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Dietary and Lifestyle Risk Factors and Metabolic Syndrome: Literature Review

Rawan H. Al-Qawasmeh, Reema F. Tayyem*

Department of Nutrition and Food Technology, Faculty of Agriculture, the University of Jordan.

Corresponding Author Email: r.tayyem@ju.edu.jo

DOI : https://dx.doi.org/10.12944/CRNFSJ.6.3.03

Article Publishing History

Received: 09-9-2018

Accepted: 16-11-2018

Published Online: 21-11-2018

Plagiarism Check: Yes

Reviewed by: Dr. Funmilayo E. Omotoye (Nigeria)

Second Review by: Prof. Fatemeh Azizi-Soleiman (Iran)

Final Approval by: Prof. Min-Hsiung Pan

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Abstract:

Metabolic syndrome (MetS) is considered a threat to public health due to its rapid growing prevalence worldwide. MetS can result from interrelated metabolic abnormalities including insulin resistance (IR), hypertension, dyslipidemia, and abdominal adiposity. Although the pathogenesis of this syndrome is not distinctly understood, it is strongly influenced by multiple genetic variations that interact with many environmental factors such as positive family history of MetS, adherence to unhealthy dietary patterns, low physical activity and smoking and that explain the variations in the prevalence of the MetS within and across populations. All of these factors were found to be associated with IR, obesity, and triglycerides elevation which therefore increase the risk of the MetS Several studies highlighted the effective preventive approach includes lifestyle changes, primarily losing weight, adopting healthy diet, and practicing exercise. All of the mentioned factors can reduce the risk of MetS.

Keywords:

Diet; Lifestyle; Metabolic syndrome; Physical activity; Smoking

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Al-Qawasmeh R. H, Tayyem R. F. Dietary and Lifestyle Risk Factors and Metabolic Syndrome: Literature Review. Curr Res Nutr Food Sci 2018;6(3). doi : http://dx.doi.org/10.12944/CRNFSJ.6.3.03


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Al-Qawasmeh R. H, Tayyem R. F. Dietary and Lifestyle Risk Factors and Metabolic Syndrome: Literature Review. Curr Res Nutr Food Sci 2018;6(3). http://www.foodandnutritionjournal.org/?p=7511


List of Abbreviations

BMI Body Mass Index
CVD Cardio Vascular Diseases
DASH Dietary Approach to Stop Hypertension
DBP Diastolic Blood Pressure
DLP Dyslipidemia
DM II Type 2 Diabetes Mellitus
FBG Fasting Blood Glucose
FFA Free Fatty Acid
FFQ Food Frequency Questionnaire
GI Glycemic Index
GL Glycemic Load
HDL-C High Density Lipoprotein Cholesterol
HTN Hypertension
IDF International Diabetes Federation
IR Insulin Resistance
LDL Low Density Lipoprotein
LPL Lipoprotein Lipase
MetS Metabolic Syndrome
MUFA Monounsaturated Fatty Acids
NCEP: ATPIII National Cholesterol Education Program: Adult Treatment Panel III
OR Odd Ratio
PA Physical Activity

 

Introduction

The metabolic syndrome (MetS) is a precursor of both cardiovascular diseases (CVD) and diabetes. It results from a general imbalance of the body’s metabolic processes that increases cardiovascular morbidity, mortality, and all-cause mortality.1 It has been recently considered as a target topic for research by health care professionals, due to its effect on the quality of life. In addition, its prevalence rate is increasing in a rapid way all over the world.2 Many factors influence the determination of the global prevalence of MetS, such as region, urban or rural environment, as well as the diagnostic criteria used to define MetS.3 Also MetS definition is influenced by other parameters such as age- as its prevalence increases with age although it may be present in children and adolescents- and sex (the prevalence of MetS in women is greater than in men).4 In general, the worldwide prevalence of MetS ranges from <10% to as much as 84%.4,5 In the United States, it is estimated that 35% of adults, and up to 50% of the population who are over 60 years, were diagnosed to have MetS (30.3% in men and 35.6% in women).6 Mexican-American women were reported to have the highest MetS prevalence.7 Depending on The International Diabetes Federation (IDF) diagnostic criteria of MetS, European prevalence has been estimated as 41% in men, and 38% in women.In Mediterranean countries, the prevalence ranges from 0.2% to 45.7% in adults <65 years of age, reaching up to 25% to 55.2% in adults >65 years.9 In Jordan as one of these Mediterranean countries, cross-sectional studies conducted to determine the prevalence of MetS and its components among Jordanians showed that the estimated prevalence rate in Jordan according to the IDF criteria was alarming at 51%, and it was higher in women (46.4% in men and 55.3% in women).10,11 Limited studies are presented in the literature that evaluates the relationship between dietary and lifestyle risk factors and the risk of MetS. Therefore, the objective of this review was to evaluate the association between macro- and micronutrients intake, eating patterns, physical activity (PA) and smoking and the risk of developing MetS.

Literature Search

A literature search was conducted using PubMed, Google Scholar, and Sciencedirect for “metabolic syndrome”, “lifestyle risk factors”, “dietary patterns” and “macro-micronutrients’.

Method and Design

Electronic databases were searched from January 2018 until June 2018 for studies investigating the association between dietary and lifestyle risk factors and metabolic syndrome.

Definition of MetS

The concept of MetS is well-known for many years, but there is a lack of a universally agreed definition of this syndrome. Three definitions of the MetS are currently in use and proposed by different health authorities: World Health Organization (WHO) in 1999, the National Cholesterol Education Program: Adult Treatment Panel III (NCEP: ATP III) in 2001, and the IDF in 2006.12

The WHO was the first organization to produce diagnostic criteria for MetS, the criteria included: aside from glucose tolerance status and IR, at least two of any other MetS risk factors should be present such as: central obesity as waist to hip ratio(WHpR) ≥0.90 for males or ≥0.85 for females and/or body mass index (BMI) ≥30 Kg/m², blood pressure ≥140/90 mmHg, and/or high-density lipo protein cholesterol (HDL-C)<35 mg/dl in males or <39 mg/dl in females, dyslipidemia as TG ≥150 mg/dl and microalbumenurea ≥20 µg min−1 or albumin: creatinine ratio ≥30 mg g−1.

But it was found that insulin resistance (IR) and microalbuminuria measurements are laborious and cannot be practically used in clinics. Thus, ATP III has released its definition of the MetS in 2001.13 The ATP III focused less on type 2 diabetes mellitus (DM II) and more on CVD risk as compared to the WHO definition.14

Therefore, ATPIII recommends the presence of any three of five components to diagnose MetS: abdominal obesity as waist circumference (WC) ≥102 cm for males or ≥88 cm for females, high blood pressure ≥130/85 mmHg, fasting hyperglycemia ≥110 mg/dl, low HDL-C <40 mg/dl in males or <50 mg/dl in females, and raised TG ≥150 mg/dl.15

However, a strong demand for a universal practical definition of MetS that can identify people who are at high risk of CVD and diabetes is still needed. Thus, the IDF has established its own criteria for the definition of MetS due to the persistent need for a single, universally accepted diagnostic tool that is easy to use in clinical practice.16 They defined patients with metabolic syndrome as suffering from central obesity (defined as WC ≥94 cm in males and ≥80 cm in females) plus any two of the following four factors: elevated triglycerides (TG) levels (≥150 mg/dL) or specific treatment for this lipid abnormality; lowered high-density lipoprotein cholesterol (HDL-C) (< 40 mg/dL in males, <50 mg/dL in females) or specific treatment for this lipid abnormality; elevated blood pressure: (systolic blood pressure (SBP) ≥130 or diastolic blood pressure (DBP) ≥85 mm Hg) or treatment of previously diagnosed hypertension; or elevated fasting blood glucose (FBG ≥100 mg/dL) , or previously diagnosed DM II.16

However, the three aforementioned definitions of MetS by the health authorities agreed on the presence of central obesity, hyperglycemia, hypertension (HTN), and dyslipidemia (DLP) as key risk factors for MetS.17,18,19 Table (1) shows the harmonized definition of MetS for these three authorities.20

Table 1: Harmonized Definition of MetS

Risk Factors Cut- off Points
Elevated WC* Population-and country-specific definitions
Elevated TG or specific treatment for this lipid abnormality ≥150 mg/dL (1.7 mmol/L)
Reduced HDL-C or specific treatment for this lipid abnormality <40 mg/dl (1.0 mmol/L) in males;<50 mg/dl (1.3 mmol/L) in females
Elevated blood pressure (treatment of previously diagnosed HTN) Systolic blood pressure (SBP) ≥ 130 and/or diastolic blood pressure ( DBP) ≥85 mm Hg
Elevated FBG (≥ 100 mg/dL), or previously diagnosed DM II ≥100 mg/dL

 

It is recommended that the IDF cut off points be used for non-Europeans and either the IDF or AHA/NHLBI cut off points used for people of European origin until more data are available.

Adopted from Alberti et al., 2009.

Abbreviation: WC: waist circumference; TG: triglycerides; HDL-C: high density lipoprotein cholesterol; HTN: hypertension; DM II: type 2 diabetes mellitus.

Pathophysiology of MetS

As aforementioned, many risk factors are related to MetS, thus it is considered to bea subject of debate. The clear mechanism or pathophysiology of this syndrome is still not well-determined, but the main causes are agreed to be IR and central obesity.21,22 These two factors lead to the development of other metabolic risk factors like hyperglycemia, DLP, and HTN which may cause CVD and DM II later on.21,23

Insulin Resistance

IR is considered to be the most accepted hypothesis to describe the pathophysiology of MetS.IR is a physiological condition in which beta-cells secrete normal amounts of insulin hormone but are unable to respond normally in the target tissues of liver, skeletal muscle and adipocytes. This reduced responsiveness is a major precursor of DM II.3

IR in skeletal muscle promotes reduction in glycogen synthesis and intracellular glucose transport, while in the liver it impairs insulin signaling pathways; however, discordant to this observation is evidence that hepatic lipogenesis continues.24

Ferris & Kahn, (2016) suggested that insulin secretion decreases fat lipolysis, gluconeogenesis, and TG secretion from liver. In addition, insulin acts on the brain, which independently reduces lipolysis through suppression of sympathetic outflow and raises hepatic TG secretion through an unknown mechanism.24 In diabetes, the decrease in insulin action on the brain and fat leads to an elevation in lipolysis. As a result, this will promote the supply of free fatty acids (FFA) to the liver which in turn will increase TG synthesis. On the other hand, the impairment of insulin action of the liver will result in increased gluconeogenesis.24 Figure 1 (A, B) illustrates the difference between (A) normal physiology vs. (B) diabetic condition regarding insulin action.

Figure 1

Figure 1: (A) normal physiology. (B) diabetic condition regarding insulin action.

Click here to View figure

 

Obesity and Abdominal Obesity

Overweight and obesity are defined as abnormal or excessive fat accumulation that presents a risk to health.25 Abdominal obesity is a major independent risk factor of insulin sensitivity, impaired glucose tolerance elevated blood pressure and DLP seen in the MetS.26,27 Overweight and obesity are associated with an increased risk for CVD, HTN, DM II, certain cancers and many other disorders.28

As the liver and pancreas, and in the MetS.29 “In addition, these FFA released from excessive It has been assumed that adipose tissue releases an excess of fatty acids and cytokines that induce insulin resistance.29 The release of these excessive FFA also induces lipotoxicity, as lipids and their metabolites create oxidative stress to the endoplasmic reticulum and mitochondria.30 This affects adipose as well as non-adipose tissue, accounting for its pathophysiology in many organs, such ly stored triacylglycerol deposits contribute to hypertriglyceridemia by the inhibition of lipogenesis, which prevents adequate clearance of serum triacylglycerol levels.31” Consequently, the secretion of FFA by endothelial lipoprotein lipase (LPL) from elevated blood TG within increased β-lipoproteins will lead to lipotoxicity which results in insulin-receptor dysfunction. IR state then will follow and cause hyperglycemia with compensated hepatic gluconeogenesis. The later consequences will increase glucose output from the liver which will enhance the hyperglycemia caused by IR. FFA also will decrease the utilization of insulin-stimulated muscle glucose, contributing further to hyperglycemia.29 As a result, lipotoxicity will decrease the secretion of pancreatic β-cell insulin, which eventually results in β-cell exhaustion.31 Grundy (2004) has explained the relationship between obesity and IR by which “obesity causes insulin resistance, whereas insulin resistance seemingly exacerbates the adverse effects of obesity”29 Figure (2) illustrates the role of lipotoxicity and inflammation in obesity.

Figure 2

Figure 2: Role of lipotoxicity and inflammation in obesity.

Click here to View figure

 

Anthropometric Measurements and MetS

MetS was strongly found to be linked to body weight, height and waist and hip circumferences. It is not only the use of these measurements that is important in this prediction, but also the estimation of the percentage of fat in the body.32 A study conducted by Khader et al., (2010) to determine cutoff values of anthropometric measurements as indicators of metabolic abnormalities among Jordanians; BMI, WC, and waist to height ratio (WHtR) were found to be associated with CVD risk factors, with WHtR being the better predictor.10 In addition, Sagun et al., (2014) conducted a study to assess the association between not routinely used body measurements (e.g., mid-upper arm, forearm, and calf circumferences) and MetS.33 The authors concluded that WC was not associated to MetS in obese and overweight subjects. However, forearm circumference was associated with MetS and visceral fat measured by bioelectric impedance, hip circumference, and WHpR.33 However, Wahrenberg et al., (2005) suggested that a WC of <100 cm prevents individuals of both sexes from being at risk of IR. Also the authors reported WC is a strong simple measurement for identifying individuals who are at high risk of IR and MetS, so it replaces BMI, WHpR, and other measures of total body fat as a predictor of IR.34

Lifestyle Risk Factors

Smoking

Smoking and physical inactivity have been identified as important modifiable risk factors for MetS and its consequences.35,36 Several studies have shown that smoking is considered as a major risk factor for CVD and DM II and it is also associated with metabolic abnormalities and increases the risk of MetS.37,38,39 Tobacco smokers had a 1.07–1.66-fold greater risk of developing MetS than non-smokers as reported by Nakanishi et al., (2005).38 Weitzman et al., (2005) conducted a study to find the relationship between tobacco smoking and the severity of MetS.40 They found that both active and passive smoking may increase the risk of MetS among adolescents who are overweight or at risk of overweight.

The mechanism by which cigarette smoking can affect glucose and lipid metabolism may partly attribute to stimulation of sympathetic nervous system.41 Nicotine released during smoking stimulates the release of several neurotransmitters and hormones such as cortisol, growth hormone and others.42

This increased cortisol production in current smokers may lead to having higher WC which results in accumulation of abdominal fat.43 In addition to the hormone disturbance; it has been shown that endothelial dysfunction and its related arterial compliance reduction were more serious in smokers than nonsmokers. Besides, smokers tend to have IR due to the effects of cotinine (a metabolite of nicotine), carbon monoxide, cortisol, and growth hormone,44 and hence could contribute to development and deterioration of metabolic syndrome.41

On the other hand, Harris et al., (2016) demonstrated that smoking cessation may also lead to the development of MetS due to the increased food intake which results in weight gain.45 It is proposed that nicotine has the ability to suppress appetite, but in the condition of smoking cessation this ability is reversed.46 In this case, replacing the rewards of food with the rewards of cigarettes will take place.47 Absence of nicotine raises the rewarding value of food and subsequently increases the intake of food rich in fat and sugar48 and may lead to excessive intake snacks that are high in carbohydrates and sugar.49 Additionally, nicotine and/or smoking help control compulsive eating and overeating; during post-cessation these activities are inhibited.50

Physical Inactivity

Sedentary PA is one of the major modifiable risk factors for the MetS.51 The second leading cause of premature morbidity and mortality is excess body weight gain due to poor diet and insufficient PA.52 PA is associated with many health-related benefits, including a reduced risk of developing several chronic diseases such as obesity,53 CVD,54 DM II,55 MetS.56,57

The adverse effect of physical inactivity on MetS components is thought to be due to reduced energy expenditure which results in increased energy intake. Cross-sectional studies reported an inverse association between PA and MetS.56,58,59

Most of the guidelines support that at least 150 minutes of moderate-intensity PA per week could be associated with a lower prevalence of MetS.60

Dietary and Food Patterns and MetS

Many studies were conducted to examine the dietary patterns that may be associated with MetS and its components.2,61,62 One of the dietary patterns that are known to be associated with reducing MetS is the Mediterranean Diet.62 The Mediterranean diet was first defined by Ancel Keys as the diet usually consumed among the populations bordering the Mediterranean Sea.63 It is characterized by the consumption of fruit, vegetables, nuts, olive oil, fish64 and low consumption of saturated fat, red meat, processed meat, refined carbohydrates, and whole-fat dairy products.63 Adherence to the Mediterranean Diet improves both physical and mental health and improves quality of life.65 Also, it has been revealed that Mediterranean Diet may lower the risk of having elevated low-density lipoprotein cholesterol (LDL-C), blood glucose values,66 and TG, and improves HDL-C levels.67 Few cross-sectional studies found a strong effect of the adherence to the Mediterranean Diet on lowering the risk of MetS and all its components (a higher effect of the entire dietary pattern than to individual food components)62,64 Some components of the Mediterranean Diet, such as olive oil and legumes,67 high fruit and vegetable consumption was generally found to be associated with lower prevalence of MetS.68 A quantitative meta-analysis of twelve studies (eight observational cross-sectional and four prospective cohort) were pooled together to estimate the association between adherence to the Mediterranean dietary pattern and MetS risk.69 The findings of this meta-analysis suggested that high adherence to the Mediterranean diet was significantly associated with reduced risk of MetS. Also the adherence to this dietary pattern had a significant inverse association with some of MetS components such as: WC, blood pressure and low HDL-C levels, but the results were conflicting about blood glucose levels.69

Association between consumption of dairy products and the risk of MetS is controversial.2,70,71 Fumeron et al., (2011) conducted a prospective study which showed that high dairy intake was generally associated with reduced risk of MetS components.70 A multi center cohort study of 15105 adults was conducted in order to investigate the association of dairy consumption, types of dairy products and dairy fat content with MetS, dairy consumption was assessed by a food frequency questionnaire (FFQ).71 The authors found out that full-fat dairy but not low fat intake was inversely and independently associated with MetS in middle-aged and older adults. Another 6-year prospective study that examined the effect of yogurt consumption on the risk of MetS concluded that there is no clear significant association between yogurt consumption and MetS and its components, but only with central adiposity which was inversely associated with high consumption of yogurt.They also found that combination of high consumption of both yogurt and fruits had a significant inverse relationship with MetS risk. Minimally processed cereals appeared to be associated with decreased risk of MetS, while highly processed cereals with high glycemic index (GI) are associated with higher risk.72

A study was conducted by Kim et al., (2011) to assess the association between usual dietary patterns and the risk of MetS in adults from South Korean. The authors found out that alcohol and meat dietary pattern was adversely associated with elevated blood pressure and hypertriglyceridemia.73 On the other hand, after adjusting for possible confounding factors for developing MetS, fish, grains, and vegetables dietary pattern was associated with a reduction in the risk of hypertriglyceridemia and inversely with MetS risk.73

Dietary Approach to Stop Hypertension (DASH) diet which is rich in fruits, vegetables, low-fat dairy products and low sodium intake, is also reported to be helpful in preventing and treating MetS.74,75 This diet is high in certain dietary macro/micro nutrients that appear to be beneficial for reducing the risk of MetS and its components such as: fiber, potassium and magnesium.75 Azadbakht et al., (2005) conducted a randomized controlled outpatient trial on 116 patients with the MetS study to determine the effects of DASH diet on metabolic risks in patients with the MetS.74 Three diets were planned and followed by participants for 6 months: a control diet, a weight-reducing diet concentrating on healthy food choices, and DASH diet. After adjustment for weight changes, DASH diet was the one which improved all components of the MetS, with improvements in WC and TG.74

“Western” dietary pattern has been shown to be associated with increased risk of components of MetS. This type of diet is characterized by high intakes of refined grains, red meat, high fat, sugar sweetened-beverages, desserts, high-fat dairy products, and eggs.68,76 Additionally, the “Empty-Calorie” pattern which is characterized by high consumption of total and saturated fat, sugars (desserts and sugar-sweetened beverages), low intake of fruits and vegetables was associated with increased prevalence of MetS.77

“Vegetarian” dietary patterns are plant-based diets that are characterized by the consumption of vegetables, fruits, grains, legumes, nuts, vegetable oils, dairy products and/or eggs and reduced or eliminated consumption of animal products.78 “Vegan” diets are more strict than the vegetarian`s since they only contain plant foods.79 These types of dietary patterns have been suggested to be associated with a lower risk for developing DM II, HTN, specific cancers, and MetS.78

Nutrients and MetS

Several studies have highlighted the evidence for the beneficial effect of some macro- and micronutrients on MetS. In general, these nutrients may have a role in energy absorption/production/utilization, pancreatic functions, modulation of systemic inflammation, and oxidative stress.80,81,82

Macronutrients and MetS

Carbohydrates

Recent data suggest that increased consumption of refined or rapidly absorbed carbohydrates including syrups, biscuits, and cakes, are closely associated with MetS, DM II, and CVD.83 This type of carbohydrates is characterized by a high glycemic load (GL)-a measure of both quantity and quality of dietary carbohydrate- which may increase the risk of coronary heart disease by increasing glucose intolerance and DLP.84 These data are consistent with a cross-sectional study that detected a positive association between GL and MetS.73 Also it is suggested that individuals who are obese and have IR are particularly prone to the adverse effects of a high dietary GL.84,85 On the other hand, whole grains contain several nutrients such as fiber and minerals that have been shown to favorably influence components of MetS such as body weight, fasting glucose or IR,84 blood pressure, HDL-C, and TG.67,86,87 Limited findings have been reported on the relation between GI and MetS. GI refers to how much a carbohydrate-containing food raises plasma glucose compared with a standard food of either glucose or white bread (50g).88 Mckeown et al., (2004) demonstrated that there was no effect of total carbohydrate intake on IR or prevalence of the MetS, on the other hand, they found that high GI is positively associated with the prevalence of MetS with a multivariable odds ratio of 1.41 (1.04-1.91) comparing the highest to the lowest quintile of GI.89

Sugar

The primary sources of added sugar are sugary beverages that contain nutritive sweeteners such as sugar, fruit juice concentrates, or high-fructose corn syrup.90 A longitudinal cohort study conducted by Schulze et al., (2004) illustrated that higher consumption of sugar-sweetened beverages may result in unfavorable metabolic changes.91 The results of this study also showed that the higher consumption of sugar-sweetened beverages is associated with a greater degree of weight gain and an increased risk of developing DM II in women which is attributed to excessive intake of calories and rapidly absorbable sugars.91

Fat    

A huge body of studies reported the evidence that saturated and trans fatty acids exert deleterious effects on metabolic health.93,94 In contrast, unsaturated fatty acids including monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) (omega-3 and omega-6) improve metabolic parameters such as: glycemic control, insulin sensitivity, blood pressure, and lipid profile.80,94

Fiber

Dietary fiber intake especially from cereals and whole grains can manage and affects body weight, blood glucose and lipid profile.95 A prospective cohort study of 9702 men and 15 365 women aged 35 to 65 years was conducted by Schulze et al., (2007) to examine associations between fiber and magnesium intake and risk of DM II. The authors found that increased consumption of cereal dietary fiber significantly reduced the risk of diabetes (relative risk, 0.67).96 Due to its viscous properties, soluble dietary fiber is found to be associated with glycemic control improvement and insulin sensitivity enhancement in both diabetic and healthy subjects. However, it didn’t show any effect on reducing the risk of DM II.97 Contrary to soluble fiber, insoluble fiber was found to be associated negatively with the risk of diabetes, even though it showed insignificant influence on postprandial glucose levels.95,94,98

Alcohol

A prospective cohort study of 3833 male and female Koreans aged between 40 and 69 years was conducted to examine the association between alcohol consumption and incident metabolic syndrome. It was observed that heavy liquor drinking is associated with an increased risk of the MetS components including: WC, TG, blood pressure, and FBG.99 Light to moderate alcohol consumption is suggested to increase HDL-C levels, thus exerting a preventive effect on cardiovascular disease.100

Micronutrients and MetS

Oxidative stress and systemic inflammation are the central mechanisms that relating energy overload and obesity to IR and consequently metabolic disorders.101 Antioxidants can reduce the level of oxidative stress and potentially prevent subsequent health complications that are associated with oxidative damage.102 Bahadoran et al., (2012) reported diets rich in antioxidants (vitamin E, vitamin C, and β-carotene) exert beneficial influences on glucose metabolism and diabetes prevention. They are also associated with a reduction in the risk of developing CVD.102 Observational evidence further suggested that higher dietary intake or supplementation of antioxidants (such as: vitamin A, C, and E, folic acid, niacin, β-carotene, selenium, and zinc) can reduce mortalities and morbidities related to CVD after a minimum of 2-year intervention. However, natural sources of these antioxidants may be more effective than synthetic forms.101,103

Liu et al., (2005) suggested that higher intakes of total, dietary, and supplemental calcium were significantly and inversely associated with the prevalence of MetS.104 It has been shown that high calcium intake improves BP and diabetes through weight loss and an increase in insulin release and sensitivity.105

Magnesium is the fourth most abundant essential mineral in the body and is involved in >300 metabolic reactions, including protein/DNA/RNA synthesis, cellular energy production, and cell growth and reproduction.106 Observational data indicated an inverse association between magnesium status and the risk of MetS among adults, but this potential benefit needs further investigation.106,107 Bian et al., (2013) concluded that “vitamin B group” pattern including thiamin, riboflavin and niacin was negatively associated with the risk of MetS.108

High sodium diet is positively associated with HTN, IR, and DLP as demonstrated by Baudrand et al., (2014).109

Management of MetS

A healthy lifestyle including weight loss through calorie restriction, healthy food choices, increased physical activity and smoking cessation has a remarkable role in preventing or delaying the onset of MetS or treating the condition when present.110 Grundy et al., (2005) suggested that besides lifestyle modification for the management of MetS, clinical therapy is also necessary in many patients for the treatment of this syndrome.111 For treating IR and delaying DM II, metformin and thiazolidinediones are effective in reducing IR and keeping serum blood glucose in normal ranges, but their effect haven`t been shown to reduce the risk of CVD in those with the MetS, prediabetes, or DM II.111

In the case of DLP, Statins are well-known to reduce all apolipoprotein B–containing lipoproteins. Fibrates improve all components of atherogenic DLP and may directly reduce the risk for CVD.18 Anti-hypertensive agents are recommended for people whose blood pressure exceeds normal ranges.111

In addition to the previous strategies; bariatric surgery is now favored to be as an effective approach for the treatment of severe and morbid obesity.21 It results in a weight loss of 25–30% and improvement of multiple comorbidities associated with obesity, including HTN, DM II, CVD and DLP.112

Conclusions

The present review provides evidence supporting the presence of an association between dietary patterns, micro- and macro nutrients intake, lifestyle factors and the risk of MetS. Higher WC and positive family history of MetS are associated with developing MetS. Also the finding of this review documented an association of the adherence to some dietary patterns; especially “fast food pattern” with MetS risk.

Acknowledgements

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Competing Interests

The authors declare that they have no competing interest.

Funding

This study did not receive any specific grant from funding agencies in the public or not-for-profit sectors.

Ethical Standards

This article does not contain any studies with human participants or animals performed by any of the authors.

References

  1. Wassink A. M., Van der Graaf Y., Olijhoek J. K., Visseren F. L. Metabolic syndrome and the risk of new vascular events and all-cause mortality in patients with coronary artery disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm. European Heart Journal. 2008;29(2):213-223.
    CrossRef
  2. Sayón-Orea C., Santiago S., Cuervo M., Martínez-González M. A., Garcia A., Martínez J. A. Adherence to Mediterranean dietary pattern and menopausal symptoms in relation to overweight/obesity in Spanish perimenopausal and postmenopausal women. 2015;22(7):750-757.
  3. McCracken E., Monaghan M., Sreenivasan S. Pathophysiology of the metabolic syndrome. Clinics in Dermatology. 2018;36(1):14-20.
    CrossRef
  4. Kolovou G. D., Anagnostopoulou K. K., Salpea K. D., Mikhailidis D. P. The prevalence of metabolic syndrome in various populations. The American Journal of the Medical Sciences. 2007;333(6):362-371.
    CrossRef
  5. Desroches S., Lamarche B. The evolving definitions and increasing prevalence of the metabolic syndrome. Applied Physiology, Nutrition, and Metabolism. 2007;32(1):23-32.
    CrossRef
  6. Aguilar M., Bhuket T., Torres S., Liu B., Wong R. J. Prevalence of the metabolic syndrome in the United States, 2003-2012. The Journal of the American Medical Association. 2015; 313(19):1973-1974.
    CrossRef
  7. Beltrán-Sánchez H., Harhay M. O., Harhay M. M., McElligott S. Prevalence and trends of metabolic syndrome in the adult US population, 1999–2010. Journal of the American College of Cardiology. 2013;62(8):697-703.
    CrossRef
  8. Gao W. Does the constellation of risk factors with and without abdominal adiposity associate with different cardiovascular mortality risk?. International Journal of Obesity.2008; 32(5),757-762.
    CrossRef
  9. Anagnostis P. Metabolic syndrome in the Mediterranean region: Current status. Indian Journal of Endocrinology and Metabolism. 2012;16(1):72.
    CrossRef
  10. Khader Y. S., Batieha A., Jaddou H., Batieha Z., El-Khateeb M., Ajlouni K. Anthropometric cutoff values for detecting metabolic abnormalities in Jordanian adults.Diabetes, Metabolic Syndrome and Obesity : Targets and Therapy. 2010;3:395–402.
    CrossRef
  11. Obeidat A. A., Ahmad M. N., Haddad F. H., Azzeh F. S. Alarming high prevalence of metabolic syndrome among Jordanian adults. Pakistan Journal of Medical Sciences. 2015;31(6):1377–1382.
    CrossRef
  12. Yasein N., Masa’d D. Metabolic syndrome in family practice in Jordan: a study of high-risk groups. Eastern Mediterranean Health Journal. 2011;17(12).
    CrossRef
  13. Genuth S., Alberti K. G. M. M., Bennett P., Buse J., DeFronzo R., Kahn R., Nathan D. Follow-up report on the diagnosis of diabetes mellitus. Diabetes Care. 2003;26(11):3160-3168.
    CrossRef
  14. Alberti K. G. M., Zimmet P., Shaw J. The metabolic syndrome—a new worldwide definition. The Lancet. 2005;366(9491):1059-1062.
    CrossRef
  15. Reaven G. M. The metabolic syndrome: is this diagnosis necessary?. The American Journal of Clinical Nutrition.2006;83(6),1237-1247.
    CrossRef
  16. IDF (International Diabetes Federation). IDF Definition of the Metabolic Syndrome: Frequently Asked Questions 2015. Retrieved from: http://www.idf.org/metabolic-syndrome/faqs.
  17. World Health Organization. Part 1: diagnosis and classification of diabetes mellitus. Definition, diagnosis and classification of diabetes and its complications: report of a WHO Consultation1999. Reported from:http://www.whqlibdoc.who.int/hq/1999/WHO_NCD_NCS_99.2.pdf .
  18. National Cholesterol Education Program Adult Treatment Panel III. 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. 2002;106:3143-3421.
  19. IDF (International Diabetes Federation). IDF Consensus Worldwide Definition of the Metabolic Syndrome 2006. Retrieved from:https://www.idf.org/e-library/consensus-statements/60-idfconsensus-worldwide-definitionof-the-metabolic-syndrome.html.
  20. Alberti K. G. M. M., Eckel R. H., Grundy S. M., Zimmet P. Z., Cleeman J. I., Donato K. A., Smith SC. Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; national heart, lung, and blood institute; American heart association; world heart federation; international atherosclerosis society; and international association for the study of obesity. Circulation.2009;120(16),1640-1645.
    CrossRef
  21. Grundy S. M, Cleeman J. I, Daniels S. R, Donato K. A, Eckel R. H, Franklin B. A, … & Spertus J. A. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement. 2005;112(17):2735-2752.
  22. Roberts C. K., Hevener A. L., Barnard R. J. Metabolic syndrome and insulin resistance: underlying causes and modification by exercise training. Comprehensive Physiology. 2013;3(1),1-58.
    CrossRef
  23. Sadikot S., Hermans M. Here we go again… The metabolic syndrome revisited!. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2010;4(2):111-120.
    CrossRef
  24. Ferris H. A., Kahn C. R. Unraveling the paradox of selective insulin resistance in the liver: the brain–liver connection. Diabetes. 2016;65(6):481-1483.
    CrossRef
  25. World Health Organization. Obesity: preventing and managing the global epidemic (No. 894). World Health Organization 2000.  Retrieved from: http://www.who.int/nutrition/publications/obesity/WHO_TRS_894/en/.
  26. Katsuki A, Sumida Y, Urakawa H, Gabazza E. C, Murashima S, Maruyama N, … & Adachi Y. Increased visceral fat and serum levels of triglyceride are associated with insulin resistance in Japanese metabolically obese, normal weight subjects with normal glucose tolerance. Diabetes Care. 2003;26(8):2341-2344.
    CrossRef
  27. Rattarasarn C., Leelawattana R., Soonthornpun S., Setasuban W., Thamprasit A., Lim A, Thamkumpee N. Relationships of body fat distribution, insulin sensitivity and cardiovascular risk factors in lean, healthy non-diabetic Thai men and women. Diabetes Research and Clinical Practice. 2003;60(2):87-94.
    CrossRef
  28. Kruger J., Ham S.A., Prohaska T. R. Peer Reviewed: Behavioral Risk Factors Associated with Overweight and Obesity Among Older Adults: the 2005 National Health Interview Survey. Preventing Chronic Disease. 2009;6(1).
  29. Grundy S. M., Hansen B., Smith S. C., Cleeman J. I., Kahn R. A. Clinical management of metabolic syndrome: report of the American Heart Association/National Heart, Lung, and Blood Institute/American Diabetes Association conference on scientific issues related to management. 2004;109(4):551-556.
  30. Evans R. M., Barish G. D., Wang Y. X. PPARs and the complex journey to obesity. Nature Medicine. 2004;10(4):355.
    CrossRef
  31. Unger R. H. Lipotoxicity in the pathogenesis of obesity-dependent NIDDM: genetic and clinical implications. Diabetes. 1995;44(8):863-870.
    CrossRef
  32. Bisschop Ch. N. S., Peters P. H. M., Monninkhoff E. M., van der Schouw Y. T. Associations of visceral fat, physical activity and muscle strength with the metabolic syndrome. Maturitas. 2013;76:139–145.
    CrossRef
  33. Sagun G., Oguz A., Karagoz E., Filizer A. T., Tamer G., Mesci B. Application of alternative anthropometric measurements to predict metabolic syndrome. 2014;69(5):347-353.
  34. Wahrenberg H., Hertel K., Leijonhufvud B. M., Persson L. G., Toft E., Arner P. Use of waist circumference to predict insulin resistance: retrospective study. British Medical Journal. 2005;330(7504):1363-1364.
    CrossRef
  35. Carnethon M. R., Loria C. M., Hill J. O., Sidney S., Savage P. J., Liu K. Risk factors for the metabolic syndrome: The Coronary Artery Risk Development in Young Adults (CARDIA) study, 1985–2001.Diabetes Care. 2004;27(11):2707-2715.
    CrossRef
  36. Oh S. W., Yoon Y. S., Lee E. S., Kim W. K., Park C., Lee S., Yoo T. Association between cigarette smoking and metabolic syndrome: the Korea National Health and Nutrition Examination Survey. Diabetes Care. 2005;28(8):2064-2066.
    CrossRef
  37. Geslain-Biquez C., Tichet J., Caradec A., D’Hour A., Balkau B. The metabolic syndrome in smokers. The DESIR study. Diabetes & Metabolism. 2003;29(3):226-234.
    CrossRef
  38. Nakanishi N., Takatorige T., Suzuki K. Cigarette smoking and the risk of the metabolic syndrome in middle-aged Japanese male office workers. Industrial Health. 2005;43(2):295-301.
    CrossRef
  39. Miyatake N., Wada J., Kawasaki Y., Nishii K., Makino H., Numata T. Relationship between metabolic syndrome and cigarette smoking in the Japanese population. Internal Medicine. 2006;45(18):1039-1043.
    CrossRef
  40. Weitzman M., Cook S., Auinger P., Florin T. A., Daniels S., Nguyen M., Winickoff J. P. Tobacco smoke exposure is associated with the metabolic syndrome in adolescents. Circulation. 2005;112(6):862-869.
    CrossRef
  41. Bigazzi R., Bianchi S. Insulin resistance, metabolic syndrome and endothelial dysfunction. Journal of Nephrology. 2007;20(1):10-14.
  42. Wilkins J. N., Carlson H. E., Van Vunakis H., Hill M. A., Gritz E., Jarvik M. E. Nicotine from cigarette smoking increases circulating levels of cortisol, growth hormone, and prolactin in male chronic smokers. Psychopharmacology. 1982;78(4):305-308.
    CrossRef
  43. Chiolero A., Jacot‐Sadowski I., Faeh D., Paccaud F., Cornuz J. Association of cigarettes smoked daily with obesity in a general adult population. 2007;15(5):1311-1318.
  44. Winkelmann B. R., Boehm B. O., Nauck M., Kleist P., März W., Verho N. K., Kneissl G. Cigarette smoking is independently associated with markers of endothelial dysfunction and hyperinsulinaemia in non-diabetic individuals with coronary artery disease. Current Medical Research and Opinion. 2001;17(2):132-141.
    CrossRef
  45. Harris K. K., Zopey M., Friedman T. C. Metabolic effects of smoking cessation. Nature Reviews Endocrinology. 2016;12(5):299.
    CrossRef
  46. Hur Y. N., Hong G. H., Choi S. H., Shin K. H., Chun B. G. High fat diet altered the mechanism of energy homeostasis induced by nicotine and withdrawal in C57BL/6 mice. Molecules and Cells. 2010;30(3):219-226.
    CrossRef
  47. Lerman C., Berrettini W., Pinto A., Patterson F., Crystal-Mansour S., Wileyto E. P., Epstein L. H. Changes in food reward following smoking cessation:a pharmacogenetic investigation. Psychopharmacology. 2004;174(4):571-577.
    CrossRef
  48. Volkow N. D., Wang G. J., Fowler J. S., Telang F. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. Philosophical Transactions of the Royal Society B: Biological Sciences. 2008;363(1507):3191-3200.
    CrossRef
  49. Johnson P. M., Hollander J. A., Kenny P. J. Decreased brain reward function during nicotine withdrawal in C57BL6 mice: evidence from intracranial self-stimulation (ICSS) studies. Pharmacology Biochemistry and Behavior. 2008;90(3):409-415.
    CrossRef
  50. White M. A., Masheb R. M., Grilo C. M. Self‐reported weight gain following smoking cessation: A function of binge eating behavior. International Journal of Eating Disorders. 2010;43(6):572-575.
    CrossRef
  51. Bertrais S., Beyeme‐Ondoua J. P., Czernichow S., Galan P., Hercberg S., Oppert J. M. Sedentary behaviors, physical activity, and metabolic syndrome in middle‐aged French subjects. Obesity. 2005;13(5):936-944.
    CrossRef
  52. Mokdad A. H., Marks J. S., Stroup D. F., Gerberding J. L. Actual causes of death in the United States, 2000. The Journal of the American Medical Association. 2004;291(10):1238-1245.
    CrossRef
  53. Ekelund U., Besson H., Luan J. A., May A. M., Sharp S. J., Brage S., Jenab M. Physical activity and gain in abdominal adiposity and body weight: prospective cohort study in 288,498 men and women–. The American Journal of Clinical Nutrition. 2011;93(4):826-835.
    CrossRef
  54. Manson J. E., Greenland P., LaCroix A. Z., Stefanick M. L., Mouton C. P., Oberman A., Siscovick D. S. Walking compared with vigorous exercise for the prevention of cardiovascular events in women.New England Journal ofMedicine. 2002;347(10):716-725.
    CrossRef
  55. Tuomilehto J., Lindström J., Eriksson J. G., Valle T. T., Hämäläinen H., Ilanne-Parikka P, Salminen V. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. New England Journal of Medicine. 2001;344(18):1343-1350.
    CrossRef
  56. Hahn V., Halle M., Schmidt-Trucksäss A., Rathmann W., Meisinger C., Mielck A. Physical activity and the metabolic syndrome in elderly German men and women: results from the population-based KORA survey. Diabetes Care. 2009;32(3):511-513.
    CrossRef
  57. Strasser B. Physical activity in obesity and metabolic syndrome. Annals of the New York Academy of Sciences. 2013;1281(1):141-159.
    CrossRef
  58. Ford E. S., Kohl H. W., Mokdad A. H., Ajani U. A. Sedentary behavior, physical activity, and the metabolic syndrome among US adults. Obesity. 2005;13(3):608-614.
    CrossRef
  59. Zhu S., St-Onge M. P., Heshka S., Heymsfield S. B. Lifestyle behaviors associated with lower risk of having the metabolic syndrome. Metabolism-Clinical and Experimental. 2004;53(11):1503-1511.
    CrossRef
  60. Wadden T. A., Webb V. L., Moran C. H., Bailer B. A. Lifestyle modification for obesity: new developments in diet, physical activity, and behavior therapy. 2012;125(9):1157-1170.
  61. Hong S., Song Y., Lee K. H., Lee H. S., Lee M., Jee S. H., Joung H. A fruit and dairy dietary pattern is associated with a reduced risk of metabolic syndrome. Metabolism-Clinical and Experimental. 2012;61(6):883-890.
    CrossRef
  62. Viscogliosi G., Cipriani E., Liguori M. L., Marigliano B., Saliola M., Ettorre E., Andreozzi P. Mediterranean dietary pattern adherence: associations with prediabetes, metabolic syndrome, and related microinflammation. Metabolic syndrome and related disorders. 2013;11(3):210-216.
    CrossRef
  63. Martínez-González M. Á., Sánchez-Villegas A. The emerging role of Mediterranean diets in cardiovascular epidemiology: monounsaturated fats, olive oil, red wine or the whole pattern?. European Journal of Epidemiology. 2004;19(1):9-13.
    CrossRef
  64. Leon E. A., Henriquez P., Serra-Majem L. Mediterranean diet and metabolic syndrome: a cross-sectional study in the Canary Islands. Public Health Nutrition. 2006;9(8A):1089-1098.
  65. Landaeta-Díaz L., Fernández J. M., Silva-Grigoletto M. D., Rosado-Alvarez D., Gómez-Garduño A, Gómez-Delgado F., Fuentes-Jimenez F. Mediterranean diet, moderate-to-high intensity training, and health-related quality of life in adults with metabolic syndrome. European Journal of Preventive Cardiology. 2013;20(4):555-564.
    CrossRef
  66. Paletas K., Athanasiadou E., Sarigianni M., Paschos P., Kalogirou A., Hassapidou M., Tsapas A. The protective role of the Mediterranean diet on the prevalence of metabolic syndrome in a population of Greek obese subjects. Journal of the American College of Nutrition.2010;29(1):41–45.
    CrossRef
  67. Babio N., Bull´o M., Basora J., Martínez-González M. A., Fernández-Ballart J., Márquez-Sandoval F., Molina C., Salas-Salvadó J. Adherence to the Mediterranean diet and risk of metabolic syndrome and its components. Nutrition.Metabolism and Cardiovascular Diseases. 2009;19(8):563–570.
    CrossRef
  68. Esmaillzadeh A., Kimiagar M., Mehrabi Y., Azadbakht L., Hu F. B., Willett W. C. Dietary patterns, insulin resistance, and prevalence of the metabolic syndrome in women–. The American Journal of Clinical Nutrition. 2007;85(3):910-918.
    CrossRef
  69. Godos., Zappalà G., Bernardini S., Giambini I., Bes-Rastrollo M., Martinez-Gonzalez M. Adherence to the Mediterranean diet is inversely associated with metabolic syndrome occurrence: a meta-analysis of observational studies. International Journal of Food Sciences And Nutrition. 2017;68(2):138-148.
    CrossRef
  70. Fumeron F., Lamri A., Emery N., Bellili N., Jaziri R., Porchay-Baldérelli I., Marre M. Dairy products and the metabolic syndrome in a prospective study, DESIR. Journal of the American College of Nutrition. 2011;30(5):454S-463S.
  71. Drehmer M., Pereira M. A., Schmidt M. I., Alvim S., Lotufo P. A., Luft V. C., Duncan B. B. Total and Full-Fat, but Not Low-Fat, Dairy Product Intakes are Inversely Associated with Metabolic Syndrome in Adults, 2. The Journal of Nutrition. 2015;146(1):81-89.
    CrossRef
  72. McKeown N. M., Meigs J. B., Liu S., Wilson P. W. F., Jacques P. F. Whole-grain intake is favorably associated with metabolic risk factors for type 2 diabetes and cardiovascular disease in the Framingham Offspring Study. The American Journal of Clinical Nutrition. 2002;76(2):390-398.
    CrossRef
  73. Kim J., Jo I. Grains, Vegetables, and Fish Dietary Pattern Is Inversely Associated with the Risk of Metabolic Syndrome in South Korean Adults. American Dietetic Association. 2011;111(8):1141-1149.
    CrossRef
  74. Azadbakht L., Mirmiran P., Esmaillzadeh A., Azizi T., Azizi F. Beneficial Effects of a Dietary Approaches to Stop Hypertension Eating Plan on Features of the Metabolic Syndrome.Diabetes Care. 2005;28(12):2823-2831.
    CrossRef
  75. Al-Solaiman Y., Jesri A., Mountford W. K., Lackland D. T., Zhao Y., Egan BM.xDASH lowers blood pressure in obese hypertensive beyond potassium, magnesium and fiber. Journal of Human Hypertension. 2005;24(4):237.
    CrossRef
  76. Lutsey P. L., Steffen L. M., Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation. 2008;117(6):754-761.
    CrossRef
  77. Sonnenberg L., Pencina M., Kimokoti R., Quatromoni P., Nam B. H., D’agostino R., Millen B. Dietary patterns and the metabolic syndrome in obese and non‐obese Framingham women. Obesity. 2005;13(1):153-162.
    CrossRef
  78. Sabaté J., Wien M. A perspective on vegetarian dietary patterns and risk of metabolic syndrome. British Journal of Nutrition. 2015;113(S2):S136-S143.
  79. Kahleova H., Levin S., Barnard N. D. Vegetarian Dietary Patterns and Cardiovascular Disease. Progress in cardiovascular diseases. 2018
  80. Roche H. M. Fatty acids and the metabolic syndrome. Proceedings of the Nutrition Society. 2005;64(1),23-29.
    CrossRef
  81. Newsholme P., Cruzat V., Arfuso F., Keane K. Nutrient regulation of insulin secretion and action. Journal of Endocrinology. 2014;221(3):R105-R120.
  82. Leidy H. J., Clifton P. M., Astrup A., Wycherley T. P., Westerterp-Plantenga M. S., Luscombe-Marsh N. D., Mattes R. D. The role of protein in weight loss and maintenance–. The American Journal of Clinical Nutrition. 2015;101(6),1320S-1329S.
  83. Shastun S., Chauhan A. K., Singh R. B., Singh M., Singh R. P., Itharat A., Halabi G. Can functional food security decrease the epidemic of obesity and metabolic syndrome? A viewpoint. World Heart Journal. 2016;8(3):273.
  84. Liu S., Manson J. E. Dietary carbohydrates, physical inactivity, obesity, and the ‘metabolic syndrome’as predictors of coronary heart disease. Current Opinion in Lipidology. 2001;12(4):395-404.
    CrossRef
  85. Brand-Miller J. C., Holt S. H., Pawlak D. B., McMillan J. Glycemic index and obesity. The American Journal of Clinical Nutrition. 2002;76(1):281S-285S.
    CrossRef
  86. Riccardi G., Rivellese A. A. Dietary treatment of the metabolic syndrome—the optimal diet. British Journal of Nutrition. 2000;83(S1):S143-S148.
    CrossRef
  87. Feldeisen S. E., Tucker K. L. Nutritional strategies in the prevention and treatment of metabolic syndrome. Applied Physiology, Nutrition, and Metabolism. 2007;32(1):46-60.
    CrossRef
  88. Jenkins D. J., Wolever T. M., Taylor R. H., Barker H., Fielden H., Baldwin J. M., Goff D. V. Glycemic index of foods: a physiological basis for carbohydrate exchange. The American Journal of Clinical Nutrition. 1981;34(3):362-366.
    CrossRef
  89. McKeown N. M., Meigs J. B., Liu S., Saltzman E., Wilson P. W., Jacques P. F. Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. Diabetes Care. 2004;27(2):538-546.
    CrossRef
  90. Duffey K. J., Popkin B. M. High-fructose corn syrup: is this what’s for dinner?. The American Journal of Clinical Nutrition. 2008;88(6):1722S-1732S.
    CrossRef
  91. Schulze M. B., Manson J. E., Ludwig D. S., Colditz G. A., Stampfer M. J., Willett W. C., Hu F. B. Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. The Journal of the American Medical Association. 2004;292(8):927-934.
    CrossRef
  92. Keller U. Dietary proteins in obesity and in diabetes. International Journal for Vitamin and Nutrition Research. 2011;81(2):125.
    CrossRef
  93. Hu F. B., Van Dam R. M., Liu S. Diet and risk of type II diabetes: the role of types of fat and carbohydrate. Diabetologia. 2001;44(7):805-817.
    CrossRef
  94. Melanson E. L., Astrup A., Donahoo W. T. The relationship between dietary fat and fatty acid intake and body weight, diabetes, and the metabolic syndrome. Annals of Nutrition and Metabolism. 2009;55(1-3):229-243.
    CrossRef
  95. Papathanasopoulos A., Camilleri M. Dietary fiber supplements: effects in obesity and metabolic syndrome and relationship to gastrointestinal functions. Gastroenterology. 2010;138(1):65-72.
    CrossRef
  96. Schulze M. B., Schulz M., Heidemann C., Schienkiewitz A., Hoffmann K., Boeing H. Fiber and magnesium intake and incidence of type 2 diabetes: a prospective study and meta-analysis. Archives of Internal Medicine. 2007;167(9):956-965.
    CrossRef
  97. Weickert M. O., Möhlig M., Schöfl C., Arafat A. M., Otto B., Viehoff H., Pfeiffer A. F. Cereal fiber improves whole-body insulin sensitivity in overweight and obese women. Diabetes Care. 2006;29(4):775-780.
    CrossRef
  98. Chiasson J. L., Josse R. G., Gomis R., Hanefeld M., Karasik A., Laakso M. STOP-NIDDM Trial Research Group. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. The Lancet. 2002;359(9323):2072-2077.
    CrossRef
  99. Baik I., Shin C. Prospective study of alcohol consumption and metabolic syndrome–. The American journal of clinical nutrition. 2008;87(5):1455-1463.
    CrossRef
  100. Yoon Y. S., Oh S. W., Baik H. W., Park H. S., Kim W. Y. Alcohol consumption and the metabolic syndrome in Korean adults: the 1998 Korean National Health and Nutrition Examination Survey. The American journal of clinical nutrition. 2004;80(1):217-224.
    CrossRef
  101. Santilli F., Guagnano M. T., Vazzana N., La Barba S., Davi G. Oxidative stress drivers and modulators in obesity and cardiovascular disease: from biomarkers to therapeutic approach. Current Medicinal Chemistry. 2015;22(5):582-595.
    CrossRef
  102. Bahadoran Z., Golzarand M., Mirmiran P., Shiva N., Azizi F. Dietary total antioxidant capacity and the occurrence of metabolic syndrome and its components after a 3-year follow-up in adults: Tehran Lipid and Glucose Study. Nutrition & Metabolism. 2012;9(1):70.
    CrossRef
  103. Whayne Jr T. F., Maulik N. Nutrition and the healthy heart with an exercise boost. Canadian Journal of Physiology and Pharmacology. 2012;90(8):967-976.
    CrossRef
  104. Liu S., Song Y. Ford E. S., Manson J. E., Buring J. E., Ridker P. M. Dietary calcium, vitamin D, and the prevalence of metabolic syndrome in middle-aged and older US women. Diabetes Care. 2005;28(12):2926-2932.
    CrossRef
  105. Zemel M. B. Nutritional and endocrine modulation of intracellular calcium: implications in obesity, insulin resistance and hypertension. Molecular and Cellular Biochemistry. 1998;188:129–136.
    CrossRef
  106. Guerrera M. P., Volpe S. L., Mao J. J. Therapeutic uses of magnesium. American Family Physician. 2009;80(2).
  107. He K., Song Y., Belin R. J., Chen Y. Magnesium intake and the metabolic syndrome: epidemiologic evidence to date. Journal Of The Cardiometabolic Syndrome. 2006;1(5):351-35.
    CrossRef
  108. Bian S., Gao Y., Zhang M., Wang X., Liu W., Zhang D., Huang G. Dietary nutrient intake and metabolic syndrome risk in Chinese adults: a case–control study. Nutrition Journal. 2013;12(1):106.
    CrossRef
  109. Baudrand R., Campino C., Carvaja C. A., Olivieri O., Guidi G., Faccini G., Fardella C. E. High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome. Clinical Endocrinology. 2014;80(5):677-684.
    CrossRef
  110. Hu F. B. Dietary pattern analysis: a new direction in nutritional epidemiology. Current Opinion in Lipidology. 2002;13(1):3-9.
    CrossRef
  111. Grundy S. M., Cleeman J. I., Daniels S. R., Donato K. A., Eckel R. H., Franklin B. A., Spertus J. A. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement. Circulation. 2005;112(17):2735-2752.
    CrossRef
  112. Sjöström L., Lindroos A. K., Peltonen M., Torgerson J., Bouchard C., Carlsson B., Sullivan M. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. New England Journal of Medicine. 2004;351(26):2683-2693.
    CrossRef


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