic syndrome
Sabrina E. Feldeisen and Katherine L. Tucker
Abstract: The metabolic syndrome (MetS) is a clustering of metabolic abnormalities that increase the risk of developing
atherosclerotic cardiovascular disease and type 2 diabetes. The exact etiology remains unclear, but it is known to be a
complex interaction between genetic, metabolic, and environmental factors. Among environmental factors, dietary habits
are of central importance in the prevention and treatment of this condition. However, there is currently no firm consensus
on the most appropriate dietary recommendations. General recommendations include decreasing obesity, increasing physical activity, and consuming an anti-atherogenic diet, and have traditionally focused on low total fat intake. A major problem with the focus on low fat is that high-carbohydrate diets can contribute to increasing triglyceride and decreasing highdensity lipoprotein (HDL) concentrations. Low-carbohydrate diets have been popular in recent years. However, such diets
are typically higher in saturated fat and lower in fruits, vegetables, and whole grains than national dietary recommendations. More recently the quality of carbohydrate has been studied in relation to MetS, including a focus on dietary fiber
and glycemic index. Similarly, there has been a move from limiting total fat to a focus on the quality of the fat, with evidence of beneficial effects of replacing some carbohydrate with monounsaturated fat. Other nutrients examined for possible
importance include calcium, vitamin D, and magnesium. Together, the evidence suggests that the components of diet currently recommended as ‘‘healthy’’ are likely also protective against MetS, including low saturated and trans fat (rather
than low total fat) and balanced carbohydrate intake rich in dietary fiber, as well as high fruit and vegetable intake (rather
than low total carbohydrate); and the inclusion of low-fat dairy foods. Accelerating research on gene–diet interactions is
likely to contribute interesting information that may lead to further individualized dietary guidance in the future.
Key words: metabolic syndrome, dietary recommendations, waist circumference, blood pressure, dietary pattern.
Re´sume´ : Le syndrome me´tabolique est un ensemble d’anomalies me´taboliques accroissant le risque de maladie cardiovasculaire tels l’athe´roscle´rose et le diabe`te de type 2. On ne connaıˆt pas les causes exactes, mais on sait qu’il s’agit d’une
interaction complexe de facteurs he´re´ditaires, me´taboliques et environnementaux. Parmi les facteurs environnementaux, les
habitudes alimentaires sont d’une importance capitale dans la pre´vention et le traitement de ce syndrome. Cependant, jusqu’a` ce jour, il n’y a aucun consensus net quant aux meilleures recommandations die´te´tiques. Comme recommandations
ge´ne´rales, on demande de re´duire l’adiposite´, d’augmenter la pratique de l’activite´ physique et de consommer des aliments
anti-athe´roge`nes et, de fac¸on classique, de re´duire la quantite´ totale de gras dans l’alimentation. En mettant l’accent sur
une faible quantite´ de gras, on cre´e un proble`me se´rieux : un re´gime hyperglucidique peut augmenter la concentration de
triglyce´rides et diminuer la concentration de HDL. Depuis quelques anne´es, on observe un engouement pour les re´gimes
hypoglucidiques ; ces derniers contiennent habituellement un plus haut taux de gras sature´ et comportent moins de fruits,
de le´gumes et de grains entiers que ne le pre´conisent les organismes nationaux. Depuis peu de temps, on s’inte´resse a` la
qualite´ des sucres et a` leur relation avec le syndrome me´tabolique et on porte une attention particulie`re aux fibres alimentaires et a` l’index glyce´mique. Paralle`lement, on est passe´ d’une recommandation de consommer une quantite´ maximale
de gras a` une recommandation be´ne´fique de substituer certains sucres par des gras monoinsature´s. Il faut aussi tenir
compte des nutriments suivants : le calcium, la vitamine D et le magne´sium. D’apre`s toutes les observations rassemble´es,
les constituants d’un re´gime alimentaire dit « bon pour la sante´ », aussi valables dans la pre´vention du syndrome me´tabolique, comportent peu de gras sature´ et de gras trans (au lieu d’une faible quantite´ totale de gras), des sucres en quantite´
raisonnable, beaucoup de fibres alimentaires, de fruits et de le´gumes (au lieu d’une faible quantite´ totale de sucres) et des
produits laitiers faibles en gras. Avec plus de recherche sur les interactions des re´gimes et des ge`nes, on pourra cumuler
plus de sources d’information utiles a` l’encadrement personnalise´ de l’alimentation.
Received 30 June 2006. Accepted 7 September 2006. Published on the NRC Research Press Web site at http://apnm.nrc.ca on 29 January
2007.
S.E. Feldeisen and K.L. Tucker.1 Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts
University, 711 Washington Street, Boston, MA 02111, USA.
1Corresponding
author (e-mail: [email protected]).
Appl. Physiol. Nutr. Metab. 32: 46–60 (2007)
doi:10.1139/H06-101
#
2007 NRC Canada
Feldeisen and Tucker
47
Mots cle´s : syndrome me´tabolique, recommandations alimentaires, tour de taille, pression sanguine, habitudes alimentaires.
[Traduit par la Re´daction]
______________________________________________________________________________________
Introduction
The metabolic syndrome (MetS) is a clustering of metabolic abnormalities that increase the risk of developing atherosclerotic cardiovascular disease (Isomaa et al. 2001;
Expert Panel on Detection, Evaluation, and Treatment of
High Blood Cholesterol in Adults 2002; Lakka et al. 2002)
and type 2 diabetes (Laaksonen et al. 2002; Grundy 2005).
Individual components that define the MetS include atherogenic dyslipidemia, elevated blood pressure, elevated plasma
glucose and (or) insulin resistance, abdominal obesity (Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults 2001, 2002) and, most recently
recognized, a pro-inflammatory and prothrombotic state
(Grundy et al. 2005; Alberti et al. 2006).
In response to a need for an internationally standardized
definition of the MetS, the International Diabetes Federation
(IDF) has recently proposed a definition for general use.
They define the MetS as central obesity, classified by ethnic
and sex-specific waist circumference cut-off points, plus 2
of the 4 following components: (i) elevated triglyceride concentration (‡1.7 mmol/L or ‡ 150 mg/dL), (ii) low high-density lipoprotein (HDL) cholesterol (<1.03 mmol/L
or <40 mg/dL in males and <1.29 mmol/L or < 50 mg/dL
in females), (iii) elevated blood pressure (systolic BP ‡ 130
or diastolic BP ‡ 85 mmHg, or treatment of previously diagnosed hypertension), and (iv) elevated fasting plasma glucose (FPG ‡ 5.6 mmol/L or ‡ 100 mg/dL, or previously
diagnosed type 2 diabetes) (Alberti et al. 2006). Additional
components, currently recommended for research purposes,
include pro-inflammatory and prothrombotic states (Alberti
et al. 2006).
Data from the National Health and Nutrition Examination
Survey (NHANES) 1999–2002 show that the age-adjusted
prevalence of MetS in the US is approximately 39.1% (men
40.7 ± 1.6%; women 37.1 ± 1.3%), when defined by the
IDF definition (Ford 2005). The increasing prevalence of
MetS has been attributed to a variety of factors including
obesity (Shirai 2004; Alberti et al. 2006), insulin resistance
(Reaven 2002; Alberti et al. 2006), population aging, and
physical inactivity (Alberti et al. 2006). The exact etiology
of MetS remains unclear, but it is known to be a complex
interaction between genetic, metabolic, and environmental
factors (Groop 2000; Wolever 2000; Lidfeldt et al. 2003).
Among environmental factors, there is no doubt that dietary
habits are of central importance in the prevention and treatment of this condition. However, there is no consensus on
the most appropriate dietary recommendations for the prevention and treatment of MetS (Table 1). General recommendations include decreasing obesity, increasing physical
activity and consuming an anti-atherogenic diet (Grundy et
al. 2005). Specific recommendations by the IDF for primary
management of the individual risk components include energy restriction, increased physical activity, reduction in total and saturated fat intake, increased fiber intake, and salt
restriction (Alberti et al. 2006).
This review aims to provide a summary of nutritional
strategies for the prevention and treatment of MetS and its
individual components. The intent is to focus on major aspects of diet and MetS based on recent evidence and trends
in the literature, rather than to be exhaustive. Nutritional
strategies specifically directed at the individual components
of the syndrome will be mentioned briefly as well.
General recommendations
The primary approach for preventing and treating MetS
includes consuming an overall healthy diet for weight reduction and long-term weight maintenance (Grundy et al. 2005;
Lichtenstein et al. 2006). Widely accepted dietary recommendations by groups such as the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III)
and the American Heart Association (AHA) include moderate fat intake (25%–35% of energy), low saturated fat intake
(<7% of total energy), avoidance of trans fat, limited cholesterol (<300 mg/d) and refined sugar intakes, and high intakes of fruits, vegetables, and whole grains (Expert Panel
on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults 2002; Lichtenstein et al. 2006). These
recommendations derive from a traditional focus on lowering LDL cholesterol to reduce the risk of heart disease. For
the MetS, however, triglyceride and HDL cholesterol concentrations are also important, requiring a more detailed examination of the recommendations.
Macronutrient intakes
Low-fat diets
Recommendations for weight loss and for MetS have traditionally focused on low total fat intakes. Several metaanalyses of the effectiveness of low-fat diets have shown
positive weight loss results (Yu-Poth et al. 1999; Astrup et
al. 2000). In an analysis of 16 trials, Astrup et al. (2000)
found that reducing dietary fat without intentionally lowering energy intake did result in greater weight loss than with
higher fat diets, especially for subjects that were more overweight. On the other hand, two reviews (Willett 2002; Pirozzo et al. 2003) provide evidence that a low-fat diet may
not be optimal for weight loss. Willett (2002) argues that
short-term trials of low-fat diets noted only small changes
in weight, and longer trials (1 y or more) showed little or
no changes in body fatness. Additionally, there appeared to
be no benefit of low-fat diets compared with other weight
loss diets at 6, 12, or 18 months in 6 randomized controlled
trials of overweight and obese individuals (Pirozzo et al.
2003). In a recent randomized trial, postmenopausal women
consuming a low-fat diet with high carbohydrate intake from
vegetables, fruits, and grains did not gain weight over an
average of 7.5 y of follow-up compared with women in the
control group (Howard et al. 2006). The question, therefore,
remains complex and it is likely that the quality of the entire
#
2007 NRC Canada
48
Appl. Physiol. Nutr. Metab. Vol. 32, 2007
Table 1. Dietary recommendations and components of MetS.
Metabolic components
Abdominal/central obesity
Elevated blood pressure
Elevated triglyceride levels and low
HDL{ cholesterol
Elevated fasting glucose concentration
Pro-inflammatory/pro-thrombotic state
Dietary recommendations
Healthy dietary pattern
Reduced caloric intake; if weight loss is needed
Low saturated and trans fats, and cholesterol intake
High fruit, vegetable, and whole grains intake
Low refined carbohydrate intake
DASH* diet
Reduced sodium intake
Low to moderate alcohol intake
Reduced caloric intake if weight loss is needed
Mediterranean-style diet
Low saturated and trans fat, and cholesterol intake
High fruit, vegetable, whole grains, and dietary fiber
Moderate fat consumption from unsaturated sources
(especially from monounsaturated fats)
Moderate fish consumption
Low to moderate alcohol intake
Reduced caloric intake if weight loss is needed
Low refined carbohydrate intake
Moderate carbohydrate intake rich in whole grains
Reduced caloric intake; if weight loss is needed
Low saturated and trans fats and cholesterol intake
*Dietary approaches to stop hypertension.
{
High-density lipoprotein.
dietary pattern is important rather than a focus on a single
nutrient. Even with a benefit of low-fat diets on overall
weight loss, more focus is needed on central adiposity,
which is associated with insulin resistance and atherogenic
dyslipidemia (Kwiterovich 2002) for those with MetS.
A major problem with the focus on low fat is that highcarbohydrate diets can contribute to increasing triglyceride
and decreasing HDL concentrations (Krauss and Dreon
1995; Dreon et al. 1999; Reaven 2005), particularly as the
low-fat recommendation may lead some individuals to consume more refined carbohydrates (Reaven 1997; Willett
1998). Excess carbohydrate consumption may be associated
with the development of MetS. Studies using low-fat, high
complex carbohydrate diets as recommended by the NCEP
found reductions in total cholesterol, low-density lipoprotein
(LDL) cholesterol, and triglycerides, but also in HDL cholesterol (Yu-Poth et al. 1999). Higher carbohydrate diets,
particularly those in the refined form, have also been associated with elevated blood pressure (Esmaillzadeh et al. 2005).
An examination of cross-sectional data from NHANES III
showed that high intake of carbohydrate (>60% energy intake) in men was associated with MetS (Zhu et al. 2004).
Low-carbohydrate diets
These observations have contributed to a recent focus on
low-carbohydrate diets. There is some evidence of beneficial
effects of low-carbohydrate diets on the risk of MetS (Volek
and Feinman 2005). Low-carbohydrate diets typically consist of <100 g/d or <30% of total energy from carbohydrate
(Bilsborough and Crowe 2003). In a randomized crossover
study of 15 overweight men, a low-carbohydrate diet was
more effective than a low-fat diet for decreasing MetS risk
factors such as fasting serum triglycerides, the TAG–HDL
cholesterol ratio, and fasting glucose and for improving the
LDL subclass distribution (Sharman et al. 2004). A recent
meta-analysis of 5 trials indicated that low-carbohydrate diets with no energy restriction produced weight loss similar
to low-fat diets with energy restriction (Nordmann et al.
2006). The low-carbohydrate diets decreased triglyceride
concentrations and increased HDL concentrations, whereas
the low-fat diets showed improvements in LDL and total
cholesterol concentrations. For MetS, the former profile is
of greater importance, although the importance of LDL cholesterol to CVD risk cannot be ignored.
High-protein, low-carbohydrate diets have been shown to
reduce weight and positively affect certain blood lipoproteins (Foster et al. 2003; Stern et al. 2004; Nordmann et al.
2006). A clinical trial of 63 obese men and women found
that a low-carbohydrate diet produced greater weight loss
than a conventional diet (high-carbohydrate, low-fat, low energy) after 6 months (Foster et al. 2003). However, subjects
tended to regain the weight after 1 y, and this study had a
high attrition rate.
Low-carbohydrate diets, including the Atkins diet, have
been popular in recent years. However, such diets are typically higher in saturated fat and lower in fruits, vegetables,
and whole grains than national dietary recommendations
(Grundy et al. 2005). Low-carbohydrate diets such as the
Atkins and Zone diets have shown some benefits for initial
weight loss, and they may improve some cardiovascular risk
factors over short periods of time (Brehm et al. 2003; Foster
et al. 2003; Samaha et al. 2003; Nordmann et al. 2006). Data
on long term effects, however, are inadequate owing to poor
adherence rates observed in trials assessing low-carbohydrate,
high-protein diets (Foster et al. 2003; Samaha et al. 2003;
Dansinger et al. 2005). One study found that a modified
low-carbohydrate diet that was higher in complex carbohydrates, protein, and monounsaturated fats led to more
weight loss than a low-fat, high-carbohydrate diet following the NCEP guidelines (Aude et al. 2004). Another,
#
2007 NRC Canada
Feldeisen and Tucker
comparing a high-carbohydrate, high-fiber diet to a high-fat
Atkins diet and a high-protein Zone diet, saw weight loss
and reduction in triglyceride concentrations in all 3
(McAuley et al. 2005). However, participants consuming
the high-fat and high-protein diets lost significantly more
weight and significantly reduced fasting triglyceride concentrations more than those following the high-carbohydrate, high-fiber diet.
Carbohydrate quality
The quality of carbohydrate has been studied in relation
to MetS. The glycemic index (GI), which is used to quantify
the effect of carbohydrate-rich foods on postprandial glucose
and insulin response, may provide more insight into the relationship between dietary carbohydrate and the MetS. In the
Framingham Offspring study, the relative risk of MetS was
1.41 (1.04–1.91) for individuals in the highest quintile of
glycemic index compared with the lowest quintile after adjusting for dietary fiber (McKeown et al. 2004). The combination of a low-glycemic, low-fat, high-protein diet has been
shown to result in a better overall lipoprotein profile relative
to an AHA phase I diet in a short-term intervention (Dumesnil et al. 2001). A review by Davy and Melby (2003)
provides evidence of potential beneficial effects of low-fat,
high-carbohydrate diets rich in dietary fiber on MetS.
The use of whole grains contributes to a lower glycemic
index while providing fiber and additional nutrients. Several
studies provide evidence of a protective effect of whole
grains on the prevalence of MetS (McKeown et al. 2004;
Esmaillzadeh et al. 2005; Sahyoun et al. 2006). However,
other studies have found no association with whole grains
(Yoo et al. 2004) and further research is needed.
Type of dietary fat
Riccardi et al. (2004) emphasize that total fat intake may
not be as important for individuals with MetS as dietary fat
composition. The type of fatty acids consumed (saturated,
polyunsaturated, monounsaturated, or trans fat) may have
greater implications for MetS and its components For example, saturated fat plays a role in atherogenic dyslipidemia,
but may also be important for insulin resistance (Riccardi et
al. 2004). A review by Grundy et al. (2002) supports these
recommendations by providing evidence of the importance
of a diet low in saturated and trans fat for managing LDLcholesterol, further noting the potential beneficial effects of
replacing some carbohydrate with monounsaturated fat for
triglyceride concentrations. A high-fat diet (40% of energy)
that is high in monounsaturated fatty acids and low in saturated fatty acids has been shown to reduce total and LDL cholesterol, similar to the effects of a low-fat, high-carbohydrate
diet (Grundy 1986). In addition, the high monounsaturated fat
diet did not lower HDL cholesterol or increase triglyceride
concentrations, as seen with a low-fat, high-carbohydrate
diet. Other studies have found similar favorable changes in
blood lipids with a high monounsaturated fatty acid diet
(Mensink et al. 1989; Ginsberg et al. 1990; Appel et al. 2005).
Consumption of long-chain omega-3 fatty acids, present
in oily fish, is beneficial for reducing risk of CVD (KrisEtherton et al. 2002) and may be beneficial for those with
MetS through a reduction of plasma triglyceride concentra-
49
tions (Harris 1997; Farmer et al. 2001; Rivellese et al.
2003) and atherogenic small, dense, lipoprotein particles
(Carpentier et al. 2006). However, these fatty acids may
also increase LDL cholesterol (Harris 1997; Farmer et al.
2001; Rivellese et al. 2003). A review of the effects of
omega-3 polyunsaturated fatty acids in persons with type 2
diabetes (Nettleton and Katz 2005) and a more recent review of omega-3 fatty acids and MetS (Carpentier et al.
2006) suggest potential benefits including lower triglyceride
concentrations, increased HDL cholesterol concentrations,
improved endothelial function, and lower blood pressure,
weighed against modest increases in LDL cholesterol.
Omega-3 fatty acids may also play a role in reducing inflammation, platelet, and leukocyte activation, (Carpentier
et al. 2006) and potentially insulin resistance (Nettleton and
Katz 2005). A review by Calder (2006) describes direct
(e.g., by inhibiting arachidonic acid metabolism) and indirect (e.g., by modifying inflammatory gene expression)
mechanisms by which omega-3 polyunsaturated fatty acids
may result in anti-inflammatory effects. This may have important implications for MetS, as inflammatory and prothrombotic states have been recently associated with the
syndrome (Dandona et al. 2005; Calder 2006). Additional
information regarding dietary factors and inflammation are
discussed below.
Alcohol
The relationship between alcohol intake and MetS remains controversial (Goude et al. 2002; Djousse et al. 2004;
Yoon et al. 2004; Fan et al. 2006). In a cross-sectional
study, moderate alcohol consumption of all types was associated with a lower prevalence of MetS in a U-shaped relation in men and a dose-dependent relation in women
(Djousse et al. 2004). For specific types of alcohol, wine appears to be protective against the prevalence of MetS in
women (Rosell et al. 2003), but this may be due to an overall healthier lifestyle associated with wine use, rather than
from the wine consumption itself (Djousse et al. 2004). In
contrast, intake of spirits has been shown to be associated
with a less favorable metabolic profile in both men and
women (Rosell et al. 2003). Data from the Korean National
Health and Nutrition Examination Survey indicate a 29%
and 20% lower prevalence of MetS for men and women, respectively, who consumed 1 to 14.9 g/d of alcohol compared
with those who consumed no alcohol, but with increasing alcohol intake, the risk of MetS and its components increased
(Yoon et al. 2004). Recent evidence indicates that lifetime
alcohol consumption may be associated with greater risk of
MetS (Fan et al. 2006). It appears that heavy alcohol intake
is associated with risk, and remains unclear as to whether
low to moderate alcohol consumption is protective against
MetS. More prospective studies are needed to elucidate this
relationship.
Micronutrients
Calcium and vitamin D
Higher intake of calcium (total, dietary, and supplemental) has been associated with a lower prevalence of MetS.
Liu et al. (2005) found a protective effect of increasing
quintiles of total calcium intake on the prevalence of MetS
#
2007 NRC Canada
50
after adjusting for smoking status, exercise, alcohol intake,
multivitamin use, and parental history of myocardial infarction before age 60 y. Total and supplemental vitamin D was
not associated with the prevalence of MetS in this study.
However, other studies have found that inadequate levels of
vitamin D are associated with MetS (Boucher 1998; Chiu et
al. 2004; Ford et al. 2005).
The major source of calcium and vitamin D in the US
population is dairy products, and several studies suggest
that dairy consumption may be protective of MetS (Pereira
et al. 2002; Azadbakht et al. 2005b; Liu et al. 2005). The
Women’s Health Study, including 10 066 women
age ‡45 y, reported a protective effect of both calcium intake and dairy products on MetS (Liu et al. 2005). However,
it has been noted that high dairy intake tends to be associated with higher consumption of fiber, fruits, vegetables,
and whole grains, and that the observed protective association may be driven by an improved overall dietary pattern
(Azadbakht et al. 2005b). The Coronary Artery Risk Development in Young Adults (CARDIA) study, a populationbased 10 y prospective study, found that overweight individuals in the highest category of dairy consumption were 72%
less likely (OR, 0.28 (0.14–0.58)) to develop insulin resistance syndrome relative to those with the lowest dairy intake
(Pereira et al. 2002). In contrast, one study found that older
women who never drank milk had a lower prevalence of the
MetS than those who drank milk (OR = 0.55; 0.33–0.94)
after adjusting for age (Lawlor et al. 2005). Subjects who
never drank milk had lower BMI, mean homeostasis model
assessment (HOMA) scores and triglyceride concentrations,
and higher HDL concentrations than those who did drink
milk. However, the actual amount of milk consumed was
not assessed in this study.
A population-based cross-sectional study in Tehranian
adults reported that those in the highest quartile of dairy
consumption showed a lower prevalence of high waist circumference, hypertension, and MetS, with p < 0.001–0.02
(Azadbakht et al. 2005b). The population-based prospective
Malmo Diet and Cancer Study found that milk fat based
food patterns showed a protective effect against hyperinsulinemia in women with an odds ratio of 0.66 (0.48, 0.91) and
suggested protective effects against dyslipidemia and hyperglycemia with odds ratios of 0.70 (0.47–1.03) and 0.74
(0.47–1.15), respectively (Wirfalt et al. 2001). Another commonly cited study conducted in France found that dairy
products were inversely associated with MetS and its components among men (Mennen et al. 2000). However, data
on fruit and vegetables were not collected, and confounding
by these foods cannot be ruled out.
Magnesium
Magnesium appears to be important for glucose metabolism and insulin homeostasis and may play a role in mediating other risk factors of MetS (Barbagallo and Dominguez
2006). Magnesium is found in many whole foods, including
dark green leafy vegetables, whole grains, some fruits, nuts,
seeds, legumes, and soy products. Few studies have examined the association between magnesium and MetS. Crosssectional studies have reported inverse associations between
dietary (Song et al. 2005) and serum magnesium levels
(Guerrero-Romero and Rodriguez-Moran 2002) and MetS
Appl. Physiol. Nutr. Metab. Vol. 32, 2007
or with fasting insulin levels in overweight women (Song et
al. 2004).
One longitudinal study showed a greater risk of incident
type 2 diabetes with low magnesium intake (Lopez-Ridaura
et al. 2004). Another study found a 31% reduced risk of incident MetS in young adults with the highest versus the lowest quartile of magnesium intake (He et al. 2006).
Magnesium intake was also inversely associated with fasting
glucose concentration, waist circumference, and HDL cholesterol in this study, after adjusting for potential confounders. When adjusted for calcium and potassium, however,
associations were attenuated, due to collinearity of intake.
Therefore, it remains unclear which of these minerals was
of greatest importance. Intervention trials can be informative
in this case, but few studies are available for MetS. A metaanalysis of magnesium supplementation and blood pressure
reported a dose-dependent effect of magnesium indicating
reductions of 4.3 mmHg systolic blood pressure and
2.3 mmHg diastolic blood pressure for each increase of
10 mmol/d magnesium (Jee et al. 2002).
Dietary patterns
Together, the data described above suggest that the components of diet currently recommended as healthy are likely
protective against MetS. Looking at the total diet together,
descriptions of ‘‘healthy dietary patterns’’ have emerged
from prospective studies using cluster and factor analysis.
These are typically characterized by higher intakes of fruits,
vegetables, reduced-fat dairy products, and whole grains (Hu
et al. 2000; Newby et al. 2003; Newby and Tucker 2004).
Dietary pattern analysis can address the complex interactions between nutrients, collinearity between nutrients, and
dietary recommendations (Newby and Tucker 2004). A
cross-sectional study identified a healthy dietary pattern using principal component analysis that was found to be protective of risk factors for MetS such as fasting glucose and
central obesity in a UK-based cohort (Williams et al. 2000).
Dietary patterns characterized by highly processed cereals
with a high glycemic index are associated with an increased
risk of MetS. Baxter et al. (2006) states in a recent review
that there appears to be no single dietary component that is
associated with MetS, but rather it is associated with an
overall dietary pattern. Food patterns that are dominated by
higher fiber intake have been associated with more favorable
risk factors for MetS, whereas patterns higher in refined
grains, cheese, cake and alcoholic beverages have been associated with more adverse effects (Wirfalt et al. 2001).
In a cross-sectional study of Tehranian adults, a higher dietary diversity score, used as an indicator of overall diet and
quality of diet, was inversely associated with MetS (Azadbakht et al. 2005a). This diversity score was associated with
relatively higher intakes of fiber, fruit, vegetables, vegetable
oil, and dairy and lower meat and cholesterol intake.
Although those with a higher diversity score also consumed
more energy and tended to be more obese, it was thought
that the increased energy intake may be from foods that are
part of a healthy dietary pattern that may reduce some of the
risk factors for MetS (Azadbakht et al. 2005a). In the Framingham Offspring Spouse study, an ‘‘empty calorie’’ dietary pattern characterized by a higher consumption of fat,
#
2007 NRC Canada
Feldeisen and Tucker
energy and sweetened beverages, and lower dietary fiber and
vegetable intake, was associated with the highest prevalence
of MetS and with low HDL levels in obese women and with
dyslipidemia in all women (Sonnenberg et al. 2005).
A 2 y intervention study using a low-calorie diet based on
NCEP ATP III recommendations including low-fat, highcarbohydrate, and high dietary fiber successfully reduced
MetS in 37% of obese subjects, especially in those who had
greater than 10% weight loss (Muzio et al. 2005). Additionally, there were no adverse effects on blood glucose, triglycerides, or HDL cholesterol. This indicates that weight
loss programs following an overall healthy diet can be beneficial for reducing the prevalence of MetS.
It appears that diets characterized by low total and saturated fat intake and higher fruit, vegetable, whole grain, and
low-fat dairy intake are protective against MetS and its individual components. The dietary approaches to stop hypertension (DASH) diet, characterized by high fruit and vegetable
intake, low-fat dairy products, whole grains, poultry, fish,
and nuts and low saturated and total fat, meats, sweets, and
sugar drinks, significantly reduced components of the MetS
compared with controls in men and women (Azadbakht et
al. 2005c). Positive results were seen for systolic blood pressure, body mass, fasting blood glucose, triglycerides, and
HDL cholesterol. The favorable changes in the metabolic
components remained after adjusting for weight loss. It is
suggested that the dietary composition of the DASH diet (dietary fiber, vitamins, minerals, and phytochemicals (Most
2004)) may drive the protective associations seen in this
study (Azadbakht et al. 2005c).
There is considerable evidence that a Mediterranean dietary pattern may have beneficial effects on cardiovascular
disease risk (de Lorgeril et al. 1999; Singh et al. 2002),
MetS (Esposito et al. 2004), and all-cause mortality (Trichopoulou et al. 2003). While there are variations in the Mediterranean diet between countries and regions, this dietary
pattern is characterized by high intake of fruit, vegetables,
whole grains, beans, nuts, and olive oil (Kris-Etherton et al.
2001). Dairy products, fish, poultry, eggs, and wine are typically consumed in low to moderate amounts and a large
proportion of energy intake from dietary fat is in the form
of monounsaturated fats. A recent review by Serra-Majem
et al. (2006) revealed the need for more clinical and observational trials to make concrete recommendations regarding
MetS and the Mediterranean diet, as most of the research is
based on observational epidemiological studies. However,
one trial of 180 men and women, randomized to consume a
Mediterranean diet or to follow a prudent diet, found an approximately 50% reduction in the prevalence of MetS with
the Mediterranean diet owing to significant decreases in
waist circumference, blood pressure, plasma glucose, total
cholesterol, and triglyceride concentrations, and a significant
increase in HDL in the intervention group (Esposito et al.
2004).
Individual risk factors for MetS
Central obesity
For the MetS, central adiposity is of primary interest.
Central adiposity, specifically visceral adiposity, has been
shown to be significantly associated with all components of
51
MetS (Carr et al. 2004). It has been shown that adiposity in
obese individuals is associated with insulin resistance
(Grundy et al. 2005) and in abnormal inflammatory responses (Grundy et al. 2005; Calder 2006), which are both
related to MetS. The importance of waist circumference as
a measure of central adiposity has recently been emphasized
as one of the major components of MetS (Alberti et al.
2006; Katzmarzyk et al. 2006). Waist circumference has
been reported to be most specifically associated with cardiovascular risk (Dobbelsteyn et al. 2001), as well as other
components of MetS including blood pressure, fasting glucose, and lipid profiles (Zhu et al. 2005). Waist circumference has been shown to be a better measure of central
adiposity (Misra et al. 2005) and has been more highly correlated than BMI with the components of MetS (Zhu et al.
2005).
Weight loss is a primary intervention recommended for
the prevention and treatment of MetS. A recent randomized,
controlled, trial of 70 premenopausal women found that increased physical activity and consumption of a low-energy
diet lead to significant reductions in body mass, BMI, waist
circumference, total fat mass, trunk fat mass, and insulin and
leptin levels (Lofgren et al. 2005). Of interest is the fact that
7 out of 8 participants who had MetS prior to the intervention no longer had it after the intervention. Aude et al.
(2004) compared an NCEP diet to a modified low-carbohydrate diet (lower in total carbohydrates, higher in protein,
monounsaturated fat, and complex carbohydrates) and found
that weight loss was significantly greater on the modified
low-carbohydrate diet than on the NCEP diet after 12 weeks.
Further, a significant reduction in the waist-to-hip ratio was
observed only within the modified low-carbohydrate diet
group and not between the groups. Dietary patterns identified from cluster or factor analysis have shown that healthy
patterns are associated with lower BMI and waist circumference (Newby et al. 2003; Newby and Tucker 2004).
Dietary patterns do not always relate similarly to BMI and
to central adiposity. One prospective study showed that a
healthy dietary pattern characterized by high fruit, vegetable,
low-fat dairy, and whole grain and low red and processed
meats, soda, and fast foods was associated with smaller
gains in BMI and waist circumference relative to others, but
that a pattern high in refined carbohydrates (white bread)
was associated with the largest gains in waist circumference,
whereas a ‘‘meat’’ pattern was associated with the largest
gains in BMI (Newby et al. 2003). In the multi-ethnic insulin resistance atherosclerosis study (IRAS 1992–1994), a
dark bread pattern derived from cluster analysis was associated with the highest fiber intake relative to total energy and
with lower waist circumference (Liese et al. 2004). This is
consistent with findings from other studies, where higher dietary fiber patterns have been related to less central obesity
(Wirfalt et al. 2001). In the IRAS, the highest intake of beer,
which emerged within the white bread group, was associated
with central and total obesity, whereas the wine group was
associated with low adiposity; this indicates that alcohol intake is associated with other health characteristics that need
to be accounted for to examine alcohol intake alone (Liese
et al. 2004).
Similar to these findings, a high intake of refined grains
was positively associated with an increase in 6 y change in
#
2007 NRC Canada
52
waist circumference among women after adjusting for BMI,
whereas potatoes were protective against gain in waist circumference for men (Halkjaer et al. 2004). This study measured diet with food factor scores and examined intakes of 10
food or beverage groups in relation to 6 y changes in waist
circumference. Beer and spirits intake was associated with
increases in waist circumference in women only. Tea and
coffee appeared to be associated with increases in waist circumference; however, the relationship was weakened when
adjusted for BMI (Halkjaer et al. 2004). Another prospective
study examining dietary intake in relation to 9 y waist gain
indicated that changes in trans fat intake but not total fat intake were related to increases in waist gain, whereas
changes in fiber intake were protective (Koh-Banerjee et al.
2003).
Blood pressure
Dietary approaches have been the focus and primary action for lowering blood pressure and preventing hypertension (Appel et al. 1997). Changes in lifestyle behaviors by
modifying dietary intake can lead to weight reduction, decreased sodium intake, and decreased alcohol intake, all factors that are beneficial and recommended for reducing blood
pressure (Chobanian et al. 2003; Champagne 2006). A systematic review of prospective studies and clinical trials with
2 years or more of follow-up concluded that, in overweight
and (or) obese adults, every 10 kg of weight loss was associated with a 6.0 mmHg decrease in systolic blood pressure
and a 4.6 mmHg decrease in diastolic blood pressure,
although changes in blood pressure were greater after initial
weight loss than they were over longer time periods (Aucott
et al. 2005). Newer evidence indicates that monounsaturated
fats, but not omega-3 fatty acids, may play a role in reducing blood pressure, specifically diastolic blood pressure
(Rasmussen et al. 2006).
Blood pressure management can be attained through
healthful dietary patterns such as the DASH trial diet (Appel
et al. 1997; Sacks et al. 2001). In an 11-week clinical trial,
the DASH diet lowered systolic blood pressure by
5.5 mmHg more and diastolic blood pressure by 3.0 mmHg
more than a control diet (Appel et al. 1997). The control
diet represented the average consumption of macronutrients
and dietary fiber in the US and approximated the 25th percentile of US consumption for potassium, magnesium, and
calcium. Greater reductions in blood pressure on a DASH
diet have been observed for individuals with hypertension
than those who are normotensive (Appel et al. 1997; Lopes
et al. 2003). However, the DASH diet has been shown to be
beneficial for participants without hypertension, indicating
the potential for preventing hypertension (Lopes et al.
2003). The potential benefits of the DASH diet on blood
pressure may occur through an increase in antioxidant capacity and reduction in oxidative stress related to hyperlipidemia in obese hypertensive participants (Lopes et al. 2003).
There is convincing evidence that a reduction of dietary
sodium intake lowers blood pressure (Cutler et al. 1997;
Sacks et al. 2001; He and MacGregor 2002; He et al.
2005). In a meta-analysis by He and MacGregor (2002), a
reduction of 6 g (100 mmol/d) of dietary salt per day predicted a significant decrease in systolic and diastolic blood
pressure in hypertensive and normotensive individuals by
Appl. Physiol. Nutr. Metab. Vol. 32, 2007
7.11/3.88 mmHg and 3.57/1.66 mmHg, respectively. The
Joint National Committee (JNC) on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure recommends a DASH diet and a decrease in dietary sodium intake
to 2.4 g (100 mmol) for improved blood pressure (Chobanian et al. 2003). Sacks et al. (2001) provided evidence that
a reduction in dietary sodium intake in combination with a
DASH diet resulted in greater effects than either intervention alone. The effects of the 2 dietary interventions, however, did not appear to be fully additive.
The DASH diet recommends foods that are good sources
of calcium, potassium, and magnesium (Appel et al. 1997).
Several studies, but not all, have shown that dairy intake
and dietary calcium are inversely associated with blood
pressure (Ruidavets et al. 2006). A recent meta-analysis of
40 randomized controlled trials concluded that supplemental
calcium is important in the reduction of systolic and diastolic blood pressure (van Mierlo et al. 2006). Although
some studies have shown a significant relationship between
systolic blood pressure and high dairy intake (Ruidavets et
al. 2006), others have found significant but weak differences
(£1–3 mmHg) in adjusted systolic and diastolic blood pressure after adjusting for potential confounders between the
highest and lowest dairy calcium intakes (Jorde and Bonaa
2000).
More consistent findings have been seen for the inverse
association between potassium and systolic and diastolic
blood pressure (Kotchen and McCarron 1998; He and MacGregor 1999; Hajjar et al. 2001). Data from NHANES III
included 17 030 individuals age 20 y or older and found
that higher intakes of potassium were negatively associated
with systolic and diastolic blood pressure (Hajjar et al.
2001). Data regarding magnesium intake are less consistent,
but some studies have also shown an inverse association between magnesium intake and blood pressure (Mizushima et
al. 1998).
A recent systematic review of randomized controlled trials concluded that a healthy diet with decreased alcohol and
sodium intakes was significantly associated with a reduction
in mean systolic and diastolic blood pressure, but there was
no support for a protective relationship with the use of calcium, magnesium, or potassium supplements (Dickinson et
al. 2006). The JNC recommends that alcohol intake be limited to no more than 2 drinks (30 mL of ethanol) per day in
most men and 1 drink (15 mL of ethanol) per day in women
and lighter-weight persons (Chobanian et al. 2003). A review (Beilin and Puddey 2006) and a meta-analysis (Xin et
al. 2001) suggest reductions in systolic and diastolic blood
pressure with decreasing alcohol consumption. Further, a
randomized crossover trial indicated that moderate alcohol
consumption increased blood pressure in normotensive men
regardless of the type of alcoholic beverage (Zilkens et al.
2005). The data regarding alcohol consumption and blood
pressure remain inconsistent (Cushman et al. 1998), but suggest that limiting alcohol intake is likely to be beneficial for
blood pressure.
Insulin resistance
Insulin resistance occurs when tissues cannot respond optimally to normal circulating concentrations of insulin,
which results in a decrease in the amount of glucose that
#
2007 NRC Canada
Feldeisen and Tucker
gets into the muscle and adipose tissue (Le Marchand-Brustel
et al. 2003). Insulin resistance has been called the ‘‘pathogenetic link’’ underlying MetS and may be influenced by different dietary factors (Riccardi et al. 2004). Individuals with
insulin resistance, especially those who are overweight or
obese, can benefit from weight loss (Reaven 2005).
In a recent review, Reaven (2005) concludes that there is
little evidence regarding a low-fat, high-carbohydrate diet
for improving insulin sensitivity and that this dietary pattern
may actually increase concentrations of glucose and insulin
in those with insulin resistance. However, diets rich in
whole grains, especially cereal fiber, are associated with
lower fasting insulin concentrations (McKeown et al. 2004).
Observational studies have not consistently shown an association between total carbohydrate intake (McKeown et al.
2004; Lau et al. 2005) or simple sugar intake (Daly 2003;
Lau et al. 2005) and insulin resistance.
There is evidence that higher intake of dietary fiber is associated with lower fasting insulin levels (Marshall et al.
1997; Ludwig et al. 1999), and inversely associated with
measures of insulin resistance (McKeown et al. 2004; Lau
et al. 2005) and improved insulin sensitivity (Liese et al.
2005). A review by McKeown (2004) found improved insulin sensitivity with diets high in whole-grain foods, that may
be mediated by magnesium and dietary fiber found in the
whole grains. Cluster analysis has shown that a dietary pattern with high intakes of white bread, meats, and fats was
associated with the worst insulin sensitivity relative to other
dietary patterns (Liese et al. 2004). In the same study, the
dark bread group and the wine group were associated with
the more desirable levels of insulin sensitivity. There also
appears to be a relationship between low magnesium status,
MetS (Guerrero-Romero and Rodriguez-Moran 2002), and
increased fasting insulin levels (Ma et al. 1995).
The role of dietary fats and MetS through impaired insulin sensitivity or insulin resistance has been recently reviewed (Roche 2005). The relationship between the amount
of fat intake (high vs. low) and insulin sensitivity is still unclear (Foster et al. 2003; Samaha et al. 2003). More consistently, there appears to be evidence that saturated fatty acids
are associated with insulin resistance and that replacing saturated fats with monounsaturated fats may improve insulin
sensitivity (Perez-Jimenez et al. 2001; Vessby et al. 2001).
However, another study did not find an effect of differing
dietary fatty acids on insulin sensitivity, especially in lean
individuals (Lovejoy et al. 2002).
After 12 years, men from the Health Professionals Followup Study in the highest quintile of dairy intake showed a relative risk for type 2 diabetes of 0.77 (0.62–0.95; p = 0.003)
compared with men in the lowest quintile; an increase of 1
serving of dairy per day was associated with a 9% lower
risk for type 2 diabetes (multivariate RR, 0.91; (0.85–0.97))
(Choi et al. 2005). Cross sectional data from NHANES III
indicate an inverse association between quintiles of vitamin
D concentrations and hyperglycemia, abdominal obesity,
and hypertriglyceridemia, which may be due to an effect of
vitamin D on insulin resistance (Ford et al. 2005).
Atherogenic dyslipidemia
Guidelines from the NCEP ATP III involve first lowering
53
LDL cholesterol for those with abnormal levels through diet
and drug therapy (Wilson and Grundy 2003). In the case of
MetS, abnormalities in HDL cholesterol and plasma triglycerides also become important targets for prevention and
treatment (Wilson and Grundy 2003). As discussed previously, dietary interventions for prevention of the syndrome
have typically focused on blood lipid management, with a
diet low in saturated and trans fat and cholesterol (Expert
Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults 2001, 2002). However, low-fat,
high-carbohydrate diets can decrease HDL cholesterol and
increase triglyceride concentrations and, therefore, are not
ideal for MetS (Garg et al. 1992; Mensink and Katan 1992).
Rather, low-carbohydrate diets have resulted in lower triglycerides and higher HDL cholesterol levels than have conventional diets (Foster et al. 2003; Stern et al. 2004;
Nordmann et al. 2006). However, the quality of fat (Riccardi
et al. 2004) and carbohydrate (McKeown et al. 2004; Aston
2006) has been a recent focus in addition to either very low
fat or low-carbohydrate diets.
Healthy dietary patterns low in saturated fat and high in
fruits, vegetables, and whole grains are among the most
common recommendations for dyslipidemia. The DASH
diet, which meets these criteria, significantly lowered total
and LDL cholesterol and did not increase triglycerides (Obarzanek et al. 2001). Recently, a randomized controlled trial
of the DASH diet resulted in higher HDL cholesterol and
lower triglycerides, which remained significant after adjusting for weight loss. This would suggest potential benefit for
the treatment of MetS (Azadbakht et al. 2005c).
High GI and glycemic load diets have been inversely associated with HDL concentrations (Frost et al. 1999; Ford
and Liu 2001) and positively associated with fasting triglycerides, which appears stronger for overweight and obese
women (Liu et al. 2001). Contrary to these findings, however, a 10 y follow-up study of elderly men examining dietary GI and unfavorable metabolic risk factors such as
decreased HDL cholesterol, increased triglyceride, or increased fasting insulin or glucose concentrations found no
association between GI and coronary heart disease (van
Dam et al. 2000). Intervention studies have also reported
conflicting results on the effect of GI on dyslipidemia
(Aston 2006). A cross-sectional Swedish study of men with
varying insulin sensitivities found that fatty acids typically
in milk products were associated with a less atherogenic
LDL profile (Sjogren et al. 2004). Further, calcium supplements and calcium fortification of foods have been reported
to decrease concentrations of LDL cholesterol and triglycerides and increase HDL concentrations (Tholstrup 2006).
Inflammation
A pro-inflammatory state has been associated with MetS
(Esposito et al. 2003; Ridker et al. 2003; Tamakoshi et al.
2003) and has been indicated as a potentially important feature to examine in addition to the other components of the
syndrome (Grundy et al. 2005; Alberti et al. 2006). Evidence from two recent reviews indicates that weight loss
(Dietrich and Jialal 2005) and modification in dietary fat
can influence inflammation (Esposito and Giugliano 2006).
For example, acute effects of a high-fat meal include in#
2007 NRC Canada
54
creased levels of some adhesion molecules (i.e., ICAM-1
and VCAM-1) and two inflammatory cytokines, plasma interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a), in
healthy subjects (Nappo et al. 2002). Several studies have
shown an association between higher consumption of saturated and trans fat and inflammatory responses such as increased C reactive protein (CRP), fibrinogen, and IL-6
(Baer et al. 2004). In a cross-sectional study of 730 women
from the Nurses’ Health Study cohort, trans fat intake was
positively associated with biomarkers of inflammation and
endothelial function including CRP, sTNFR-2, E-selectin,
sICAM-1 and sVCAM-1 (Lopez-Garcia et al. 2005). Others,
however, have reported only weak to no association between
CRP and dietary factors (Fredrikson et al. 2004).
A review by Esposito and Giugliano (2006) emphasizes
the importance of healthy dietary patterns as a potential
strategy to reduce inflammation and related metabolic risks.
A Mediterranean style diet significantly reduced serum highsensitivity CRP, IL-6, IL-7, and IL-8 compared with a control diet (Esposito et al. 2004). Additionally, a very low-carbohydrate and an energy-restricted, low-fat diet significantly
decreased some biomarkers of inflammation, although this is
thought to be a result of weight loss associated with the diets (Sharman and Volek 2004). This relatively new area of
research requires more attention.
Gene–diet interaction
Roche et al. (2005) note that there are multiple genes involved in the development and progression of MetS.
Although the prevalence of MetS has increased dramatically
and continues to rise, the human genome has not changed
much over this period of time. For this reason, environmental influences like diet have been identified as central factors
contributing to incidence of the syndrome. Recently, researchers have identified a number of gene–diet interactions.
For example, an interaction between the APOA1 G?A polymorphism and dietary intake of polyunsaturated fat led to
differences in HDL cholesterol concentrations in women
from the Framingham Offspring Study (Ordovas et al.
2002). Higher intake of polyunsaturated fats was associated
with increased HDL cholesterol concentrations for women
who were carriers of the A allele and, for women in the G/
G group, the effect was reversed. Additionally, two studies
discussed in the review by Roche et al. (2005) found that a
polymorphism in the PPAR gene (Pro12Ala) modifies the
relationship between dietary fat intake and MetS components (Robitaille et al. 2003; Luan et al. 2001). Clearly,
given the complexity of both the MetS and dietary intake,
many such interactions will become apparent in this active
research area, further clarifying whether individual differences can be identified in the future that would result in tailored dietary recommendations.
Conclusions
MetS has many components that are modifiable by diet,
thereby providing important opportunities for prevention
and treatment. Although a consensus has not been reached
regarding the most appropriate dietary recommendations,
the summary of research suggests that low saturated and
trans fat (rather than low total fat) intakes, a balanced carbo-
Appl. Physiol. Nutr. Metab. Vol. 32, 2007
hydrate intake rich in dietary fiber, high fruit and vegetable
intake (rather than a focus on low total carbohydrate), and
the inclusion of low-fat dairy intake may be most beneficial
for improving each of the individual components and thus
reduce the risk of MetS. These recommendations closely resemble those for an overall healthy dietary pattern. Accelerating research on gene–diet interactions is likely to
contribute interesting information that may lead to further
individualized dietary guidance in the future.
Acknowledgements
This work was supported in part by the US Department of
Agriculture Agricultural Research Service under USDA contract No. 53-3K06-5-10.
References
Alberti, K.G., Zimmet, P., and Shaw, J. 2006. Metabolic syndrome–
a new world-wide definition. A Consensus Statement from the
International Diabetes Federation. Diabet. Med. 23: 469–480.
doi:10.1111/j.1464-5491.2006.01858.x. PMID:16681555.
Appel, L.J., Moore, T.J., Obarzanek, E., Vollmer, W.M., Svetkey,
L.P., Sacks, F.M., et al. 1997. A clinical trial of the effects of
dietary patterns on blood pressure. DASH Collaborative Research Group. N. Engl. J. Med. 336: 1117–1124. doi:10.1056/
NEJM199704173361601. PMID:9099655.
Appel, L.J., Sacks, F.M., Carey, V.J., Obarzanek, E., Swain, J.F.,
Miller, E.R., 3rd, et al. 2005. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum
lipids: results of the OmniHeart randomized trial. JAMA, 294:
2455–2464. doi:10.1001/jama.294.19.2455. PMID:16287956.
Aston, L.M. 2006. Glycaemic index and metabolic disease risk.
Proc. Nutr. Soc. 65: 125–134. doi:10.1079/PNS2005485.
PMID:16441952.
Astrup, A., Grunwald, G.K., Melanson, E.L., Saris, W.H., and Hill,
J.O. 2000. The role of low-fat diets in body weight control: a
meta-analysis of ad libitum dietary intervention studies. Int. J.
Obes. Relat. Metab. Disord. 24: 1545–1552. doi:10.1038/sj.ijo.
0801453. PMID:11126204.
Aucott, L., Poobalan, A., Smith, W.C., Avenell, A., Jung, R., and
Broom, J. 2005. Effects of weight loss in overweight/obese individuals and long-term hypertension outcomes: a systematic review. Hypertension, 45: 1035–1041. doi:10.1161/01.HYP.
0000165680.59733.d4. PMID:15897373.
Aude, Y.W., Agatston, A.S., Lopez-Jimenez, F., Lieberman, E.H.,
Marie, A., Hansen, M., et al. 2004. The national cholesterol education program diet vs. a diet lower in carbohydrates and higher
in protein and monounsaturated fat: a randomized trial. Arch. Intern. Med. 164: 2141–2146. doi:10.1001/archinte.164.19.2141.
PMID:15505128.
Azadbakht, L., Mirmiran, P., and Azizi, F. 2005a. Dietary diversity
score is favorably associated with the metabolic syndrome in
Tehranian adults. Int. J. Obes. (Lond), 29: 1361–1367. doi:10.
1038/sj.ijo.0803029. PMID:16116493.
Azadbakht, L., Mirmiran, P., Esmaillzadeh, A., and Azizi, F.
2005b. Dairy consumption is inversely associated with the prevalence of the metabolic syndrome in Tehranian adults. Am. J.
Clin. Nutr. 82: 523–530. PMID:16155263.
Azadbakht, L., Mirmiran, P., Esmaillzadeh, A., Azizi, T., and
Azizi, F. 2005c. Beneficial effects of a Dietary Approaches to
Stop Hypertension eating plan on features of the metabolic syndrome. Diabetes Care, 28: 2823–2831. PMID:16306540.
Baer, D.J., Judd, J.T., Clevidence, B.A., and Tracy, R.P. 2004.
Dietary fatty acids affect plasma markers of inflammation in
#
2007 NRC Canada
Feldeisen and Tucker
healthy men fed controlled diets: a randomized crossover study.
Am. J. Clin. Nutr. 79: 969–973. PMID:15159225.
Barbagallo, M., and Dominguez, L.J. 2006. Magnesium metabolism
in type 2 diabetes mellitus, metabolic syndrome and insulin resistance. Arch. Biochem. Biophys. Available online at: http://
www.sciencedirect.com.
Baxter, A.J., Coyne, T., and McClintock, C. 2006. Dietary patterns
and metabolic syndrome- a review of epidemiological evidence.
Asia Pac. J. Clin. Nutr. 15: 134–142. PMID:16672196.
Beilin, L.J., and Puddey, I.B. 2006. Alcohol and hypertension: an
update. Hypertension, 47: 1035–1038. doi:10.1161/01.HYP.
0000218586.21932.3c. PMID:16585405.
Bilsborough, S.A., and Crowe, T.C. 2003. Low-carbohydrate diets:
what are the potential short- and long-term health implications?
Asia Pac. J. Clin. Nutr. 12: 396–404. PMID:14672862.
Boucher, B.J. 1998. Inadequate vitamin D status: does it contribute
to the disorders comprising syndrome ’X’? Br. J. Nutr. 79: 315–
327. doi:10.1079/BJN19980055. PMID:9624222.
Brehm, B.J., Seeley, R.J., Daniels, S.R., and D’Alessio, D.A. 2003.
A randomized trial comparing a very low carbohydrate diet and
a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J. Clin. Endocrinol. Metab.
88: 1617–1623. doi:10.1210/jc.2002-021480. PMID:12679447.
Calder, P.C. 2006. n-3 polyunsaturated fatty acids, inflammation,
and inflammatory diseases. Am. J. Clin. Nutr. 83: 6 Suppl,
1505S–1519S. PMID:16841861.
Carpentier, Y.A., Portois, L., and Malaisse, W.J. 2006. n-3 fatty
acids and the metabolic syndrome. Am. J. Clin. Nutr. 83: 6
Suppl, 1499S–1504S. PMID:16841860.
Carr, D.B., Utzschneider, K.M., Hull, R.L., Kodama, K., Retzlaff,
B.M., Brunzell, J.D., et al. 2004. Intra-abdominal fat is a major
determinant of the National Cholesterol Education Program
Adult Treatment Panel III criteria for the metabolic syndrome.
Diabetes, 53: 2087–2094. PMID:15277390.
Champagne, C.M. 2006. Dietary interventions on blood pressure:
the Dietary Approaches to Stop Hypertension (DASH) trials.
Nutr. Rev. 64: S53–S56. doi:10.1301/nr.2006.feb.S53-S56.
PMID:16532899.
Chiu, K.C., Chu, A., Go, V.L., and Saad, M.F. 2004. Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Am. J. Clin. Nutr. 79: 820–825. PMID:15113720.
Chobanian, A.V., Bakris, G.L., Black, H.R., Cushman, W.C., Green,
L.A., Izzo, J.L., Jr., et al. 2003. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure. Hypertension, 42: 1206–
1252.
doi:10.1161/01.HYP.0000107251.49515.c2.
PMID:14656957.
Choi, H.K., Willett, W.C., Stampfer, M.J., Rimm, E., and Hu, F.B.
2005. Dairy consumption and risk of type 2 diabetes mellitus in
men: a prospective study. Arch. Intern. Med. 165: 997–1003.
doi:10.1001/archinte.165.9.997. PMID:15883237.
Cushman, W.C., Cutler, J.A., Hanna, E., Bingham, S.F., Follmann,
D., Harford, T., et al. 1998. Prevention and Treatment of Hypertension Study (PATHS): effects of an alcohol treatment program
on blood pressure. Arch. Intern. Med. 158: 1197–1207. doi:10.
1001/archinte.158.11.1197. PMID:9625399.
Cutler, J.A., Follmann, D., and Allender, P.S. 1997. Randomized
trials of sodium reduction: an overview. Am. J. Clin. Nutr. 65:
2 Suppl, 643S–651S. PMID:9022560.
Daly, M. 2003. Sugars, insulin sensitivity, and the postprandial
state. Am. J. Clin. Nutr. 78: 865S–872S. PMID:14522751.
Dandona, P., Aljada, A., Chaudhuri, A., Mohanty, P., and Garg, R.
2005. Metabolic syndrome: a comprehensive perspective based
on interactions between obesity, diabetes, and inflammation.
55
Circulation, 111: 1448–1454. doi:10.1161/01.CIR.0000158483.
13093.9D. PMID:15781756.
Dansinger, M.L., Gleason, J.A., Griffith, J.L., Selker, H.P., and
Schaefer, E.J. 2005. Comparison of the Atkins, Ornish, Weight
Watchers, and Zone diets for weight loss and heart disease risk
reduction: a randomized trial. JAMA, 293: 43–53. doi:10.1001/
jama.293.1.43. PMID:15632335.
Davy, B.M., and Melby, C.L. 2003. The effect of fiber-rich carbohydrates on features of Syndrome X. J. Am. Diet. Assoc. 103:
86–96. doi:10.1053/jada.2003.50005. PMID:12525799.
de Lorgeril, M., Salen, P., Martin, J.L., Monjaud, I., Delaye, J., and
Mamelle, N. 1999. Mediterranean diet, traditional risk factors,
and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation,
99: 779–785. PMID:9989963.
Dickinson, H.O., Mason, J.M., Nicolson, D.J., Campbell, F., Beyer,
F.R., Cook, J.V., et al. 2006. Lifestyle interventions to reduce
raised blood pressure: a systematic review of randomized controlled trials. J. Hypertens. 24: 215–233. PMID:16508562.
Dietrich, M., and Jialal, I. 2005. The effect of weight loss on a
stable biomarker of inflammation, C-reactive protein. Nutr. Rev.
63: 22–28. doi:10.1301/nr.2004.janr.22-28. PMID:15730232.
Djousse, L., Arnett, D.K., Eckfeldt, J.H., Province, M.A., Singer,
M.R., and Ellison, R.C. 2004. Alcohol consumption and metabolic syndrome: does the type of beverage matter? Obes. Res.
12: 1375–1385. PMID:15483202.
Dobbelsteyn, C.J., Joffres, M.R., MacLean, D.R., and Flowerdew,
G. 2001. A comparative evaluation of waist circumference,
waist-to-hip ratio and body mass index as indicators of cardiovascular risk factors. The Canadian Heart Health Surveys. Int.
J. Obes. Relat. Metab. Disord. 25: 652–661. doi:10.1038/sj.ijo.
0801582. PMID:11360147.
Dreon, D.M., Fernstrom, H.A., Williams, P.T., and Krauss, R.M.
1999. A very low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins. Am. J. Clin. Nutr. 69: 411–418.
PMID:10075324.
Dumesnil, J.G., Turgeon, J., Tremblay, A., Poirier, P., Gilbert, M.,
Gagnon, L., et al. 2001. Effect of a low-glycaemic index–lowfat–high protein diet on the atherogenic metabolic risk profile
of abdominally obese men. Br. J. Nutr. 86: 557–568.
PMID:11737954.
Esmaillzadeh, A., Mirmiran, P., and Azizi, F. 2005. Whole-grain
consumption and the metabolic syndrome: a favorable association in Tehranian adults. Eur. J. Clin. Nutr. 59: 353–362.
doi:10.1038/sj.ejcn.1602080. PMID:15536473.
Esposito, K., and Giugliano, D. 2006. Diet and inflammation: a
link to metabolic and cardiovascular diseases. Eur. Heart J. 27:
15–20. PMID:16219650.
Esposito, K., Pontillo, A., Giugliano, F., Giugliano, G., Marfella,
R., Nicoletti, G., et al. 2003. Association of low interleukin-10
levels with the metabolic syndrome in obese women. J. Clin.
Endocrinol. Metab. 88: 1055–1058. doi:10.1210/jc.2002021437. PMID:12629085.
Esposito, K., Marfella, R., Ciotola, M., Di Palo, C., Giugliano, F.,
Giugliano, G., et al. 2004. Effect of a mediterranean-style diet
on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA,
292:
1440–1446.
doi:10.1001/jama.292.12.1440.
PMID:15383514.
Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults. 2001. Executive Summary of the
Third Report of the National Cholesterol Education Program
(NCEP) Expert Panel on Detection, Evaluation, and Treatment
#
2007 NRC Canada
56
of High Blood Cholesterol in Adults (Adult Treatment Panel
III). JAMA, 285: 2486–2497. doi:10.1001/jama.285.19.2486.
PMID:11368702.
Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults. 2002. Third Report of the National
Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in
Adults (Adult Treatment Panel III) final report. Circulation,
106: 3143–3421. PMID:12485966.
Fan, A.Z., Russell, M., Dorn, J., Freudenheim, J.L., Nochajski, T.,
Hovey, K., et al. 2006. Lifetime alcohol drinking pattern is related to the prevalence of metabolic syndrome. The Western
New York Health Study (WNYHS). Eur. J. Epidemiol. 21:
129–138. doi:10.1007/s10654-005-5457-y. PMID:16518681.
Farmer, A., Montori, V., Dinneen, S., and Clar, C. 2001. Fish oil in
people with type 2 diabetes mellitus. Cochrane Database Syst.
Rev. 3: CD003205. PMID:11687050.
Ford, E.S. 2005. Prevalence of the metabolic syndrome defined by
the International Diabetes Federation among adults in the US.
Diabetes Care, 28: 2745–2749. PMID:16249550.
Ford, E.S., and Liu, S. 2001. Glycemic index and serum high-density lipoprotein cholesterol concentration among us adults. Arch.
Intern. Med. 161: 572–576. doi:10.1001/archinte.161.4.572.
PMID:11252117.
Ford, E.S., Ajani, U.A., McGuire, L.C., and Liu, S. 2005. Concentrations of serum vitamin D and the metabolic syndrome among
U.S. adults. Diabetes Care, 28: 1228–1230. PMID:15855599.
Foster, G.D., Wyatt, H.R., Hill, J.O., McGuckin, B.G., Brill, C.,
Mohammed, B.S., et al. 2003. A randomized trial of a low-carbohydrate diet for obesity. N. Engl. J. Med. 348: 2082–2090.
doi:10.1056/NEJMoa022207. PMID:12761365.
Fredrikson, G.N., Hedblad, B., Nilsson, J.A., Alm, R., Berglund,
G., and Nilsson, J. 2004. Association between diet, lifestyle, metabolic cardiovascular risk factors, and plasma C-reactive protein
levels. Metabolism, 53: 1436–1442. doi:10.1016/j.metabol.2004.
06.010. PMID:15536598.
Frost, G., Leeds, A.A., Dore, C.J., Madeiros, S., Brading, S., and
Dornhorst, A. 1999. Glycaemic index as a determinant of serum
HDL-cholesterol concentration. Lancet, 353: 1045–1048. doi:10.
1016/S0140-6736(98)07164-5. PMID:10199351.
Garg, A., Grundy, S.M., and Unger, R.H. 1992. Comparison of effects of high and low carbohydrate diets on plasma lipoproteins
and insulin sensitivity in patients with mild NIDDM. Diabetes,
41: 1278–1285. PMID:1397701.
Ginsberg, H.N., Barr, S.L., Gilbert, A., Karmally, W., Deckelbaum,
R., Kaplan, K., et al. 1990. Reduction of plasma cholesterol levels in normal men on an American Heart Association Step 1
diet or a Step 1 diet with added monounsaturated fat. N. Engl.
J. Med. 322: 574–579. PMID:2304504.
Goude, D., Fagerberg, B., and Hulthe, J. 2002. Alcohol consumption, the metabolic syndrome and insulin resistance in 58-yearold clinically healthy men (AIR study). Clin. Sci. (Lond.), 102:
345–352. PMID:11869176.
Groop, L. 2000. Genetics of the metabolic syndrome. Br. J. Nutr.
83: Suppl 1, S39–S48. PMID:10889791.
Grundy, S.M. 1986. Comparison of monounsaturated fatty acids
and carbohydrates for lowering plasma cholesterol. N. Engl. J.
Med. 314: 745–748. PMID:3951504.
Grundy, S.M. 2005. Metabolic Syndrome Scientific Statement by
the American Heart Association and the National Heart, Lung
and Blood Institute. Arterioscler. Thromb. Vasc. Biol. 25:
2243–2244. PMID:16258150.
Grundy, S.M., Abate, N., and Chandalia, M. 2002. Diet composition and the metabolic syndrome: what is the optimal fat intake?
Appl. Physiol. Nutr. Metab. Vol. 32, 2007
Am. J. Med. 113: Suppl 9B, 25S–29S. doi:10.1016/S00029343(01)00988-3. PMID:12566135.
Grundy, S.M., Cleeman, J.I., Daniels, S.R., Donato, K.A., Eckel,
R.H., Franklin, B.A., et al. 2005. Diagnosis and management of
the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation, 112: 2735–2752. doi:10.1161/CIRCULATIONAHA.
105.169404. PMID:16157765.
Guerrero-Romero, F., and Rodriguez-Moran, M. 2002. Low serum
magnesium levels and metabolic syndrome. Acta Diabetol. 39:
209–213. doi:10.1007/s005920200036. PMID:12486495.
Hajjar, I.M., Grim, C.E., George, V., and Kotchen, T.A. 2001. Impact of diet on blood pressure and age-related changes in blood
pressure in the US population: analysis of NHANES III. Arch.
Intern. Med. 161: 589–593. doi:10.1001/archinte.161.4.589.
PMID:11252120.
Halkjaer, J., Sorensen, T.I., Tjonneland, A., Togo, P., Holst, C.,
and Heitmann, B.L. 2004. Food and drinking patterns as predictors of 6-year BMI-adjusted changes in waist circumference. Br.
J.
Nutr.
92:
735–748.
doi:10.1079/BJN20041246.
PMID:15522143.
Harris, W.S. 1997. n-3 fatty acids and serum lipoproteins: human
studies. Am. J. Clin. Nutr. 65: 5 Suppl, 1645S–1654S.
PMID:9129504.
He, F.J., and MacGregor, G.A. 1999. Potassium intake and blood
pressure. Am. J. Hypertens. 12: 849–851. PMID:10480482.
He, F.J., and MacGregor, G.A. 2002. Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health. J. Hum. Hypertens. 16: 761–770.
doi:10.1038/sj.jhh.1001459. PMID:12444537.
He, F.J., Markandu, N.D., and MacGregor, G.A. 2005. Modest salt
reduction lowers blood pressure in isolated systolic hypertension
and combined hypertension. Hypertension, 46: 66–70. doi:10.
1161/01.HYP.0000171474.84969.7a. PMID:15956111.
He, K., Liu, K., Daviglus, M.L., Morris, S.J., Loria, C.M., Van Horn,
L., et al. 2006. Magnesium intake and incidence of metabolic syndrome among young adults. Circulation, 113: 1675–1682. doi:10.
1161/CIRCULATIONAHA.105.588327. PMID:16567569.
Howard, B.V., Manson, J.E., Stefanick, M.L., Beresford, S.A.,
Frank, G., Jones, B., et al. 2006. Low-fat dietary pattern and
weight change over 7 years: the Women’s Health Initiative Dietary Modification Trial. JAMA, 295: 39–49. doi:10.1001/jama.
295.1.39. PMID:16391215.
Hu, F.B., Rimm, E.B., Stampfer, M.J., Ascherio, A., Spiegelman,
D., and Willett, W.C. 2000. Prospective study of major dietary
patterns and risk of coronary heart disease in men. Am. J. Clin.
Nutr. 72: 912–921. PMID:11010931.
Isomaa, B., Almgren, P., Tuomi, T., Forsen, B., Lahti, K., Nissen,
M., et al. 2001. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care, 24: 683–
689. PMID:11315831.
Jee, S.H., Miller, E.R., 3rd, Guallar, E., Singh, V.K., Appel, L.J.,
and Klag, M.J. 2002. The effect of magnesium supplementation
on blood pressure: a meta-analysis of randomized clinical trials.
Am. J. Hypertens. 15: 691–696. doi:10.1016/S0895-7061(02)
02964-3. PMID:12160191.
Jorde, R., and Bonaa, K.H. 2000. Calcium from dairy products, vitamin D intake, and blood pressure: the Tromso Study. Am. J.
Clin. Nutr. 71: 1530–1535. PMID:10837295.
Katzmarzyk, P.T., Janssen, I., Ross, R., Church, T.S., and Blair,
S.N. 2006. The importance of waist circumference in the definition of metabolic syndrome: prospective analyses of mortality in
men. Diabetes Care, 29: 404–409. doi:10.2337/diacare.29.02.06.
dc05-1636. PMID:16443895.
#
2007 NRC Canada
Feldeisen and Tucker
Koh-Banerjee, P., Chu, N.F., Spiegelman, D., Rosner, B., Colditz,
G., Willett, W., et al. 2003. Prospective study of the association
of changes in dietary intake, physical activity, alcohol consumption, and smoking with 9-y gain in waist circumference among
16 587 US men. Am. J. Clin. Nutr. 78: 719–727.
PMID:14522729.
Kotchen, T.A., and McCarron, D.A. 1998. Dietary electrolytes and
blood pressure: a statement for healthcare professionals from the
American Heart Association Nutrition Committee. Circulation,
98: 613–617. PMID:9714124.
Krauss, R.M., and Dreon, D.M. 1995. Low-density-lipoprotein subclasses and response to a low-fat diet in healthy men. Am. J.
Clin. Nutr. 62: 478S–487S. PMID:7625363.
Kris-Etherton, P., Eckel, R.H., Howard, B.V., St Jeor, S., and Bazzarre, T.L. 2001. AHA Science Advisory: Lyon Diet Heart
Study. Benefits of a Mediterranean-style, National Cholesterol
Education Program/American Heart Association Step I Dietary
Pattern on Cardiovascular Disease. Circulation, 103: 1823–
1825. PMID:11282918.
Kris-Etherton, P.M., Harris, W.S., and Appel, L.J. 2002. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation, 106: 2747–2757. doi:10.1161/01.CIR.
0000038493.65177.94. PMID:12438303.
Kwiterovich, P.O., Jr. 2002. Clinical relevance of the biochemical,
metabolic, and genetic factors that influence low-density lipoprotein heterogeneity. Am. J. Cardiol. 90: 8A, 30i–47i. doi:10.
1016/S0002-9149(02)02749-2. PMID:12419479.
Laaksonen, D.E., Lakka, H.M., Niskanen, L.K., Kaplan, G.A., Salonen, J.T., and Lakka, T.A. 2002. Metabolic syndrome and development of diabetes mellitus: application and validation of
recently suggested definitions of the metabolic syndrome in a
prospective cohort study. Am. J. Epidemiol. 156: 1070–1077.
doi:10.1093/aje/kwf145. PMID:12446265.
Lakka, H.M., Laaksonen, D.E., Lakka, T.A., Niskanen, L.K., Kumpusalo, E., Tuomilehto, J., et al. 2002. The metabolic syndrome
and total and cardiovascular disease mortality in middle-aged
men. JAMA, 288: 2709–2716. doi:10.1001/jama.288.21.2709.
PMID:12460094.
Lau, C., Faerch, K., Glumer, C., Tetens, I., Pedersen, O., Carstensen, B., et al. 2005. Dietary glycemic index, glycemic load, fiber, simple sugars, and insulin resistance: the Inter99 study.
Diabetes Care, 28: 1397–1403. PMID:15920058.
Lawlor, D.A., Ebrahim, S., Timpson, N., and Smith, G.D. 2005.
Avoiding milk is associated with a reduced risk of insulin resistance and the metabolic syndrome: findings from the British
Women’s Heart and Health Study. Diabet. Med. 22: 808–811.
doi:10.1111/j.1464-5491.2005.01537.x. PMID:15910636.
Le Marchand-Brustel, Y., Gual, P., Gremeaux, T., Gonzalez, T.,
Barres, R., and Tanti, J.F. 2003. Fatty acid-induced insulin resistance: role of insulin receptor substrate 1 serine phosphorylation
in the retroregulation of insulin signalling. Biochem. Soc. Trans.
31: 1152–1156. PMID:14641015.
Lichtenstein, A.H., Appel, L.J., Brands, M., Carnethon, M., Daniels, S., Franch, H.A., et al. 2006. Diet and lifestyle recommendations revision 2006: a scientific statement from the American
Heart Association Nutrition Committee. Circulation, 114: 82–96.
doi:10.1161/CIRCULATIONAHA.106.176158.
PMID:16785338.
Lidfeldt, J., Nyberg, P., Nerbrand, C., Samsioe, G., Schersten, B.,
and Agardh, C.D. 2003. Socio-demographic and psychosocial
factors are associated with features of the metabolic syndrome.
The Women’s Health in the Lund Area (WHILA) study. Diabetes Obes. Metab. 5: 106–112. doi:10.1046/j.1463-1326.2003.
00250.x. PMID:12630935.
57
Liese, A.D., Schulz, M., Moore, C.G., and Mayer-Davis, E.J. 2004.
Dietary patterns, insulin sensitivity and adiposity in the multiethnic Insulin Resistance Atherosclerosis Study population. Br.
J.
Nutr.
92:
973–984.
doi:10.1079/BJN20041279.
PMID:15613260.
Liese, A.D., Schulz, M., Fang, F., Wolever, T.M., D’Agostino,
R.B., Jr., Sparks, K.C., et al. 2005. Dietary glycemic index and
glycemic load, carbohydrate and fiber intake, and measures of
insulin sensitivity, secretion, and adiposity in the Insulin Resistance Atherosclerosis Study. Diabetes Care, 28: 2832–2838.
PMID:16306541.
Liu, S., Manson, J.E., Stampfer, M.J., Holmes, M.D., Hu, F.B.,
Hankinson, S.E., et al. 2001. Dietary glycemic load assessed by
food-frequency questionnaire in relation to plasma high-densitylipoprotein cholesterol and fasting plasma triacylglycerols in
postmenopausal women. Am. J. Clin. Nutr. 73: 560–566.
PMID:11237932.
Liu, S., Song, Y., Ford, E.S., Manson, J.E., Buring, J.E., and Ridker, P.M. 2005. Dietary calcium, vitamin D, and the prevalence
of metabolic syndrome in middle-aged and older U.S. women.
Diabetes Care, 28: 2926–2932. PMID:16306556.
Lofgren, I.E., Herron, K.L., West, K.L., Zern, T.L., Brownbill,
R.A., Ilich, J.Z., et al. 2005. Weight loss favorably modifies
anthropometrics and reverses the metabolic syndrome in premenopausal women. J. Am. Coll. Nutr. 24: 486–493.
PMID:16373945.
Lopes, H.F., Martin, K.L., Nashar, K., Morrow, J.D., Goodfriend,
T.L., and Egan, B.M. 2003. DASH diet lowers blood pressure
and lipid-induced oxidative stress in obesity. Hypertension, 41:
422–430.
doi:10.1161/01.HYP.0000053450.19998.11.
PMID:12623938.
Lopez-Garcia, E., Schulze, M.B., Meigs, J.B., Manson, J.E., Rifai,
N., Stampfer, M.J., et al. 2005. Consumption of trans fatty acids
is related to plasma biomarkers of inflammation and endothelial
dysfunction. J. Nutr. 135: 562–566. PMID:15735094.
Lopez-Ridaura, R., Willett, W.C., Rimm, E.B., Liu, S., Stampfer,
M.J., Manson, J.E., et al. 2004. Magnesium intake and risk of
type 2 diabetes in men and women. Diabetes Care, 27: 134–
140. PMID:14693979.
Lovejoy, J.C., Smith, S.R., Champagne, C.M., Most, M.M., Lefevre, M., DeLany, J.P., et al. 2002. Effects of diets enriched in
saturated (palmitic), monounsaturated (oleic), or trans (elaidic)
fatty acids on insulin sensitivity and substrate oxidation in
healthy adults. Diabetes Care, 25: 1283–1288. PMID:12145222.
Luan, J., Browne, P.O., Harding, A.H., Halsall, D.J., O’Rahilly, S.,
Chatterjee, V.K., et al. 2001. Evidence for gene-nutrient interaction at the PPARgamma locus. Diabetes, 50: 686–689.
PMID:11246892.
Ludwig, D.S., Pereira, M.A., Kroenke, C.H., Hilner, J.E., Van Horn,
L., Slattery, M.L., et al. 1999. Dietary fiber, weight gain, and cardiovascular disease risk factors in young adults. JAMA, 282:
1539–1546. doi:10.1001/jama.282.16.1539. PMID:10546693.
Ma, J., Folsom, A.R., Melnick, S.L., Eckfeldt, J.H., Sharrett, A.R., Nabulsi, A.A., et al. 1995. Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin,
and carotid arterial wall thickness: the ARIC study. Atherosclerosis
Risk in Communities Study. J. Clin. Epidemiol. 48: 927–940.
doi:10.1016/0895-4356(94)00200-A. PMID:7782801.
Marshall, J.A., Bessesen, D.H., and Hamman, R.F. 1997. High saturated fat and low starch and fibre are associated with hyperinsulinaemia in a non-diabetic population: the San Luis Valley
Diabetes Study. Diabetologia, 40: 430–438. doi:10.1007/
s001250050697. PMID:9112020.
McAuley, K.A., Hopkins, C.M., Smith, K.J., McLay, R.T., Wil#
2007 NRC Canada
58
liams, S.M., Taylor, R.W., et al. 2005. Comparison of high-fat
and high-protein diets with a high-carbohydrate diet in insulinresistant obese women. Diabetologia, 48: 8–16. doi:10.1007/
s00125-004-1603-4. PMID:15616799.
McKeown, N.M. 2004. Whole grain intake and insulin sensitivity:
evidence from observational studies. Nutr. Rev. 62: 286–291.
PMID:15384920.
McKeown, N.M., Meigs, J.B., Liu, S., Saltzman, E., Wilson, P.W.,
and Jacques, P.F. 2004. Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. Diabetes Care, 27: 538–546.
PMID:14747241.
Mennen, L.I., Lafay, L., Feskens, E.J., Novak, M., Lepinay, P., and
Balkau, B. 2000. Possible protective effect of bread and dairy
products on the risk of the metabolic syndrome. Nutr. Res.
20(3): 335–347.
Mensink, R.P., and Katan, M.B. 1992. Effect of dietary fatty acids
on serum lipids and lipoproteins. A meta-analysis of 27 trials.
Arterioscler. Thromb. 12: 911–919. PMID:1386252.
Mensink, R.P., de Groot, M.J., van den Broeke, L.T., SeverijnenNobels, A.P., Demacker, P.N., and Katan, M.B. 1989. Effects
of monounsaturated fatty acids v complex carbohydrates on
serum lipoproteins and apoproteins in healthy men and women.
Metabolism, 38: 172–178. doi:10.1016/0026-0495(89)90258-8.
PMID:2536459.
Misra, A., Wasir, J.S., and Vikram, N.K. 2005. Waist circumference criteria for the diagnosis of abdominal obesity are not applicable uniformly to all populations and ethnic groups.
Nutrition, 21: 969–976. PMID:15993041.
Mizushima, S., Cappuccio, F.P., Nichols, R., and Elliott, P. 1998.
Dietary magnesium intake and blood pressure: a qualitative
overview of the observational studies. J. Hum. Hypertens. 12:
447–453. doi:10.1038/sj.jhh.1000641. PMID:9702930.
Most, M.M. 2004. Estimated phytochemical content of the dietary
approaches to stop hypertension (DASH) diet is higher than in
the Control Study Diet. J. Am. Diet. Assoc. 104: 1725–1727.
doi:10.1016/j.jada.2004.08.001. PMID:15499362.
Muzio, F., Mondazzi, L., Sommariva, D., and Branchi, A. 2005.
Long-term effects of low-calorie diet on the metabolic syndrome
in obese nondiabetic patients. Diabetes Care, 28: 1485–1486.
PMID:15920073.
Nappo, F., Esposito, K., Cioffi, M., Giugliano, G., Molinari, A.M.,
Paolisso, G., et al. 2002. Postprandial endothelial activation in
healthy subjects and in type 2 diabetic patients: role of fat and
carbohydrate meals. J. Am. Coll. Cardiol. 39: 1145–1150.
doi:10.1016/S0735-1097(02)01741-2. PMID:11923038.
Nettleton, J.A., and Katz, R. 2005. n-3 long-chain polyunsaturated
fatty acids in type 2 diabetes: a review. J. Am. Diet. Assoc. 105:
428–440. doi:10.1016/j.jada.2004.11.029. PMID:15746832.
Newby, P.K., and Tucker, K.L. 2004. Empirically derived eating
patterns using factor or cluster analysis: a review. Nutr. Rev. 62:
177–203. doi:10.1301/nr.2004.may.177-203. PMID:15212319.
Newby, P.K., Muller, D., Hallfrisch, J., Qiao, N., Andres, R., and
Tucker, K.L. 2003. Dietary patterns and changes in body mass
index and waist circumference in adults. Am. J. Clin. Nutr. 77:
1417–1425. PMID:12791618.
Nordmann, A.J., Nordmann, A., Briel, M., Keller, U., Yancy, W.S.,
Jr., Brehm, B.J., et al. 2006. Effects of low-carbohydrate vs.
low-fat diets on weight loss and cardiovascular risk factors: a
meta-analysis of randomized controlled trials. Arch. Intern.
Med.
166:
285–293.
doi:10.1001/archinte.166.3.285.
PMID:16476868.
Obarzanek, E., Sacks, F.M., Vollmer, W.M., Bray, G.A., Miller,
E.R., 3rd, Lin, P.H., et al. 2001. Effects on blood lipids of a
Appl. Physiol. Nutr. Metab. Vol. 32, 2007
blood pressure-lowering diet: the Dietary Approaches to Stop
Hypertension (DASH) Trial. Am. J. Clin. Nutr. 74: 80–89.
PMID:11451721.
Ordovas, J.M., Corella, D., Cupples, L.A., Demissie, S., Kelleher,
A., Coltell, O., et al. 2002. Polyunsaturated fatty acids modulate
the effects of the APOA1 G-A polymorphism on HDL-cholesterol concentrations in a sex-specific manner: the Framingham
Study. Am. J. Clin. Nutr. 75: 38–46. PMID:11756058.
Pereira, M.A., Jacobs, D.R., Jr., Van Horn, L., Slattery, M.L., Kartashov, A.I., and Ludwig, D.S. 2002. Dairy consumption, obesity, and the insulin resistance syndrome in young adults: the
CARDIA Study. JAMA, 287: 2081–2089. doi:10.1001/jama.
287.16.2081. PMID:11966382.
Perez-Jimenez, F., Lopez-Miranda, J., Pinillos, M.D., Gomez, P.,
Paz-Rojas, E., Montilla, P., et al. 2001. A Mediterranean and a
high-carbohydrate diet improve glucose metabolism in healthy
young persons. Diabetologia, 44: 2038–2043. doi:10.1007/
s001250100009. PMID:11719836.
Pirozzo, S., Summerbell, C., Cameron, C., and Glasziou, P. 2003.
Should we recommend low-fat diets for obesity? Obes. Rev. 4:
83–90. doi:10.1046/j.1467-789X.2003.00099.x. PMID:12760443.
Rasmussen, B.M., Vessby, B., Uusitupa, M., Berglund, L., Pedersen, E., Riccardi, G., et al. 2006. Effects of dietary saturated,
monounsaturated, and n-3 fatty acids on blood pressure in
healthy subjects. Am. J. Clin. Nutr. 83: 221–226.
PMID:16469978.
Reaven, G.M. 1997. Do high carbohydrate diets prevent the development or attenuate the manifestations (or both) of syndrome X?
A viewpoint strongly against. Curr. Opin. Lipidol. 8: 23–27.
PMID:9127707.
Reaven, G. 2002. Metabolic syndrome: pathophysiology and implications for management of cardiovascular disease. Circulation,
106:
286–288.
doi:10.1161/01.CIR.0000019884.36724.D9.
PMID:12119239.
Reaven, G.M. 2005. The insulin resistance syndrome: definition and
dietary approaches to treatment. Annu. Rev. Nutr. 25: 391–406.
doi:10.1146/annurev.nutr.24.012003.132155. PMID:16011472.
Riccardi, G., Giacco, R., and Rivellese, A.A. 2004. Dietary fat, insulin sensitivity and the metabolic syndrome. Clin. Nutr. 23:
447–456. doi:10.1016/j.clnu.2004.02.006. PMID:15297079.
Ridker, P.M., Buring, J.E., Cook, N.R., and Rifai, N. 2003. C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow-up of 14 719 initially healthy
American women. Circulation, 107: 391–397. doi:10.1161/01.
CIR.0000055014.62083.05. PMID:12551861.
Rivellese, A.A., Maffettone, A., Vessby, B., Uusitupa, M., Hermansen, K., Berglund, L., et al. 2003. Effects of dietary saturated,
monounsaturated and n-3 fatty acids on fasting lipoproteins,
LDL size and post-prandial lipid metabolism in healthy subjects.
Atherosclerosis, 167: 149–158. doi:10.1016/S0021-9150(02)
00424-0. PMID:12618280.
Robitaille, J., Despres, J.P., Perusse, L., and Vohl, M.C. 2003. The
PPAR-gamma P12A polymorphism modulates the relationship between dietary fat intake and components of the metabolic syndrome:
results from the Quebec Family Study. Clin. Genet. 63: 109–116.
doi:10.1034/j.1399-0004.2003.00026.x. PMID:12630956.
Roche, H.M. 2005. Fatty acids and the metabolic syndrome. Proc.
Nutr. Soc. 64: 23–29. doi:10.1079/PNS2004405. PMID:15877919.
Roche, H.M., Phillips, C., and Gibney, M.J. 2005. The metabolic
syndrome: the crossroads of diet and genetics. Proc. Nutr. Soc.
64: 371–377. doi:10.1079/PNS2005445. PMID:16048671.
Rosell, M., De Faire, U., and Hellenius, M.L. 2003. Low prevalence of the metabolic syndrome in wine drinkers–is it the alco#
2007 NRC Canada
Feldeisen and Tucker
hol beverage or the lifestyle? Eur. J. Clin. Nutr. 57: 227–234.
doi:10.1038/sj.ejcn.1601548. PMID:12571653.
Ruidavets, J.B., Bongard, V., Simon, C., Dallongeville, J., Ducimetiere, P., Arveiler, D., et al. 2006. Independent contribution of
dairy products and calcium intake to blood pressure variations
at a population level. J. Hypertens. 24: 671–681.
PMID:16531795.
Sacks, F.M., Svetkey, L.P., Vollmer, W.M., Appel, L.J., Bray,
G.A., Harsha, D., et al. 2001. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research
Group. N. Engl. J. Med. 344: 3–10. doi:10.1056/
NEJM200101043440101. PMID:11136953.
Sahyoun, N.R., Jacques, P.F., Zhang, X.L., Juan, W., and
McKeown, N.M. 2006. Whole-grain intake is inversely associated with the metabolic syndrome and mortality in older
adults. Am. J. Clin. Nutr. 83: 124–131. PMID:16400060.
Samaha, F.F., Iqbal, N., Seshadri, P., Chicano, K.L., Daily, D.A.,
McGrory, J., et al. 2003. A low-carbohydrate as compared with
a low-fat diet in severe obesity. N. Engl. J. Med. 348: 2074–
2081. doi:10.1056/NEJMoa022637. PMID:12761364.
Serra-Majem, L., Roman, B., and Estruch, R. 2006. Scientific evidence of interventions using the Mediterranean diet: a systematic review. Nutr. Rev. 64: S27–S47. doi:10.1301/nr.2006.feb.
S27-S47. PMID:16532897.
Sharman, M.J., and Volek, J.S. 2004. Weight loss leads to reductions in inflammatory biomarkers after a very-low-carbohydrate
diet and a low-fat diet in overweight men. Clin. Sci. (Lond.),
107: 365–369. PMID:15265001.
Sharman, M.J., Gomez, A.L., Kraemer, W.J., and Volek, J.S. 2004.
Very low-carbohydrate and low-fat diets affect fasting lipids and
postprandial lipemia differently in overweight men. J. Nutr. 134:
880–885. PMID:15051841.
Shirai, K. 2004. Obesity as the core of the metabolic syndrome and
the management of coronary heart disease. Curr. Med. Res.
Opin.
20:
295–304.
doi:10.1185/030079903125003008.
PMID:15025838.
Singh, R.B., Dubnov, G., Niaz, M.A., Ghosh, S., Singh, R., Rastogi, S.S., et al. 2002. Effect of an Indo-Mediterranean diet on
progression of coronary artery disease in high risk patients
(Indo-Mediterranean Diet Heart Study): a randomized singleblind trial. Lancet, 360: 1455–1461. doi:10.1016/S01406736(02)11472-3. PMID:12433513.
Sjogren, P., Rosell, M., Skoglund-Andersson, C., Zdravkovic, S.,
Vessby, B., de Faire, U., et al. 2004. Milk-derived fatty acids
are associated with a more favorable LDL particle size distribution in healthy men. J. Nutr. 137(7): 1729–1735.
Song, Y., Manson, J.E., Buring, J.E., and Liu, S. 2004. Dietary
magnesium intake in relation to plasma insulin levels and risk
of type 2 diabetes in women. Diabetes Care, 27: 59–65.
PMID:14693967.
Song, Y., Ridker, P.M., Manson, J.E., Cook, N.R., Buring, J.E., and
Liu, S. 2005. Magnesium intake, C-reactive protein, and the prevalence of metabolic syndrome in middle-aged and older U.S.
women. Diabetes Care, 28: 1438–1444. PMID:15920065.
Sonnenberg, L., Pencina, M., Kimokoti, R., Quatromoni, P., Nam,
B.H., D’Agostino, R., et al. 2005. Dietary patterns and the metabolic syndrome in obese and non-obese Framingham women.
Obes. Res. 13: 153–162. PMID:15761175.
Stern, L., Iqbal, N., Seshadri, P., Chicano, K.L., Daily, D.A.,
McGrory, J., et al. 2004. The effects of low-carbohydrate versus
conventional weight loss diets in severely obese adults: one-year
follow-up of a randomized trial. Ann. Intern. Med. 140: 778–
785. PMID:15148064.
59
Tamakoshi, K., Yatsuya, H., Kondo, T., Hori, Y., Ishikawa, M.,
Zhang, H., et al. 2003. The metabolic syndrome is associated
with elevated circulating C-reactive protein in healthy reference
range, a systemic low-grade inflammatory state. Int. J. Obes.
Relat. Metab. Disord. 27: 443–449. doi:10.1038/sj.ijo.0802260.
PMID:12664077.
Tholstrup, T. 2006. Dairy products and cardiovascular disease.
Curr. Opin. Lipdol. 17(1):1–10.
Trichopoulou, A., Costacou, T., Bamia, C., and Trichopoulos, D.
2003. Adherence to a Mediterranean diet and survival in a
Greek population. N. Engl. J. Med. 348: 2599–2608. doi:10.
1056/NEJMoa025039. PMID:12826634.
van Dam, R.M., Visscher, A.W., Feskens, E.J., Verhoef, P., and
Kromhout, D. 2000. Dietary glycemic index in relation to metabolic risk factors and incidence of coronary heart disease: the
Zutphen Elderly Study. Eur. J. Clin. Nutr. 54: 726–731. doi:10.
1038/sj.ejcn.1601086. PMID:11002385.
van Mierlo, L.A., Arends, L.R., Streppel, M.T., Zeegers, M.P.,
Kok, F.J., Grobbee, D.E., et al. 2006. Blood pressure response
to calcium supplementation: a meta-analysis of randomized controlled trials. J. Hum. Hypertens. 20: 571–580. doi:10.1038/sj.
jhh.1002038. PMID:16673011.
Vessby, B., Unsitupa, M., Hermansen, K., Riccardi, G., Rivellese,
A.A., Tapsell, L.C., et al. 2001. Substituting dietary saturated
for monounsaturated fat impairs insulin sensitivity in healthy
men and women: The KANWU Study. Diabetologia, 44: 312–
319. doi:10.1007/s001250051620. PMID:11317662.
Volek, J.S., and Feinman, R.D. 2005. Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate
restriction. Nutr. Metab. (Lond), 2: 31. doi:10.1186/1743-70752-31. PMID:16288655.
Willett, W.C. 1998. Is dietary fat a major determinant of body fat?
Am. J. Clin. Nutr. 67: 3 Suppl, 556S–562S. PMID:9497170.
Willett, W.C. 2002. Dietary fat plays a major role in obesity: no.
Obes. Rev. 3: 59–68. doi:10.1046/j.1467-789X.2002.00060.x.
PMID:12120421.
Williams, D.E., Prevost, A.T., Whichelow, M.J., Cox, B.D., Day,
N.E., and Wareham, N.J. 2000. A cross-sectional study of dietary patterns with glucose intolerance and other features of the
metabolic syndrome. Br. J. Nutr. 83: 257–266. PMID:10884714.
Wilson, P.W., and Grundy, S.M. 2003. The metabolic syndrome: a
practical guide to origins and treatment: Part II. Circulation,
108: 1537–1540. doi:10.1161/01.CIR.0000089506.12223.F1.
PMID:14517148.
Wirfalt, E., Hedblad, B., Gullberg, B., Mattisson, I., Andren, C.,
Rosander, U., et al. 2001. Food patterns and components of the
metabolic syndrome in men and women: a cross-sectional study
within the Malmo Diet and Cancer cohort. Am. J. Epidemiol.
154: 1150–1159. doi:10.1093/aje/154.12.1150. PMID:11744521.
Wolever, T.M. 2000. Dietary carbohydrates and insulin action in
humans. Br. J. Nutr. 83: Suppl 1, S97–102. PMID:10889799.
Xin, X., He, J., Frontini, M.G., Ogden, L.G., Motsamai, O.I., and
Whelton, P.K. 2001. Effects of alcohol reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension, 38: 1112–1117. PMID:11711507.
Yoo, S., Nicklas, T., Baranowski, T., Zakeri, I.F., Yang, S.J., Srinivasan, S.R., et al. 2004. Comparison of dietary intakes associated with metabolic syndrome risk factors in young adults: the
Bogalusa Heart Study. Am. J. Clin. Nutr. 80: 841–848.
PMID:15447888.
Yoon, Y.S., Oh, S.W., Baik, H.W., Park, H.S., and Kim, W.Y. 2004.
Alcohol consumption and the metabolic syndrome in Korean
#
2007 NRC Canada
60
adults: the 1998 Korean National Health and Nutrition Examination Survey. Am. J. Clin. Nutr. 80: 217–224. PMID:15213051.
Yu-Poth, S., Zhao, G., Etherton, T., Naglak, M., Jonnalagadda, S.,
and Kris-Etherton, P.M. 1999. Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention
programs on cardiovascular disease risk factors: a meta-analysis.
Am. J. Clin. Nutr. 69: 632–646. PMID:10197564.
Zhu, S., St-Onge, M.P., Heshka, S., and Heymsfield, S.B. 2004.
Lifestyle behaviors associated with lower risk of having the me-
Appl. Physiol. Nutr. Metab. Vol. 32, 2007
tabolic syndrome. Metabolism, 53: 1503–1511. doi:10.1016/j.
metabol.2004.04.017. PMID:15536610.
Zhu, S., Heymsfield, S.B., Toyoshima, H., Wang, Z., Pietrobelli,
A., and Heshka, S. 2005. Race-ethnicity-specific waist circumference cutoffs for identifying cardiovascular disease risk factors. Am. J. Clin. Nutr. 81: 409–415. PMID:15699228.
Zilkens, R.R., Burke, V., Hodgson, J.M., Barden, A., Beilin, L.J.,
and Puddey, I.B. 2005. Red wine and beer elevate blood pressure in normotensive men. Hypertension, 45: 874–879. doi:10.
1161/01.HYP.0000164639.83623.76. PMID:15837829.
#
2007 NRC Canada