Phytochemistry Reviews

, Volume 17, Issue 2, pp 351–377 | Cite as

Biomarkers of the metabolic syndrome: influence of selected foodstuffs, containing bioactive components

  • Harry Robberecht
  • Tess De Bruyne
  • Nina Hermans


The influence of various non-nutritive bioactive foodstuffs and food components on the biomarkers of the metabolic syndrome in humans is critically reviewed. Tea, coffee, cocoa, soy, olive oil, fruit and nuts are most of the time found to be effective in improving lipid profiles, CRP and adiponectin. Spices (garlic, curcumin and cinnamon), carotenoids and the phytosterol/-stanols are frequently related to lower risk of metabolic syndrome and improved biomarkers. Since food is a complex matrix and the heterogeneity of studied population and served diets are not always well-defined, this could explain some contradictory results found in literature. Other factors jeopardizing definite conclusions are mentioned.


Metabolic syndrome Biomarkers Foodstuffs Bioactive components 



α-Linoleic acid


Alanine aminotransferase


Body mass index


C-reactive protein


Cardiovascular disease


Docosahexaenoic acid




Eicosapentaenoic acid


Gamma aminobutyric acid


High-density lipoprotein




Homeostasis assessment-insulin resistance index


High sensitivity-CRP




Inducible nitric oxide synthetase


Low-density lipoprotein




Monocyte chemoattractant protein-1




Metabolic syndrome


Monounsaturated fatty acids


Nitric oxide


Oxidized LDL


Polyunsaturated fatty acids


Retinol-binding protein 4


Soluble intercellular adhesion molecule




Total cholesterol




Tumor necrosis factor-α


Very-low density lipoprotein




Metabolic syndrome (MetS), also called “insulin resistance syndrome” (DeFronzo and Ferrannini 1991), “deadly quartet” (Kaplan 1989), or “syndrome X” (Reaven 1988), is characterized by abdominal obesity, hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol level, increased blood pressure, and elevated serum glucose concentration (Grundy et al. 2005).

Although the exact mechanism underlying metabolic syndrome has not yet been completely elucidated, many cross-sectional or longitudinal studies have shown that MetS is strongly associated with insulin resistance (Lann and LeRoith 2007), oxidative stress (Onat et al. 2006), inflammation (Festa et al. 2000), endothelial dysfunction (Isomaa et al. 2001) and risk of cardiovascular diseases (Lakka et al. 2002; Hajer et al. 2007).

The basis of this endemic is either a diet too often characterized by excessive consumption of saturated and trans-esterified fatty acids, simple sugars and salt, either a sedentary lifestyle or a combination of both.

Most research groups use a mixture of biomarkers as risk factors for the occurrence of metabolic syndrome (Mansoub et al. 2006). Metabolic overload (high caloric intake) evokes oxidative stress, which can lead to low-grade inflammation and result in a cardiovascular risk. Therefore, due to this sequence of actions, dividing the biomarkers of MetS into four groups (dyslipidemias, markers of oxidative stress and inflammation, and cardio-metabolic markers) seems quite logic. We have discussed the biochemical action and clinical significance of these markers in an extensive review article (Robberecht and Hermans 2016).

Effect of various types of diets on biomarkers of MetS are reviewed (Robberecht et al. 2016a), while in two other articles we discussed the influences of minerals, oligo and trace elements (Robberecht et al. 2016b) and of caloric intake, various food groups and vitamins (Robberecht et al. 2017) on the biomarkers of MetS.

While some review papers focus on the dietary management of the MetS beyond macronutrients (Minich and Bland 2008; Graf et al. 2010; Davi et al. 2010; Cicero et al. 2014; Cicero and Colletti 2015), here we intend to discuss some foodstuffs, spices, containing various biologically active components and their effect on biomarkers of MetS.

Literature is screened by using keywords “metabolic syndrome”, “biomarkers” in combination with the selected foodstuffs and bioactive components. References from 2000 onwards are used or some important previous references cited therein.

We have tried to limit this report to papers reporting reviews, meta-analyses, or original clinical trials studying influence of the foodstuffs with bioactive components on biomarkers in humans with MetS.

However, the selection is not always that straightforward, since description of sampled population is sometimes poor defined.

Biological active food components


Certain dietary components and various plants can help in the prevention or amelioration of MetS by assisting homeostatic mechanisms.

Functional foods are foods (or food constituents) providing health benefits beyond the expected nutritional function, and including prevention and treatment of a disease (Davi et al. 2010; Suhaila 2014). Nutraceuticals are those foods or compounds thereof, marketed in a pharmaceutical dosage from such as tablets or capsules. Unfortunately, terminology is confusing, and sometimes both terms are being interchanged (Espin et al. 2007; Rubio-Ruiz et al. 2013; Kaur et al. 2015; Brown et al. 2015a, b; Cicero and Colletti 2015).

Also herbal-, food- or dietary supplements can contain those compounds, and sometimes they are referred to as phytochemicals or plant-derived therapeutics.

One way of dividing them up into major classes can be as follows:
  • dietary fibers (from fruit, beans, barley, oats)

  • antioxidant vitamins and provitamins (vitamin C, vitamin E and carotenoids)

  • polyphenols, also having antioxidant capacities (non-flavonoids, flavonoids and tannins, phyto-estrogens)

  • ω-3 fatty acids

  • spices (garlic, curcumin, cinnamon) (Cicero et Colletti 2015).

Key issues, such as bioavailability, metabolism, dose/response and toxicity of these food bioactive components are reviewed elsewhere (Espin et al. 2007; Ozen et al. 2012).

We are aware of the fact that bioactive components present are of various types of which some have different mechanisms of action and can display their activity in an additive, synergistic or antagonistic way. Sometimes there is a thin line between a nutraceutical and a drug. Therefore we have omitted the discussion on effect of fermented red yeast rice on biomarkers of the MetS (Patel 2016; Cicero et al. 2016), since this product can be classified as a food supplement or even as a drug.

Various foodstuffs


Although all types of Camellia siniensis derived beverages contain polyphenols, important differences exist between green, white and black tea.

Several different biologically active polyphenolic compounds might offer variable protection against a variety of human diseases.

The tea catechin epigallocatechin-3-gallate (EGCG) is generally considered to be the most active component (Lorenz 2013; Keske et al. 2015; Legeay et al. 2015). In cell cultures and animal models of obesity, tea components reduce adipocyte differentiation and proliferation, lipogenesis, fat mass, body weight, fat absorption, plasma levels of triglycerides, free fatty acids, cholesterol, glucose, insulin and leptin, as well as increase beta-oxidation and thermogenesis (Wolfram et al. 2006; Oh et al. 2009). Green tea extracts reduce adipogenesis by decreasing expression of transcription factor C/EBPα and PPArϒ during adipocyte differentiation (Yang et al. 2014a, b).

Human studies report reduced body weight and fat (Vieira Senger et al. 2012; Zhong et al. 2015), as well as increased fat oxidation and thermogenesis, as confirmed in animal findings (Hursel and Westerterp-Plantenga 2013). Green tea consumption (3 cups/day, 1 g/sachet) or extract supplementation (2 capsules/day) for 60 days significantly decreased body weight and BMI (Vieira Senger et al. 2012). Moreover it lowered lipid peroxidation (decreased malondialdehyde and hydroxynonenals) versus age- and gender-matched controls (Basu et al. 2010a, b, c). Green tea (4 cups/day) and polyphenolic extracts (2 capsules/day) significantly increased plasma antioxidant capacity and whole blood glutathione versus controls after 8 weeks (Basu et al. 2013). This supports the hypothesis that green tea may provide antioxidant protection in MetS (Gao et al. 2015), but the optimal dose has not yet been established (Hosoda et al. 2003; Tsuneki et al. 2004).

An exact report on the composition of the tea or tested extract is often lacking, and therefore the tested dose (e.g. 2 capsules/day with the extract) offers no information on the amount of specific components responsible for the observed activity. Moreover, also indications like “1 g tea/sachet” yield little information, since time of contact and water temperature strongly influence the amount of dissolved compounds.

Pooled analysis of six studies exploring the association between tea consumption and MetS resulted in the conclusion of decreased odds of MetS for individuals consuming more tea (type of tea not specified; Marventano et al. 2016).

The cardiovascular health promoting effects are primarily attributed to the antioxidant properties of EGCG (Imai and Nakachi 1995; Pearson et al. 1998; Princen et al. 1998; Serafini et al. 2000; Nakachi et al. 2000; Sasazuki et al. 2000; Sano et al. 2004; Sung et al. 2005; Basu et al. 2010a, b, c, 2013), although research in recent years has also uncovered their prooxidant properties (Lorenz 2013).

LDL-oxidation is found to be decreased in most cases (Pearson et al. 1998; Serafini et al. 2000; Sung et al. 2005; Basu et al. 2010a) and soluble vascular cell adhesion molecule-1 was decreased (Sung et al. 2005). CRP-concentration (Vernarelli and Lambert 2013) and a lipid profile modulation have been observed (Pearson et al. 1998; Sasazuki et al. 2000; Vernarelli and Lambert 2013; Grosso et al. 2014; Onakpoya et al. 2014), while other studies report no differences (Princen et al. 1998; Sung et al. 2005; Wolfram et al. 2006; Mielgo-Ayuso et al. 2014; Zhong et al. 2015). Sometimes this beneficial effect is observed only in women (Grosso et al. 2015).

Rye-bread enriched with green tea extract (intake of 210 mg of EGCG) did not influence the lipid parameters (Bajerska et al. 2015).

On the other hand, one publication could be traced which mentioned that frequent tea drinking is a risk factor for the MetS (Yu et al. 2014), without a clear cause/effect relationship.


Coffee is one of the most widely consumed beverages and rich in polyphenols, acting as antioxidants (Devasagayam et al. 1996; Shen 2012), but multiple mechanisms should underlie the beneficial effects of coffee consumption. Many different mechanisms have been proposed to contribute to the biological activity of polyphenols in affecting the MetS (Annuzzi et al. 2014; Amiot et al. 2016), including the regulation of cellular signals (Virgili and Marino 2008) and the modulation of the activity of numerous enzymes and redox-sensitive transcription factors.

Results of animal studies focusing on the effect of coffee consumption on the risk of MetS showed that supplementation attenuated the expected onset of an adverse profile in animals fed high-fat diets (Fukushima et al. 2009; Panchai et al. 2012a, b; Abrahao et al. 2013).

Human clinical and epidemiological studies and conclusions from review articles generally show an inverse association between coffee consumption and the risk of MetS (Hino et al. 2007; Matsuuraa et al. 2012; Takami et al. 2013; Mure et al. 2013; Uemura et al. 2013; Yesil and Yilmaz 2013; Nordestgaard et al. 2015; Shang et al. 2016), however the question of causality remains unsolved (Shang et al. 2016).

All components of MetS (blood pressure, glucose level, triglyceride concentration) except HDL-cholesterol were significant (p < 0.01) and inversely related to coffee consumption (Hino et al. 2007; Matsuuraa et al. 2012; Takami et al. 2013; Mure et al. 2013; Uemura et al. 2013; Yesil and Yilmaz 2013; Nordestgaard et al. 2015; Shang et al. 2016; Sarria et al. 2016).

The two longitudinal studies not showing statistically significant results were both from the same cohort (the Amsterdam Growth and Health Longitudinal Study) consisting of young persons with a low prevalence of MetS (Driessen et al. 2009; Balk et al. 2009). Therefore the lack of the association between coffee consumption and the MetS in that case might have been due to the specific characteristics of the investigated cohort, consisting of relatively healthy people.

Also in a Mediterranean population no direct association between caffeine intake and the biomarkers of MetS have been observed, however coffee and tea consumption was significantly related to reduced odds of MetS (Onakpoya et al. 2014).

Moderate coffee consumption showed a significant inverse association with MetS-related biomarkers possibly involving adiponectin, which is inversely associated with visceral fat accumulation (Mure et al. 2013).

Coffee consumption was also inversely associated with arterial stiffness (Uemura et al. 2013). This association may be partly mediated by reducing circulating triglycerides (Shang et al. 2016).

On the other hand, consumption of coffee, particularly instant coffee mix, may have harmful effects on MetS, perhaps deriving from a probable concomitant excessive intake of sugar and powder creamer (Kim et al. 2014).

The manuscript of Platt et al. (2016) claimed that caffeine impact on metabolic syndrome components is modulated by a CYP1A2 variant.


Cocoa (Theobroma cacao) is a dietary ingredient with worldwide popularity. It is often associated with the high-caloric confection and chocolate, but it is also consumed via diverse foods and beverages.

Mechanisms by which cocoa flavanols improve MetS and related disorders were recently published by Strat et al. (2016). A number of observational and clinical studies indicated that cocoa or cocoa-containing products may improve CVD-related risk factors such as LDL-oxidation, inflammation (Ding et al. 2006; Fernandez-Murga et al. 2011; Gu and Lambert 2013; Amiot et al. 2016), endothelial function (Davison et al. 2008; Davison and Howe 2015) and the blood lipid profile (Jia et al. 2010; Shrime et al. 2011; Tokede et al. 2011). Dose–response relationship (Uemura et al. 2013), as well as the underlying mechanisms of action still need to be clarified more (Gu and Lambert 2013).

Several clinical studies showed that cocoa increases HDL-cholesterol concentrations (Mursu et al. 2004; Baba et al. 2007; Mellor et al. 2010; Khan et al. 2012), although other studies did not confirm such a beneficial effect (Wan et al. 2001; Engler et al. 2004; Balzer et al. 2008; Muniyappa et al. 2008; Tokede et al. 2012). The reason for this still remains to be explained. However, amount of consumption (Buitrago-Lopez et al. 2011), type of chocolate and percentage of containing cocoa should be considered (Tokede et al. 2012). Polyphenol-rich dark chocolate offers metabolic benefits on biomarkers of cardiovascular risk (Almoosawi et al. 2012).

It is not clear whether flavonoids (Galleano et al.; 2012) or possibly another bioactive component of cocoa (f.i., theobromine; Nuefingerl et al. 2013) are responsible for the reported increase in serum or plasma HDL-cholesterol.

A randomized controlled trial proved that theobromine independently increased serum HDL-cholesterol concentrations (Nuefingerl et al. 2013). However, to deliver 850 mg theobromine (the daily dose which was provided in that study) about 100 g dark or 200 g milk chocolate are needed (Smit 2011).

Combinations of whey protein isolate and cocoa polyphenols improved adiponectin level as was proven in a recent study (Campbell et al. 2016).


Soy products, which are a rich source of antioxidants and isoflavones also contain specific proteins and peptides, which attracted significant attention for their possible health effects (Matthan et al. 2007).

The cholesterol-lowering effect of soy is one of the well-documented physiological effects.
  1. (a)



Earlier studies have attributed the health benefits of soy primarily to its isoflavonoids (Wong et al. 1998). This fraction, consisting primarily of genistein, dadzein and glycitein, has been shown to have a hypocholesterolemic effect in animals and humans (Potter 1998).

Although meta-analysis revealed that the isoflavonoid content of soy might be responsible for this, there is no direct dose–response relationship between soy isoflavone content and its lipid-lowering effect (Zhuo et al. 2004).

Data on the effects of separate isoflavones on metabolic health are limited (Amani et al. 2005). Some studies have indicated that genistein, as a main isoflavone in soy products, might affect cardiovascular health through its inhibitory effect on tyrosine kinase (Anderson et al. 1995).
  1. (b)

    Proteins and peptides


In addition to the isoflavonoids, many other compounds in soy products, such as saponins, beta-conglycinin (7S globulin) protein fractions, dietary fiber, and unsaturated fats might be beneficial.

Some in vitro studies have shown that a 7S globulin protein present in soy possibly up-regulates LDL receptors thereby reducing serum LDL concentrations (Wong et al. 1998).

Regular consumption of soy proteins can result in significant reductions in total cholesterol (9.3%), LDL-cholesterol (12.9%), and triglycerides (10.5%), with a small but insignificant increase (2.4%) in high-density lipoprotein cholesterol. Linear regression analysis indicated that the threshold level of soy intake at which the effects on blood lipids became significant was 25 g.

Although the findings on lipid profiles are somewhat conflicting, the combined results of a meta-analysis have suggested significant reductions of 9% in total serum cholesterol concentration, 13% in LDL-c, and 12% in triglycerides with an average consumption of 47 g/day of soy protein (Potter 1998).

It has been hypothesized that also the unique amino acid profile of soybean might have an influence on the effects (Taku et al. 2007; de Souza Ferreira et al. 2011). Experimental data have shown hypercholesterolemic effects of lysine and methionine, but a hypocholesterolemic effect of arginine. Therefore, the higher arginine to lysine and methionine ratio in soy might explain, in part, its hypocholesterolemic effect (Cederroth and Nef 2009).
  1. (c)

    Soy, as a whole product


Soy bean is a whole-soy product that contains all beneficial ingredients of soy. Various soy products are obtained through different processing methods. Due to processing-induced ingredient loss, each product has different composition of soybean ingredients. For instance, alcohol extraction and acid precipitation used to produce soy protein results in isoflavone loss (Zhang et al. 2009). Other procedures can alter soy bean fiber, fat, sugars, phytic acid, and saponin content (Zhang et al. 2009).

The potential mechanisms by which soy protein and/or isoflavonoids induce a decrease of blood cholesterol concentrations include thyroid status, bile acid balance and the estrogenic effects of genistein and daidzein. Studies have further indicated that isoflavones exhibit antioxidant properties (Khan et al. 2013).

Findings on the effect of soy consumption on serum apolipoprotein levels in both normal and hyperlipidemic individuals are inconsistent (McVeigh et al. 2006; Blachier et al. 2010).

Earlier studies on soy and inflammation have shown conflicting results too (Blum et al. 2003; Beavers et al. 2009; Bakhtiary et al. 2012). It seems that the effects of soy consumption on inflammation are product-dependent. While the beneficial effects of soy bean and soy milk consumption on inflammation have been shown, textured soy protein or isoflavone supplements alone are reported to be neutral (Reinwald et al. 2010). Co-existence of unsaturated fats along with lecithin, isoflavones, essential fatty acids, phytosterols, polyphenols, inositol, and dietary fiber as well as other bioactive compounds make soy bean a more effective food than other soy products in improving metabolic abnormalities (Reinwald et al. 2010; Bakhtiary et al. 2012).

Consumption of soy and soy-products also seems to affect cardio-metabolic health to a variable extent, which sometimes was gender-dependent (Azadbakht et al. 2007a; Pan et al. 2008).

The reduction in cardiovascular risk in postmenopausal women was greater among producers of equol, an estrogen metabolite (Azadbakht et al. 2007a).

The reduced risk can occur via various components and mechanisms (lowering total and LDL-cholesterol and glucose; Simao et al. 2014), to which blood pressure lowering effect can be added.

Increased adiponectin and NO values could be responsible for this effect (Simao et al. 2010; Simão et al. 2012).

Studies are required to determine the optimal amounts of soy bean and soy protein for inclusion in the diets of patients with MetS (Azadbakht and Esmaillzadeh 2012).

Experimental studies as well as randomized clinical trials have demonstrated a role for soy products in the management of MetS (Dyrskog et al. 2005; Azadbakht et al. 2007a, b, c; Bahls et al. 2011; Bakhtiary et al. 2012). Bakhtiary et al. (2012) found that both textured soy protein or soy bean consumption for 12 weeks resulted in reduced levels of serum total- and LDL-cholesterol, apolipoprotein B100, and VLDL concentration in addition to increased levels of serum apolipoprotein A1. However, the authors have failed to find significant effects on serum hs-CRP, fibrinogen, triglyceride, and HDL levels, as well as on blood pressure.

Azadbakht et al. (2007c) reported a similarity in the lipid profile, however they also observed beneficial effects of soy bean consumption on inflammatory biomarkers (2007b) and proved an enhanced antioxidant status (Azadbakht et al. 2007a).

In postmenopausal women with MetS on a soy diet, significant reductions in blood pressure, TG, CRP and sICAM were noted among equol (an estrogen metabolite) producers (Acharjee et al. 2015).

Supplementation of soy products in combination with other phytochemicals resulted in better lipid profiles (Lerman et al. 2008, 2010; Jones et al. 2012; Lee et al. 2012; Guevara-Cruz et al. 2012; Simao et al. 2014) or increased adiponectin (Guevara-Cruz et al. 2012).

Olive oil

Olive oil consumption has proven beneficial effects on lipid profile (Anderson-Vasquez et al. 2015), fatty acid composition (Mayneris-Perxachs et al. 2014), insulin sensitivity, lipid and DNA oxidation (Mtjavila et al. 2013; Venturini et al. 2015), inflammation, endothelial function, thrombotic factors and blood pressure (Lopez-Miranda et al. 2008). Therefore olive oil is considered as a key food for preventing metabolic syndrome, related micro-inflammation (Viscogliosi et al. 2013) and a reduced cardiovascular risk (Ros et al. 2014; Covas et al. 2015).

Several studies have suggested that olive oil in hyperlipidemic patients could reduce the susceptibility of LDL to oxidation, not only because of its high monounsaturated fatty acid content (Ruidavets et al. 2007), but probably also because of the antioxidative activity of its phenolic compounds (Masella et al. 2001). Virgin olive oil containing phenolics (Rigacci and Stefani 2016) shows a more pronounced antioxidant effect on this LDL oxidation than refined olive oil (Fito et al. 2000; Sialvera et al. 2012; Oliveras-Lopez et al. 2014) and reduces the postprandial inflammatory response (Camargo et al. 2014).

Hydroxytyrosol, an ingredient of olive oil, reduces triglyceride accumulation and promotes lipolysis in adipocytes (Stefanon and Colitti 2016).

Vissers et al. (2004) however claimed, after reviewing bioavailability and antioxidant effect of olive oil phenols, that there was no evidence that consumption of polyphenols in the amounts provided by dietary olive oil will protect LDL against oxidative modification to any important extent.

Virgin olive seems to repress in vivo expression of several pro-inflammatory genes (Camargo et al. 2010).

A Mediterranean dietary pattern, characterized by a high consumption of nuts and olive oil, has been associated with a reduced risk of MetS (Martinez-Gonzalez and Martin-Calvo 2013).

The relationship between Mediterranean diet, olive oil and MetS and potential mechanisms by which this food can help in disease prevention and treatment are discussed (Soriguer et al. 2007; Perez-Martinez et al. 2011).

An olive oil diet rich in MUFA, but with low α-linolenic acid (ALA) content, resulted after a 6-month period in reduced levels of total and LDL-cholesterol (Baxheinrich et al. 2012).

Olive oil consumption has only marginal beneficial effects on serum resistin levels in healthy men (Machowetz et al. 2008).


This group contains a lot of different fruits, berries, juices, and phytochemicals. We intend to divide them in berries, citrus fruits and miscellaneous others, although any division has some limitations (common use of term “berry”, instead of botanical use). The intention is not to go to different botanical plant parts, but rather categorize herbal foods according to their common consumption.


Interventional studies on the therapeutic roles of strawberries, blueberries and cranberries in MetS have demonstrated the following effects: strawberries lowered total and LDL-cholesterol, but not triglycerides and decreased biomarkers of atherosclerosis (malondialdehyde and adhesion molecules); blueberries lowered systolic and diastolic blood pressure and lipid oxidation and improved insulin resistance; and low-caloric cranberry juice selectively decreased biomarkers of inflammation (adhesion molecules) in MetS (Basu and Lyons 2012).

These observations could be due to an up-regulation of endothelial nitric acid synthase activity, reduction of renal oxidative damage, and inhibition of carbohydrate digestive enzymes or angiotensin-converting enzyme by the berries (Basu and Lyons 2012).

Strawberries are an especially good source of phytochemicals, particularly anthocyanins and ellagic acid, which have potent antioxidant and anti-inflammatory functions (Hannum 2004).

Short-term supplementation of freeze-dried strawberries appeared to exert hypocholesterolemic effects and decreased lipid peroxidation in women with MetS (Basu et al. 2009).

Plasma oxidized LDL, serum malondialdehyde and hydroxynonenal concentration decreased in a group with MetS eating blueberries. The authors claimed that selected features of the syndrome and related cardiovascular risk factors can be improved at dietary achievable dosis (Basu et al. 2010b).

Vascular cell-adhesion molecule-1 levels decreased after strawberry supplementation (50 g/day) (Basu et al. 2010c).

Cranberry juice significantly increased plasma antioxidant capacity and decreased oxidized low-density lipoprotein and malondialdehyde. However, the consumption does not cause a significant improvement in blood pressure, glucose, lipid profiles, C-reactive protein, and IL-6 (Basu et al. 2011). Folic acid and adiponectin were increased and homocysteine and oxidative stress were reduced (Simao et al. 2013).

On the other hand, low-calorie cranberry juice lowers markers of cardiometabolic risk, including blood pressure and circulating CRP, triglyceride, and glucose concentration in healthy adults (Novotny et al. 2015).

In addition to the widely recognized antioxidant power of berry extracts, both commercial berry varieties and wild species have been linked to hypoglycemic activity, inhibition of adipogenesis, amelioration of CVD risk factors, anti-inflammatory capacity and ability to induce satiety and counteract overweight (Lila 2011). Proanthocyanidins or anthocyanins may be the active agents.

Lowering the levels of alanine aminotransferase (ALAT) may be regarded as nutritionally significant by enhancing the liver function (Lehtonen et al. 2010), but berries and berry fractions have various other but slightly positive effects on vascular cell adhesion molecule and intercellular adhesion molecules (Lehtonen et al. 2011).

Consumption of fruit pulp from berries of Euterpe oleracea Mart. resulted in a reduction of total cholesterol, but no effect on blood pressure was hs-CRP was observed (Udani et al. 2011).

Bilberries (Vaccinium myrtillus) reduce low-grade inflammation in individuals with features of MetS: lower hs-CRP, IL-6, IL-12 and lipopolysaccharides (Kolehmainen et al. 2012). Diets high in fatty fish, bilberries and whole grain products lower plasma E-selectin and hs-CRP (de Mello et al. 2011).

A recent review indicates that regular long-term consumption of different berries could potentially delay the progression of MetS and comorbidities (Kowalska and Olejnik 2016).

Citrus fruits

Citrus flavonoids constitute an important source of flavonoids and were found to display strong anti-inflammatory and antioxidant activities. Several lines of investigations suggest that naringin supplementation is beneficial for the treatment of obesity, diabetes, hypertension, and MetS. A number of molecular mechanisms underlying these activities have been elucidated (Alam et al. 2014). Their effect on obesity and MetS still remains to be fully established.

Naringenin is claimed to prevent dyslipidemia, apoB overproduction and hyperinsulinemia in LKL-receptor null mice with diet-induced insulin resistance (Mulvihill et al. 2009).

Daily intake of 300 ml of a citrus-based juice during 6 months improved the biomarkers of oxidative stress in MetS (Bernabé et al. 2013). Also lipid profile and inflammation markers were improved after consumption of a citrus-based juice (Mulero et al. 2012).

Hesperidin, a citrus flavonoid glycoside, and its metabolite hesperetin have vascular actions with health benefits. Hesperidin treatment increased flow-mediated dilation and reduced concentration of circulating inflammatory biomarkers (hs-CRP, serum amyloid A protein and soluble E-selectin) (Rizza et al. 2011).

Daily consumption (twice a day) of grape fruit for 6 weeks reduces urine F2-isoprostanes in overweight adults but has no effect on plasma hs-CRP or soluble vascular cellular adhesion molecule-1 (Dow et al. 2013).

Pure orange juice consumption is associated with lower total and LDL-cholesterol and LDL-cholesterol serum levels (O’Neil et al. 2012a).

Other fruits

Higher intakes of fruit and vegetables are associated with a lower risk of MetS. This may be the result of lower CRP concentrations (Esmaillzadeh et al. 2006). However, encapsulated fruit and vegetable fruit powder concentrates did not alter insulin or glucose measures in a sample of adults with MetS (Ali et al. 2011).

A meta-analysis of randomized controlled trials suggested that there is an inverse association between fruit and vegetable consumption and diastolic blood pressure in MetS-patients (Shin et al. 2015).

Consumption of 46 g of lyophilized grape powder resulted in an increased level of plasma adiponectin, and IL-10 and in increased expression of inducible nitric oxide synthase (iNOS) only in patients without dyslipidemia. This suggested that grape consumption shows an anti-oxidative and anti-inflammatory action in absence of the inflammatory status associated with dyslipidemias (Barona et al. 2012a, b). It increases anti-inflammatory markers and upregulates nitric oxide synthase even in the absence of dyslipidemias in men with MetS (Barona et al. 2012a, b).

Resveratrol is a stilbene with main dietary sources grapes, rhubarb and red wine. Supplementation with this compound in various amounts and duration does not result in significant changes of oxidative and inflammatory markers, neither did it changes the lipid profiles (Fujita et al. 2011; Dash et al. 2013; Mendez-del Villar et al. 2014; Van der Made et al. 2015).

Consumption of fruit and vegetables in the US were lower among people with MetS (Ford et al. 2003). These foodstuffs contribute to an increased dietary intake of antioxidants, resulting in an oxLDL decrease. Moreover, a decrease in BMI, waist circumference, fat mass and triglyceride levels was associated with the decreased oxLDL levels (De la Iglesia et al. 2013).

The presence of antioxidant vitamins (Robberecht et al. 2017) in fruit may be a contributing factor to a risk reduction of MetS as was observed in a long-term supplementation study. Baseline serum antioxidant concentrations of β-carotene and vitamin C were negatively associated with the risk of MetS (Czernichow et al. 2009).

A mangosteen juice blend reduced CRP-levels, but other markers of inflammation (inflammatory cytokines) or a marker of lipid peroxidation (F2-isoprostane) did not show any significant differences when compared with placebo (Udani et al. 2009).


The commonly used term”nut” encompasses a wide range of seeds that based on botanical definitions, may not actually be nuts. While hazelnuts meet the botanical definition of nut, almonds, pistachios and walnuts, which are all seeds of stone fruits or drupes, do not. Despite this inconsistency, this variable group of seeds has been clustered together under the collective term “tree nuts”.

Tree nuts are healthy foods because of their fatty acid profile (low in saturated fats and high in mono- and polyunsaturated fats (MUFA and PUFA, respectively) and low available carbohydrate content, as well as being good sources of vegetable protein, fibre, phytosterols, polysterols, vitamins and minerals (Phillips et al. 2005; Segura et al. 2006).

Nuts may therefore be a useful component of a dietary strategy aimed at improving the risk factors of the MetS, diabetes and CVD (O’Neil et al. 2015; Brown et al. 2015a, b).

The ability of nuts to improve the blood lipid profile (Blanco Mejia et al. 2014) and reduce the CVD risk is now well established (Kendall et al. 2010; Lee et al. 2014).

Pooled analyses of clinical trials showed that nut intake is inversely related to triglyceride concentrations only in subjects with hypertriglyceridemia. An inverse association was found between the frequency of nut consumption and the incidence of MetS (Salas-Salvado et al. 2014).

Out-of-hand nut consumption (1/4 oz or more per day) is associated with higher HDL-cholesterol and lower CRP-levels (O’Neil et al. 2012b). This biomarkers of low-grade inflammation (CRP), together with leucocyte and platelet count) is reduced in nut consumers (Bonaccio et al. 2015).

Compared with a low-fat diet, a Mediterranean diet enriched in nuts (Salas-Salvado et al. 2008), or olive oil and nuts (Babio et al. 2014) could be beneficial for MetS management (Urpi-Sarda et al. 2012). Nuts and virgin olive oil are regarded as key foods of the Mediterranean diet affecting inflammatory biomarkers (IL-6, TNF-receptor, intercellular adhesion molecule 1), related to atherosclerosis (Urpi-Sarda et al. 2012). Probably this could be explained by the moderation of inflammation and oxidation, resulting in an improved endothelial function (Salas-Salvado et al. 2008).

Protection against LDL oxidation by nut intake has been documented in some, but not all, clinical studies (Mukuddem-Petersen et al. 2007; Lopez-Uriarte et al. 2010). Regarding inflammation, cross-sectional studies have shown that nut consumption is associated with lower concentrations of circulating inflammatory molecules and higher levels of adoponectin, a potent anti-inflammatory adipokine (Ros 2009).

Short-term walnut consumption increased circulating total adiponectin and apolipoprotein A concentrations, but does not affect other markers of inflammation in obese humans with MetS (Aronis et al. 2012). A diet enriched with this type of nuts reduced fasting non-HDL-cholesterol and apolipoprotein B in healthy subjects (Wu et al. 2014).

Beneficial effects of walnut consumption on vascular activity and endothelial function may be ascribed to several constituents of the nut: l-arginine, α-linolenic acid and polyphenolic antioxidants (Katz et al. 2012). The effect on haemostatic factors was not observed for high walnut and cashew diets (Pieters et al. 2005).

The inclusion of 2 portions of pistachios in a moderate-fat diet favourably affects the cardiometabolic profile (lower LDL level and TAG/HDL-ratio) (Holligan et al. 2014).

Contradictory results found in literature [a weak (Jaceldo-Siegl et al. 2014), no correlation (Mukuddem-Petersen et al. 2007) or only an improved insulin sensitivity (Casas-Agustench et al. 2011)] could be due to the variability of the diet and additional components (olive oil, nuts).

Table 1 summarizes most important effect of the various foodstuffs on biomarkers of MetS.
Table 1

Effect of various foodstuffs on biomarkers of MetS



Risk of MetS




Six studies


Imai and Nakachi (1995)


Devasagayam et al. (1996)


Nakachi et al. (2000), Vernarelli et al. (2013), Basu et al.(2013)

Cell adhesion molecule↓

Vernarelli et al. (2013)


Grosso et al. (2014)

Improved lipid profile

Princen et al. (1998), Serafini et al. (2000), Sasazuki et al. (2000)


Sano et al. (2004), Grosso et al. (2014)


Mielgo-Ayuso et al. (2014), Onakpoya et al. (2014), Grosso et al. (2015)


Serafini et al. (2000), Oh et al. (2009), Vernarelli and Lambert (2013)

No difference

Bajerska et al. (2015)



Imai and Nakachi (1995), Matsuuraa et al. (2012), Takami et al. (2013)


Mure et al. (2013), Uemura et al. (2013), Yesil and Yilmaz (2013)


Nordestgaard et al. (2015), Shang et al. (2016), Sarria et al. (2016)

TG↓, HDL-c↑

Driessen et al. (2009), Matsuuraa et al. (2012)

No relation

Balk et al. (2009), Kim et al. (2014)

Reduced odd

Grosso et al. (2015)



Uemura et al. (2013)



Sarria et al. (2016)



Davison et al. (2008), Fernandez-Murga et al. (2011)


Gu and Lambert (2013), Amiot et al. (2016)



Wan et al. (2001), Mursu et al. (2004), Wang-Polagruto et al. (2006), Mellor et al. (2010), Khan et al. (2012)


Engler et al. (2004), Balzer et al. (2008). Muniyappa et al. (2008)

No effect


Buitrago-Lopez et al. (2011), Tokede et al. (2012)


Galleano et al. (2012)

Polyphenol-rich chocolate

Improved cardiomarkers

Nuefingerl et al. (2013)



Smit (2011)








Zhuo et al. (2004)



Potter (1998)


TC↓, LDL-c↓

Zhuo et al. (2004), Reinwald et al. (2010)



Zhuo et al. (2004)


apoA1↑, apoB100↓

Reinwald et al. (2010)



Cederroth and Nef (2009), Zhang et al. (2009)


de Souza Ferreira et al. (2011)


Improved lipid profile

Bahls et al. (2011)


Inflammation markers↓

Bahls et al. (2011)



Lerman et al. (2008)


Improved lipid profile

Lerman et al. (2010), Jones et al. (2012), Lee et al. (2012)


Azadbakht and Esmaillzadeh (2012), Guevara-Cruz et al. (2012)


Simao et al. (2014), Anderson-Vasquez et al. (2015)



Simao et al. (2014)

Olive oil

Improved lipid profile

Mayneris-Perxachs et al. (2014)


Ros et al. (2014)


TC↓, LDL-c↓

Machowetz et al. (2008)




Hannum (2004), Basu et al. (2010a)



Hannum (2004)



Hannum (2004), Basu et al. (2010b)

Cranberry juice


Novotny et al. (2015)

Cranberry juice


Lila (2011)


hs-CRP↓, IL-6↓, IL-12↓

Kolehmainen et al. (2012)

Citrus fruit

Oxidative stress↓

Bernabé et al. (2013)

Citrus fruit

hs-CRP↓, amyloidA↓,selectin↓

Rizza et al. (2011)

Grape fruit

No effect on hs-CRP

Dow et al. (2013)

Orange juice

TC↓, LDL-c↓

O’Neil et al. (2012a)



Udani et al. (2009)


High walnut, cashew nut

No effect

Mukuddem-Petersen et al. (2007)

Improved lipid profiles

Lee et al. (2014)

HDL-c↑, CRP↓

O’Neil et al. (2012b)


Ros (2009)


Adiponectin↑, apoA↑

Aronis et al. (2012)


apoB↑, non-HDL-c↓

Wu et al. (2014)

Brazil nut

Improved lipid profiles

Maranhao et al. (2011)

Brazil nut

Oxidative markers↓

Maranhao et al. (2011)

apoA1: apolipoprotein A1; apoB: apolipoproteinB; apoB100: apolipoprotein B100; CRP: C-reactive protein; HDL-c: high-density lipoprotein cholesterol; hs-CRP: high-sensitivity CRP; IL-6: interleukin-6; interleukin-10; LDL-c: low-density lipoprotein cholesterol; non-HDL-c: non-HDL-cholesterol; sICAM: soluble intercellular adhesion molecule; TC: total cholesterol; TG: triglycerides



Garlic (Allium sativum) belongs to the group of plants with medicinal and health supporting activity. Garlic health benefits result from the content of over 200 biologically active substances (Swiderski et al. 2007).

Individuals with MetS frequently have significantly higher levels of IL-6, TNF-α and lower levels of adiponectin, than those without MetS (Swiderski et al. 2007; Maury and Brichard 2010; Koster et al. 2010; Chakraborty et al. 2010). Of the clinical trials conducted to evaluate the effect of garlic on inflammatory cytokines, three have shown that garlic has an effect on these biomarkers (Williams et al. 2005; Van Doorn et al. 2006; Sharifi et al. 2010). One study (Gomez-Arbelaez et al. 2013) claimed that 12 weeks administration of aged garlic extracts increased plasma adiponectin in patients with MetS. This suggests that garlic might be useful to increase this biomarker and prevent cardiovascular complications in individuals with MetS.

Supplementation of aged black garlic (6 g/day for 12 weeks) reduced atherogenic markers (increased HDL-cholesterol and decreased apo-lipoprotein B) in patients with mild hypercholesterolemia (Jung et al. 2014).

Garlic, fermented with Monascus pilosus, decreased triglyceride and cholesterol in serum of normal to mildly hyperlipidemic individuals (Higashikawa et al. 2012).

Human reports are quite scarce (Hosseini and Hosseinzadeh 2015), however, studies in rats demonstrate that raw garlic homogenate (Padiya et al. 2011; Al-Rasheed et al. 2014) or S-methyl-l-cysteine, a hydrophilic cysteine-containing compound found in garlic (Thomas et al. 2015), is effective in improving insulin sensitivity while attenuating MetS and oxidative stress in fructose-fed rats.

The abundant data in literature on the beneficial influence of garlic on lipid parameters in animal studies are not confirmed in clinical trials, maybe due to (1) the doses of garlic used in the human trials are far below those used in animal studies; (2) the different garlic products (fresh or cooked, aged or fresh, fermented, black garlic or garlic extracts) (Gorinstein et al. 2005), which are composed of different organosulfur compounds, of which the concentration changes after the treatment; (3) the omitted importance of bioavailability; (4) the different response to garlic by specific groups, and (5) soil composition, in which the garlic is cultivated (Zheng et al. 2013).


Curcumin (diferuloylmethane) is a yellow-orange pigment of Curcuma longa rhizomes (turmeric). This molecule has been shown to be safe (Di Pierro et al. 2015) and interact with multiple molecular targets that are involved in the pathogenesis of MetS (Sahebkar 2013) and other diseases (Pulido-Moran et al. 2016).

Curcumin has antihyperglycemic and insulin sensitizer effects (Ghorbani et al. 2014).

The anti-diabetic activity was partly due to the induction of heme-oxygenase-1 activity (Son et al. 2013).

Other experiments demonstrated the lipid-lowering effect of curcumin in cell culture and animal models (Yao et al. 2014) or of curcumin or a curcuminoids-piperine combination in humans (Panahi et al. 2014; Yang et al. 2014a, b). Curcumin improved serum levels of adiponectin and leptin in patients with MetS (Panahi et al. 2016).

A systemic review and meta-analysis of randomized controlled trials investigating the effects of curcumin on blood lipid levels proved that there was apparently no effect when considering heterogeneous populations (Sahebkar 2014). Therefore, proposed cardiovascular protective effects of curcumin could be attributed to mechanisms other than lipid lowering and HDL-C enhancing activities. Some examples may be improvement of lipid peroxidation (Soni and Kuttan 1992) and LDL-oxidation (Xu et al. 2007), platelet aggregation (Mayanglambam et al. 2010), thrombosis (Srivastava et al. 1985; Shah et al. 1999), vascular smooth muscle cell proliferation (Chen and Huang 1998), endothelial dysfunction (Ramaswammi et al. 2004; Rungseesantivanon et al. 2010) and inflammation (Jurenka 2009). Curcumin is considered as an orally applied blocker of TNF and other pro-inflammatory biomarkers (Aggarwal et al. 2013).

Studies to prove that curcumin can be used as an alternative approach against MetS have involved a small number of subjects and been of short duration (Perez-Torres et al. 2013). Future studies are needed to prove the preventive effect.

The possible limited bioavailability of this compound and the combination with other components also ought to be taken into account (Cherniak 2011). Very recently a manuscript reviews the essential medicinal chemistry of curcumin and provides evidence that curcumin is an unstable, reactive, nonbioavailable compound (Nelson et al. 2017).


Common cinnamon (Cinnamomum verum, C. zeylanicum) has a long history of use as a spice, flavoring agent, preservative, and pharmacological agent. It is traditionally used to treat elevated blood sugar levels (Broadhurst et al. 2000).

Different publications deal with this spice on reducing risk factors associated with diabetes (Khan et al. 2003), MetS and cardiovascular disease in animal models (Couturier et al. 2010) and man (Ziegenfuss et al. 2006; Qin et al. 2010; Power and Pratley 2011; Shen et al. 2012; Cicero et al. 2014). Especially lipid profiles are improved (Khan et al. 2003).

Table 2 summarizes most important effect of spices on biomarkers of MetS.
Table 2

Effect of spices on biomarkers of MetS

Type of spice

Risk of MetS




No effect

Inflammatory cytokines

Sharifi et al. (2010)

Aged garlic


Gomez-Arbelaez et al. (2013)

Aged black garlic

HDL-c↑, apoB↓

Jung et al. (2014)

Fermented garlic

TG↓, TC↓

Higashikawa et al. (2012)


Improved lipid profiles

Yang et al. (2014a, 2014b)

Adiponectin↑, improved leptin

Panahi et al. (2016)

No effect on lipid profile

Sahebkar (2014)



Ziegenfuss et al. (2006), Qin et al. (2010)


Power and Pratley (2011)


Shen et al. (2012)


Cicero et al. (2014)


Improved lipid profiles

Khan et al. (2003)

apo B: apolipoprotein B: HDL-c: high-density lipoprotein-cholesterol; TC: total cholesterol; TG: triglycerides

Specific bioactive components in foodstuffs

We have selected some specific groups of biologically active compounds with promising effects on the biomarkers of MetS. Representatives of a certain group show similar activities, thus, although the compounds are present in various foodstuffs, we chose to discuss these groups separately.

ω-3 Fatty acids

Reviews on the role of ω-3 fatty acids in obesity, metabolic syndrome, and cardiovascular diseases are published (Carpentier et al. 2006; Gillingham et al. 2011; Hosseinpour-Niazi et al. 2015).

Beneficial effects of type of fatty acids on lipid profiles (Ebrahimi et al. 2009; Pirillo and Catapano 2013; Tardiva et al. 2015; Bays et al. 2015), markers of inflammation (Ebrahimi et al. 2009; Khorsan et al. 2014; Tardiva et al. 2015; Tortosa-Caparros et al. 2016; Masquio et al. 2016) or autoimmunity (Ebrahimi et al. 2009) have been published and very recently reviewed (Robberecht et al. 2017).

Phytosterols and stanols

The term “phytosterols’ refers to sterols and stanols, lipophilic triterpenes of plant origin (Rondanelli et al. 2013).

Plant sterols and stanols are structurally related to cholesterol, but are characterized by an extra ethyl (sitosterol) or methyl group (campesterol) in the side chain (Grundy 1983; Normen et al. 2000).

Sitosterol, campesterol and stigmasterol are the most common plant sterols in nature (Heinemann et al. 1993). Stanols, like sitostanol and campestanol are saturated plant sterols, which are found in nature in much smaller amounts than plant sterols.

Recent meta-analyses have summarized the results of more than 100 randomized clinical trials and have established that LDL-cholesterol is reduced by 9–12% with consumption of phytosterol-fortified foods at doses of 2–3 g/day (Cofan and Ros 2015).

Molecular actions of phytosterols and stanols in synthesis and absorption of cholesterol (Assmann et al. 2007; Carpe-Berdiel et al. 2009) or lipoprotein metabolism (Plat and Mensink 2009; Gylling and Simonen 2015) are published.

It seems obvious that the most atherogenic lipoprotein particles are diminished by phytosterol and stanol treatment (Gylling and Simonen 2015).

After 2 months supplementation with phytosterols and -stanols, a significant reduction in total cholesterol, LDL-cholesterol, small and dense LDL levels, as well as, apoB and triglyceride concentrations were observed. No differences were found in levels of HDL-c, apoA1, glucose, CRP, fibrinogen levels and blood pressure (Sialvera et al. 2012).

One publication claimed that a low intestinal cholesterol absorption is associated with a reduced efficacy of phytosterols as hypolipemic agents in patients with MetS (Hernandez-Mijares et al. 2011), which could explain the observations of Ooi and coworkers, who did not observe an influence of plant sterol supplementation on lipid or lipoprotein metabolism (Ooi et al. 2007).

Phytosterols and/or stanols are claimed to improve endothelial dysfunction in subjects at risk for cardiovascular diseases (Baumgartner et al. 2011).

Regular intake of phytosterols-enriched food did not significantly change CRP, but further studies with higher doses may provide more definite conclusions on a potential anti-inflammatory effect of this phytosterol intake (Rocha et al. 2016).

Supplementation does not affect plasma antioxidant capacity in patients with MetS (Sialvera et al. 2013).

Nutritional supplementation with essential amino acids and phytosterols (Coker et al. 2015), as well as with soy protein, phytosterols, hops rho iso-alpha acids and Acacia nilotica (gum Arabic tree) proanthocyanidins may reduce risk for MetS and cardiovascular disease in overweight individuals with hyperlipidemia (Lerman et al. 2010) or hypercholesterolemia (Lerman et al. 2008).

Low glycemic index diet with 30 g soy protein and 4 g of phytosterols/day showed statistically significant decreases of total cholesterol (15%) and triglycerides (45%) (Lukaczer et al. 2006).

Consumption of a plant stanolester-containing spread by moderately hypercholesterolemic patients reduced TC, LDL-c, and also the inflammation marker hs-CRP (Athyros et al. 2011).

Intake of fermented milk products containing lactotripeptides and plant sterol esters showed a lipid-lowering effect of borderline significance (Hautaniemi et al. 2015).


Carotenoids (lutein, zeaxanthin, cryptoxanthin, lycopene, α- and β-carotene, and vitamin A and retinol) are components primarily from plants and their chemistry, metabolism, absorption, nutritional value and allied health claims are comprehensively reviewed (Perveen et al. 2015). Some have shown to be potent antioxidant nutrients, which play a role in MetS (Gregorio et al. 2016). Researchers working in this field should carefully check the components studied in the experiments (retinol, β-carotene, vitamin A, zeaxanthin, lutein or lycopenes), before taking up references into their conclusions.

Total carotenoid intakes were inversely related to adiposity (Zulet et al. 2008), subclinical inflammation (Zimmermann and Aeberli 2008) and risk of MetS (Sluijs et al. 2009).

Inverse association of serum concentration of carotenoids with MetS was evident (Sugiura et al. 2008; Czernichow et al. 2009; Villaca Chaves et al. 2010; Suzuki et al. 2011; Li et al. 2013; Liu et al. 2014; Kabat et al. 2015; Sugiura et al. 2015; Wei et al. 2016), in smokers (Sugiura et al. 2008), as well as in non-smokers (Suzuki et al. 2011).

A Mediterranean-style low glycemic-load diet increases plasma carotenoids and decreases LDL-oxidation in women with MetS (Barona et al. 2012a, b). Higher circulating plasma levels of carotenoids resulted in higher levels of anti-inflammatory cytokine IL-10 and lower MDA (Azzini et al. 2011). Total carotenoids were inversely related to HOMA-IR (Beydoun et al. 2012) and CRP (Beydoun et al. 2012; Zeba et al. 2013) in MetS patients.

There was a positive association of plasma β-carotene concentration with adiponectin in obese subjects (Ben Amara et al. 2015) and leptin and RBP-4 in overweight children (Zimmermann and Aeberli 2008).

Plasma vitamin A levels (Godala et al. 2014; Teske et al. 2014), as well as skin carotenoid concentration (Zhang et al. 2012; Holt et al. 2014) were significantly lower in MetS patients than in healthy individuals.

Egg intake, with the carotenoids lutein and zeaxanthin (Andersen 2015) improves carotenoid status and results in increased plasma HDL-cholesterol in adults with MetS (Blesso et al. 2013).

Administration of natural astaxanthin lowers triglycerides and increases serum HDL-cholesterol and adiponectin in subjects with mild hyperlipidemia (Yoshida et al. 2010).

A recent systematic review and meta-analysis claimed that higher lutein concentration was associated with a lower risk of MetS (Leermakers et al. 2016).

Most of the time these studies are observational (Leermakers et al. 2016), therefore a large population-based prospective cohort study do not support the hypothesis that lutein intake early in life has a beneficial role for later cardio-metabolic health (Leermakers et al. 2015).

Longitudinal studies may further help to determine whether the inverse association for the various carotenoids is causally related to the MetS, or a result of the pathology (Coyne et al. 2009).

Two publications could be traced, where no association was found between the dietary carotenoid (Wei et al. 2015) or serum vitamin A (Suriyaprom et al. 2014) and MetS.

The most probable explanation for this could be the fact that most of the time more than one carotenoid form is taken in and also combinations of biologically active components (Barona et al. 2012a, b; Park et al. 2015; Silveira et al. 2015) can jeopardize the conclusions.

This is the best illustrated by the red-fleshed sweet orange juice, where the antioxidant activity of citrus flavonoids and carotenoids are added to the lycopene content of this type of juice, resulting in a decreased LDL-cholesterol and CRP-level (Silveira et al. 2015).

Table 3 summarizes most important results of the biologically active components on biomarkers of MetS.
Table 3

Effect of biological active components in foodstuffs on biomarkers of MetS


Risk of MetS



ω-3 fatty acids

Improved lipid profiles

Ebrahimi et al. (2009)


Pirillo and Catapano (2013)


Tardiva et al. (2015)


Bays et al. (2015)


Robberecht et al. (2017)

Markers of inflammation↓

Ebrahimi et al.(2009)


Tardiva et al. (2015)


Tortosa-Caparros et al. (2016)


Masquio et al. (2016)


Robberecht et al. (2017)

Markers of autoimmunity↓

Ebrahimi et al. (2009)


Robberecht et al. (2017)


TC↓, TG↓

de Jong et al. (2003)


Sirtori et al. (2009)

LDL-c↓ (9–12%)

Cofan and Ros (2015)

TC↓, TG↓, LDL-c↓, apoB↓

Sialvera et al. (2012)


No effect on HDL-c, apoA1, CRP, fibrinogen

Sialvera et al. (2012)

Carotenoids (−)


Sugiura et al. (2008), Czernichow et al. (2009)


Villaca Chaves et al. (2010), Suzuki et al. (2011), Li et al. (2013)


Liu et al. (2014), Kabat et al. (2015), Sugiura et al. (2015)


Wei et al. (2016)

Carotenoids (−)

IL-10↑, MDA↓

Azzini et al. (2011)

Carotenoids (−)


Beydoun et al. (2012)

Carotenoids (−)


Beydoun et al. (2012), Zeba et al. (2013)

Carotenoids (−)


Ben Amara et al. (2015)

carotenoids (−)

leptin↑, RBP-4↑

Zimmermann and Aeberli (2008)

Carotenoids (egg intake)


Blesso et al. (2013)

Carotenoids (astaxantin)

TG↓, HDL-c↑, adiponectin↑

Yoshida et al. (2010)

Carotenoids (lutein)


Leermakers et al. (2015)

Carotenoids (−)

No association

Suriyaprom et al. (2014)


Wei et al. (2015)

apoA1: apolipoprotein A1; apoB: apolipoprotein B; CRP: C-reactive protein; HDL-c: high-density lipoprotein cholesterol; HOMA-IR: homeostasis-associated –insulin resistance index; IL-10: interleukin 10; LDL-c: low-density lipoprotein colesterol; MDA: malondialdehyde; RPB-4: retinol-binding protein 4; TC: total cholesterol; TG: triglycerides


Tea, coffee, cocoa, soy, olive oil, fruit (berries and juices) and nuts are most of the time found to be effective in improving lipid profiles (TC, TG, HDL-c), the inflammatory marker CRP and the cytokine adiponectin.

The potential role of green tea catechines in the prevention of MetS can result from (1) a reduction of body fat, (2) improved glucose tolerance, (3) maintaining a healthy cardiovascular system by the antioxidant activity and (4) blood pressure control (Thielecke and Boschmann 2009).

Because of the cholesterol- and triglyceride-lowering effects (Plat et al. 2009), and this in a dose-dependent manner (Sirtori et al. 2009) plant sterols/stanols are incorporated nowadays into a wide variety of food products, referred to as functional foods (de Jong et al. 2003).

Key points to maximum effectiveness and safety are the following: (a) plant sterols should be taken with meals; (b) the optimal dosage is 2–2.5 g/day in a single dose (more than 3 g/day has not been found to have any additional effect and increases the risk of side effects); and, (c) the food matrix used to dissolve the sterols should contain a certain amount of fat (like e.g. milk-based matrix) (Rondanelli et al. 2013). The treatment may be considered (1) in individuals with high cholesterol levels at intermediate or low global cardiovascular risk who do not qualify for pharmacotherapy, (2) as an adjunct to pharmacologic therapy in high and very high risk patients who fail to achieve LDL-c targets on statins or are statin-intolerant, (3) and in adults and children (> 6 years) with familial hypercholesterolaemia (Gylling et al. 2014).

The contradictory results sometimes found in literature could be due to the variability of the diet with additionally or synergistically/antagonistically acting other components. The effects on MetS may be due to the entire dietary pattern, rather than to the individual food components.

Also for the same foodstuff (tea), which contains polyphenols, important differences exist between green, white and black tea.

Most of the time limited information on bioavailability is available.

Furthermore the studied population, the duration and size of the served portions are influencing factors. Fruits and nuts have different bioactive components with varying content (antioxidants, MUFAs, carotenoids, vitamins and trace elements). Sometimes a component, not taken into consideration, may be responsible for the observed effect. The high selenium content of Brazil nuts may be acting by enhancing the selenium status (Thomson et al. 2008), resulting in an improvement of lipid profiles, oxidative and microvascular markers (Maranhao et al. 2011).

And finally, more definite conclusions are limited due to the set-up of some trials. Cross-sectional studies restrict the interpretation of the observed associations in terms of cause and effect. Longitudinal studies are required for further investigation. Also a single assessment of blood samples or food intake may introduce some errors.

Significant between-study heterogeneity (Blanco Mejia et al. 2014) plays an additional role. Not only a low amount of patients, but also a variation in description of the studied population. This can vary from MetS, hypercholesterolemic (Blum et al. 2003; Wang-Polagruto et al. 2006; Matthan et al. 2007; Lerman et al. 2008; Cicero et al. 2016), obese (Davison et al. 2008; Udani et al. 2009; Villaca Chaves et al. 2010; Lehtonen et al. 2011; Teske et al. 2014; Bajerska et al. 2015), overweight (van Doorn et al. 2006; Zimmermann and Aeberli 2008; Lehtonen et al. 2011; Udani et al. 2011; Coker et al. 2015; Van der Made et al. 2015), people with dyslipidemia (Masella et al. 2001; Yoshida et al. 2010; Tardiva et al. 2015) risk of MetS (Davi et al. 2010) to diabetics (Mellor et al. 2010).


  1. Abrahao SH, Pereira RG, de Sousa RV et al (2013) Influence of coffee brew in metabolic syndrome and type 2 diabetes. Plant Foods Hum Nutr 68:184–189PubMedCrossRefGoogle Scholar
  2. Acharjee S, Zhou JR, Elajami TK et al (2015) Effect of soy nuts and equol status on blood pressure, lipids and inflammation in postmenopausal women stratified by metabolic syndrome status. Metabolism 64:236–243PubMedCrossRefGoogle Scholar
  3. Aggarwal BB, Gupta SC, Sung B (2013) Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers. Br J Pharmacol 169:1672–1692PubMedPubMedCentralCrossRefGoogle Scholar
  4. Alam MA, Subhan N, Rahman MM et al (2014) Effect of citrus flavonoids, naringin and naringenin, on metabolic syndrome and their mechanisms of action. Adv Nutr 5:404–417PubMedPubMedCentralCrossRefGoogle Scholar
  5. Ali A, Yazaki Y, Njike VY et al (2011) Effect of fruit and vegetable concentrates on endothelial function in metabolic syndrome: a randomized controlled trial. Nutr J 10:72.
  6. Almoosawi S, Tsang C, Ostertag LM et al (2012) Differential effect of polyphenol-rich dark chocolate on biomarkers of glucose metabolism and cardiovascular risk factors in healthy, overweight and obese subjects: a randomized clinical trial. Food Funct 3:1035–1043PubMedCrossRefGoogle Scholar
  7. Al-Rasheed N, Al-Rasheed N, Bassiouni Y et al (2014) Potential protective effects of Nigella sativa and Allium sativum against fructose-induced metabolic syndrome in rats. J Oleo Sci 63:839–848PubMedCrossRefGoogle Scholar
  8. Amani RA, Baghdadchi JB, Zand-Moghaddam AA (2005) Effects of soy protein isoflavones on serum lipids, lipoprotein profile and serum glucose of hypercholesterolemic rabbits. Int J Endocrinol Metab 2:87–92Google Scholar
  9. Amiot MJ, Riva C, Vinet A (2016) Effects of dietary polyphenols on metabolic syndrome features in humans: a systematic review. Obes Rev 17:573–586PubMedCrossRefGoogle Scholar
  10. Andersen CJ (2015) Bioactive egg components and inflammation. Nutrients 16:7889–7913CrossRefGoogle Scholar
  11. Anderson JW, Johnstone BM, Cook-Newell ME (1995) Meta-analysis of the effects of soy protein intake on serum lipids. N Engl J Med 333:276–282PubMedCrossRefGoogle Scholar
  12. Anderson-Vasquez HE, Perez-Martinez P, Ortega Fernandez P et al (2015) Impact of the consumption of a rich diet in butter and it replacement for a rich diet in extra virgin olive oil on the anthropometric, metabolic and lipid profile in postmenopausal women. Nutr Hosp 31:2561–2570PubMedGoogle Scholar
  13. Annuzzi G, Bozzetto L, Costabile G et al (2014) Diets naturally rich in polyphenols improve fasting and postprandial dyslipidemia and reduce oxidative stress: a randomized controlled trial. Am J Clin Nutr 99:463–471PubMedCrossRefGoogle Scholar
  14. Aronis KN, Vamvini MT, Chamberland JP et al (2012) Short-term walnut consumption increases circulating total adiponectin and apolipoprotein A concentrations, but does not affect markers of inflammation or vascular injury in obese humans with the metabolic syndrome: data from a double-blinded, randomized, placebo-controlled study. Metab Clin Experim 61:577–582CrossRefGoogle Scholar
  15. Assmann G, Cullen P, Kannenberg F et al (2007) Relationship between phytosterol levels and components of the metabolic syndrome in the PROCAM study. Eur J Cardiovasc Prev Rehabil 14:208–214PubMedCrossRefGoogle Scholar
  16. Athyros VG, Kakafika AL, Papageorgiou AA et al (2011) Nutr Metab Cardiovasc Dis 21:213–221PubMedCrossRefGoogle Scholar
  17. Azadbakht L, Esmaillzadeh A (2012) Soy intake and metabolic health: beyond isoflavones. Arch Iran Med 15:460–461PubMedGoogle Scholar
  18. Azadbakht L, Kimiagar M, Mehrabi Y et al (2007a) Dietary soy intake alters plasma antioxidant status and lipid peroxidation in postmenopausal women with the metabolic syndrome. Br J Nutr 98:807–813PubMedGoogle Scholar
  19. Azadbakht L, Kimiagar M, Mehrabi Y et al (2007b) Soy consumption, markers of inflammation, and endothelial function. A cross-over study in postmenopausal women with the metabolic syndrome. Diabetes Care 30:967–973PubMedCrossRefGoogle Scholar
  20. Azadbakht LL, Kimiagar M, Mehrabi Y et al (2007c) Soy inclusion in the diet improves features of the metabolic syndrome: a randomized crossover study in post menopausal women. Am J Clin Nutr 85:735–741PubMedCrossRefGoogle Scholar
  21. Azzini E, Plito A, Fumagalli A et al (2011) Mediterranean diet effect: an Italian picture. Nutr J 10:125. doi: 10.1186/1475-2891-10-125 PubMedPubMedCentralCrossRefGoogle Scholar
  22. Baba S, Osakabe N, Kato Y et al (2007) Continuous intake of polyphenolic compounds containing cocoa powder reduces LDL oxidative susceptibility and has beneficial effects on plasma HDL-cholesterol concentrations in humans. Am J Clin Nutr 85:709–717PubMedCrossRefGoogle Scholar
  23. Babio N, Toledo E, Estruch R et al (2014) Mediterranean diets and metabolic syndrome status in the PREDIMED randomized trial. Canad Med Assoc J. doi: 10.1503/cmaj.140764 CrossRefGoogle Scholar
  24. Bahls LD, Venturini D, Scripes Nde A et al (2011) Evaluation of the intake of a low daily amount of soybeans in oxidative stress, lipid and inflammatory profile, and insulin resistance in patients with metabolic syndrome. Arq Bras Endocrinol Metabol 55:399–405PubMedCrossRefGoogle Scholar
  25. Bajerska J, Milkner-Szudlarz S, Walkoviak J (2015) Effects of rye bread enriched with green tea extract on weight maintenance and the characteristics of metabolic syndrome following weight loss: a pilot study. J Med Food 18:698–705PubMedCrossRefGoogle Scholar
  26. Bakhtiary A, Yassin Z, Hanachi P et al (2012) Effects of soy on metabolic biomarkers of cardiovascular disease in elderly women with metabolic syndrome. Arch Iran Med 15:462–468PubMedGoogle Scholar
  27. Balk L, Hoekstra T, Twisk J (2009) Relationship between long-term coffee consumption and components of the metabolic syndrome: the Amsterdam Growth and Health Longitudinal Study. Eur J Epidemiol 24:203–209PubMedCrossRefGoogle Scholar
  28. Balzer J, Rassaf T, Heiss C et al (2008) Sustained benefits in vascular function through flavanol-containing cocoa in medicated diabetic patients -a double-masked, randomized, controlled trial. J Am Coll Cardiol 51:2141–2149PubMedCrossRefGoogle Scholar
  29. Barona J, Blesso CN, Andersen CJ et al (2012a) Grape consumption increases anti-inflammatory markers and upregulates peripheral nitric oxide synthase in the absence of dyslipidemias in men with metabolic syndrome. Nutrients 4:1945–1957PubMedPubMedCentralCrossRefGoogle Scholar
  30. Barona J, Jones JJ, Kopec RE et al (2012b) A Mediterranean-style low-glycemic-load diet increases plasma carotenoids and decreases LDL oxidation in women with metabolic syndrome. J Nutr Biochem 23:609–615PubMedCrossRefGoogle Scholar
  31. Basu A, Lyons TJ (2012) Strawberries, blueberries, and cranberries in the metabolic syndrome: clinical perspectives. J Agric Food Chem 30:5687–5692CrossRefGoogle Scholar
  32. Basu A, Wilkinson M, Penugonda K et al (2009) Freeze-dried strawberry powder improves lipid profile and lipid peroxidation in women with metabolic syndrome: baseline and post intervention effects. Nutr J 8:43. doi: 10.1186/1475-2891-8-43 PubMedPubMedCentralCrossRefGoogle Scholar
  33. Basu A, Sanchez K, Leyva MJ et al (2010a) Green tea supplementation affects body weight, lipids, and lipid peroxidation in obese subjects with metabolic syndrome. J Am Coll Nutr 29:31–40PubMedCrossRefGoogle Scholar
  34. Basu A, Du M, Leyva MJ et al (2010b) Blueberries decrease cardiovascular risk factors in obese men and women with metabolic syndrome. J Nutr 140:1582–1587PubMedPubMedCentralCrossRefGoogle Scholar
  35. Basu A, Fu DX, Wilkinson M et al (2010c) Strawberries decrease atherosclerotic markers in subjects with metabolic syndrome. Nutr Res 30:462–469PubMedPubMedCentralCrossRefGoogle Scholar
  36. Basu A, Betts NM, Ortiz J et al (2011) Low-energy cranberry juice decreases lipid oxidation and increases plasma antioxidant capacity in women with metabolic syndrome. Nutr Res 31:190–196PubMedPubMedCentralCrossRefGoogle Scholar
  37. Basu A, Betts NM, Mulugeta A et al (2013) Green tea supplementation increases glutathione and plasma antioxidant capacity in adults with the metabolic syndrome. Nutr Res 33:180–187PubMedPubMedCentralCrossRefGoogle Scholar
  38. Baumgartner S, Mensink RP, Plat J (2011) Plant sterols and stanols in the treatment of dyslipidemia: new insights into targets and mechanisms related to cardiovascular risk. Curr Pharm Des 17:922–932PubMedCrossRefGoogle Scholar
  39. Baxheinrich A, Stratmann B, Lee-Barkey YH et al (2012) Effects of a rapeseed oil-enriched hypoenergetic diet with a high content of α-linolenic acid on body weight and cardiovascular risk profile in patients with the metabolic syndrome. Br J Nutr 108:682–691PubMedCrossRefGoogle Scholar
  40. Bays HE, Ballantyne CM, Braeckman RA et al (2015) Icosapent Ethyl (Eicosapentaenoic acid ethyl ester): effects upon high-sensitivity C-reactive protein and lipid parameters in patients with metabolic syndrome. Metab Syndr Relat Disord 13:239–247PubMedCrossRefGoogle Scholar
  41. Beavers KM, Serra MC, Beavers DP et al (2009) Soy milk supplementation does not alter plasma markers of inflammation and oxidative stress in postmenopausal women. Nutr Res 29:619–622CrossRefGoogle Scholar
  42. Ben Amara N, Tourniaire F, Maraninchi M et al (2015) Independent positive association of plasma β-carotene concentrations with adiponectin among non-diabetic obese subjects. Eur J Nutr 54:447–454PubMedCrossRefGoogle Scholar
  43. Bernabé J, Mulero J, Cerda B et al (2013) Effects of a citrus based juice on biomarkers of oxidative stress in metabolic syndrome patients. J Functional Foods 5:1031–1038CrossRefGoogle Scholar
  44. Beydoun MA, Canas JA, Beydoun HA et al (2012) Serum antioxidant concentrations among U.S. adolescents in recent national surveys. J Nutr 142:1693–1704PubMedPubMedCentralCrossRefGoogle Scholar
  45. Blachier F, Lancha AH Jr, Boutry C et al (2010) Alimentary proteins, amino acids an cholesterolemia. Amino Acids 38:15–22PubMedCrossRefGoogle Scholar
  46. Blanco Mejia S, Dendall CW, Viguiliouk E et al (2014) Effect of tree nuts on metabolic syndrome criteria: a systemic review and meta-analysis of randomized controlled trials. BMJ Open 4:e004660PubMedPubMedCentralCrossRefGoogle Scholar
  47. Blesso CN, Andersen CJ, Bolling BW et al (2013) Egg intake improves carotenoid status by increasing plasma HDL cholesterol in adults with metabolic syndrome. Food Funct 4:213–221PubMedCrossRefGoogle Scholar
  48. Blum A, Lang N, Peleg A et al (2003) Effects of oral soy protein on markers of inflammation in postmenopausal women with mild hypercholesterolemia. Am Heart J 145:N1–N4CrossRefGoogle Scholar
  49. Bonaccio M, Di Castenuovo A, De Curtis A et al (2015) Nut consumption is inversely associated with both cancer and total mortality in a Mediterranean population: prospective results from the Moli-sani study. Br J Nutr 114:804–811PubMedCrossRefGoogle Scholar
  50. Broadhurst CL, Polansky MM, Anderson RA (2000) Insulin-like biological activity of culinary and medicinal plant extracts in vitro. J Agric Food Chem 48:849–852PubMedCrossRefGoogle Scholar
  51. Brown L, Poudyal H, Panchal SK (2015a) Functional foods as potential therapeutic options for metabolic syndrome. Obes Rev 16:914–941PubMedCrossRefGoogle Scholar
  52. Brown RC, Tey SL, Gray AR et al (2015b) Association of nut consumption with cardiometabolic risk factors in the 2008/2009 New Zealand Adult Nutrition Survey. Nutrients 7:7523–7542PubMedPubMedCentralCrossRefGoogle Scholar
  53. Buitrago-Lopez A, Sanderson J, Johnson L et al (2011) Chocolate consumption and cardiometabolic disorders: systematic review and meta-analysis. BMJ 343:d4488. doi. 10.1136/bmjd4488
  54. Camargo A, Ruano J, Fernandez JM et al (2010) Gene expression changes in mononuclear cells in patients with metabolic syndrome after acute intake of phenol-rich virgin oil. BMC Genom 11:253. doi: 10.1186/1471-2164-11-253 CrossRefGoogle Scholar
  55. Camargo A, Rangel-Zuniga OA, Haro C et al (2014) Olive oil phenolic compounds decrease the postprandial inflammatory response by reducing postprandial plasma lipopolysaccharide levels. Food Chem 162:161–171PubMedCrossRefGoogle Scholar
  56. Campbell CL, Foegeding EA, Harris GK (2016) Cocoa and whey protein differentially affect markers of lipid and glucose metabolism and satiety. J Med Food 19:219–227PubMedCrossRefGoogle Scholar
  57. Carpe-Berdiel L, Escolo-Gil JC, Blanco-Vaca F (2009) New insights into the molecular actions of plant sterols and stanols in cholesterol metabolism. Atherosclerosis 203:18–31CrossRefGoogle Scholar
  58. Carpentier YA, Portois L, Malaisse WJ (2006) N-3 fatty acids and the metabolic syndrome. Am J Clin Nutr 83:1499S–1504SPubMedCrossRefGoogle Scholar
  59. Casas-Agustench P, Lopez-Uriarte P, Bullo M et al (2011) Effects of one serving of mixed nuts on serum lipids, insulin resistance and inflammatory markers in patients with the metabolic syndrome. Nutr Metab Cardiovasc Dis 21:126–135PubMedCrossRefGoogle Scholar
  60. Cederroth CR, Nef S (2009) Soy, phytoestrogens and metabolism: a review. Mol Cell Endocrinol 304:30–42PubMedCrossRefGoogle Scholar
  61. Chakraborty S, Zawieja S, Wang W et al (2010) Lymphatic system: a vital link between metabolic syndrome and inflammation. Ann NY Acad Sci 1207:E94–E102PubMedPubMedCentralCrossRefGoogle Scholar
  62. Chen HW, Huang HC (1998) Effect of curcumin on cell cycle progression and apoptosis in vascular smooth muscle cells. Br J Pharmacol 124:1029–1040PubMedPubMedCentralCrossRefGoogle Scholar
  63. Cherniak EP (2011) Polyphenols: planting the seeds of treatment for the metabolic syndrome. Nutrition 27:617–623CrossRefGoogle Scholar
  64. Cicero AF, Colletti A (2015) Role of phytochemicals in the management of metabolic syndrome. Phytomedicine. doi: 10.1016/j.phymed.2015.11.009 CrossRefPubMedGoogle Scholar
  65. Cicero AF, Tartagni E, Ertek S (2014) Nutraceuticals for metabolic syndrome management: from laboratory to benchside. Curr Vasc Pharmacol 12:565–571PubMedCrossRefGoogle Scholar
  66. Cicero AF, Morbini M, Parini A et al (2016) Effect of red yeast rice combined with antioxidants on lipid pattern, hs-CRP level, and endothelial function in moderately hypercholesterolemic subjects. Therapeutics and Clin Risk Management 12:281–286CrossRefGoogle Scholar
  67. Cofan M, Ros E (2015) Clinical application of plant sterol and stanol products. J AOAC Int 98:701–706PubMedCrossRefGoogle Scholar
  68. Coker RH, Deutz NE, Schutzler S et al (2015) Nutritional supplementation with essential amino acids and phytosterols may reduce risk for metabolic syndrome in overweight individuals with mild hyperlipidemia. J Endocrinol Diabetes Obes 3:1069. ISSN: 2333-6692Google Scholar
  69. Couturier K, Batandier C, Awada M et al (2010) Cinnamon improves insulin sensitivity and alters the body composition in an animal model of the metabolic syndrome. Arch Biochem Biophys 501:158–161PubMedCrossRefGoogle Scholar
  70. Covas M-I, de la Torre R, Fito M (2015) Virgin olive oil: a key food for cardiovascular risk protection. Br J Nutr 113:S19–S28PubMedCrossRefGoogle Scholar
  71. Coyne T, Iebele TI, Baade PD et al (2009) Metabolic syndrome and serum carotenoids: findings of a cross-sectional study in Queensland, Australia. Br J Nutr 102:1668–1677PubMedCrossRefGoogle Scholar
  72. Czernichow S, Vergnaud A-C, Galan P et al (2009) Effects of long-term antioxidant supplementation and association of serum antioxidant concentrations with risk of metabolic syndrome in adults. Am J Clin Nutr 90:329–335PubMedCrossRefGoogle Scholar
  73. Dash S, Xiao C, Morgantini C et al (2013) High-dose resveratrol treatment for 2 weeks inhibits intestinal and hepatic lipoprotein production in overweight/obese men. Arterioscler Thromb Vasc Biol 33:2895–2901PubMedCrossRefGoogle Scholar
  74. Davi G, Santilli F, Patrono C (2010) Nutraceuticals in diabetes and metabolic syndrome. Cardiovasc Therap 28:216–226CrossRefGoogle Scholar
  75. Davison K, Howe PR (2015) Potential implications of dose and diet for the effects of cocoa flavanols on cardiometabolic function. J Agric Food Chem 63:9942–9947PubMedCrossRefGoogle Scholar
  76. Davison K, Coate AM, Buckley JD et al (2008) Effect of cocoa flavanols and exercise on cardiometabolic risk factors in overweight and obese subjects. Int J Obes 32:1289–1296CrossRefGoogle Scholar
  77. de Jong A, Plat J, Mensink RP (2003) Metabolic effects of plant sterols and stanols (Review). J Nutr Biochem 14:362–369PubMedCrossRefGoogle Scholar
  78. De la Iglesia R, Lopez-Legarrea P, Celada P et al (2013) Beneficial effects of the RESMENA dietary pattern on oxidative stress in patients suffering from metabolic syndrome with hyperglycemia are associated to dietary TAC and fruit consumption. Int J Mol Sci 14:6903–6919PubMedPubMedCentralCrossRefGoogle Scholar
  79. de Mello VD, Schwab U, Kolehmainen M et al (2011) A diet high in fatty fish, bilberries and wholegrain products improves markers of endothelial function and inflammation in individuals with impaired glucose metabolism in a randomized controlled trial: the Sysdimet study. Diabetologia 54:2755–2767PubMedCrossRefGoogle Scholar
  80. de Souza Ferreira E, Silva MA, Demonte A et al (2011) Soy β-conglycinin (7S globulin) reduces plasma and liver cholesterol in rats fed hypercholesterolic diet. J Med Food 14:94–100CrossRefGoogle Scholar
  81. DeFronzo RA, Ferrannini E (1991) Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 14:173–194PubMedCrossRefGoogle Scholar
  82. Devasagayam T, Kamat J, Mohan H et al (1996) Caffeine as an antioxidant: inhibition of lipid peroxidation induced by reactive oxygen species. Biochem Biophys Acta 1282:63–70PubMedCrossRefGoogle Scholar
  83. Di Pierro F, Bressan A, Ranaldi D et al (2015) Potential role of bioavailable curcumin in weight loss and omental adipose tissue decrease: preliminary data of a randomized, controlled trial in overweight people with metabolic syndrome. Preliminary study. Eur Rev Med Pharmacol Sci 19:4195–4202PubMedGoogle Scholar
  84. Ding EL, Hutfless SM, Ding X et al (2006) Chocolate and prevention of cardiovascular disease: a systematic review. Nutr Metab 3:2. doi: 10.1186/1743-7075-3-2 CrossRefGoogle Scholar
  85. Dow CA, Wertheim BC, Patil BS et al (2013) Daily consumption of grapefruit for 6 weeks reduces urine F2-isoprostanes in overweight adults with high baseline values but has no effect on plasma high-sensitivity C-reactive protein or soluble vascular cellular adhesion molecule 1. J Nutr 143:1586–1592PubMedPubMedCentralCrossRefGoogle Scholar
  86. Driessen MT, Koppes LLJ, Veldhuis L et al (2009) Coffee consumption is not related to the metabolic syndrome at the age of 36 years: the Amsterdam Growth and Health Longitudinal Study. Eur J Clin Nutr 63:536–542PubMedCrossRefGoogle Scholar
  87. Dyrskog SE, Jeppesen PB, Colomba M et al (2005) Preventive effects of a soy-based diet supplemented with stevioside on the development of the metabolic syndrome and type 2 diabetes in Zucker diabetic fatty rats. Metabolism 54:1181–1188PubMedCrossRefGoogle Scholar
  88. Ebrahimi M, Ghayour-Mobarhan M, Rezaiean S et al (2009) Omega-3 fatty acid supplements improve the cardiovascular risk profile of subjects with metabolic syndrome, including markers of inflammation and auto-immunity. Acta Cardiol 64:321–327PubMedCrossRefGoogle Scholar
  89. Engler MB, Engler MM, Chen CY et al (2004) Flavonoid-rich dark chocolate improves endothelial function and increases plasma epicatechin concentrations in healthy adults. J Am Coll Nutr 23:197–204PubMedCrossRefGoogle Scholar
  90. Esmaillzadeh A, Kimiagar M, Mehrabi Y et al (2006) Fruit and vegetable intakes, C-reactive protein, and the metabolic syndrome. Am J Clin Nutr 84:1489–1797PubMedCrossRefGoogle Scholar
  91. Espin JC, Garcia-Conesa MT, Tomas-Barberan FA (2007) Nutraceuticals: facts and fiction. Phytochemistry 68:2986–3008PubMedCrossRefGoogle Scholar
  92. Fernandez-Murga L, Tarin JJ, Garcia-Perez MA et al (2011) The impact of chocolate on cardiovascular health. Maturitas 69:312–321PubMedCrossRefGoogle Scholar
  93. Festa A, D’Agostino R Jr, Howard C et al (2000) Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation 102:42–47PubMedCrossRefGoogle Scholar
  94. Fito M, Covas MI, Lamuela-Raventos RM et al (2000) Protective effect of olive oil and its phenolic compounds against low density lipoprotein oxidation. Lipids 35:633–638PubMedCrossRefGoogle Scholar
  95. Ford ES, Mokdad AH, Giles WH et al (2003) The metabolic syndrome and antioxidant concentrations: findings from the Third National Health and Nutrition Examination Survey. Diabetes 52:2346–2352PubMedCrossRefGoogle Scholar
  96. Fujita K, Otani H, Jo F et al (2011) Modified resveratrol Longevinex improves endothelial function in adults with metabolic syndrome receiving standard treatment. Nutr Res 31:842–847CrossRefGoogle Scholar
  97. Fukushima Y, Kasuga M, Nakav K et al (2009) Effects of coffee on inflammatory cytokine gene expression in mice fed high-fat diets. J Agric Food Chem 57:11100–11105PubMedCrossRefGoogle Scholar
  98. Galleano M, Calabro V, Prince PD et al (2012) Flavonoids and metabolic syndrome. Ann NY Acad Sci 1259:87–94PubMedCrossRefGoogle Scholar
  99. Gao M, Zhao Z, Lv P et al (2015) Quantitative combination of natural anti-oxidants prevents metabolic syndrome by reducing oxidative stress. Redox Biol 6:206–217PubMedPubMedCentralCrossRefGoogle Scholar
  100. Ghorbani Z, Hekmatdoost A, Mirmiran P (2014) Anti-hyperglycemic and insulin sensitizer effects of turmeric and its principle constituent curcumin. Int J Endocrinol Metab 12:e18081. doi: 10.5812/ijem.18081 PubMedPubMedCentralCrossRefGoogle Scholar
  101. Gillingham LG, Harris-Janz S, Jones PJ (2011) Dietary monounsaturated fatty acids are protective against metabolic syndrome and cardiovascular disease risk factors. Lipids 46:209–228PubMedCrossRefGoogle Scholar
  102. Godala M, Materek-Kusmierkiewicz I, Moczulski D et al (2014) Estimation of plasma vitamin A, C and E levels in patients with metabolic syndrome. Pol Merkur Lekarski 36:320–323PubMedGoogle Scholar
  103. Gomez-Arbelaez D, Lahera V, Oubina P et al (2013) Aged garlic extract improves adiponectin levels in subjects with metabolic syndrome: a double-blind, placebo-controlled, randomized, crossover study. Mediators Inflamm. doi: 10.1155/2013/285795 PubMedPubMedCentralCrossRefGoogle Scholar
  104. Gorinstein S, Drzewiecki J, Leontowicz H et al (2005) Comparison of the bioactive compounds and antioxidant potentials of fresh and cooked Polish, Ukrainian, and Israeli garlic. J Agric Food Chem 53:2726–2732PubMedCrossRefGoogle Scholar
  105. Graf BL, Raskin I, Cefaly WT et al (2010) Plant-derived therapeutics for the treatment of metabolic syndrome. Curr Opin Investig Drugs 11:1107–1115PubMedPubMedCentralGoogle Scholar
  106. Gregorio BM, De Souza DB, de Morais Nascimento FA et al (2016) The potential role of antioxidants in metabolic syndrome. Curr Pharm Des 22:859–869PubMedCrossRefGoogle Scholar
  107. Grosso G, Marventano S, Galvano F et al (2014) Factors associated with metabolic syndrome in a Mediterranean population: role of caffeinated beverages. J Epidemiol 24:327–333PubMedPubMedCentralCrossRefGoogle Scholar
  108. Grosso G, Stepaniak U, Micek A et al (2015) Association of daily coffee and tea consumption and metabolic syndrome: results from the Polish arm of the HAPIEE study. Eur J Nutr 54:1129–1137PubMedCrossRefGoogle Scholar
  109. Grundy SM (1983) Absorption and metabolism of dietary cholesterol. Ann Rev Nutr 3:71–96CrossRefGoogle Scholar
  110. Grundy SM, Cleeman JI, Daniels SR et al (2005) Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 112:2735–2752PubMedCrossRefGoogle Scholar
  111. Gu Y, Lambert JD (2013) Modulation of metabolic syndrome-related inflammation by cocoa. Mol Nutr Food Res 57:948–961PubMedCrossRefGoogle Scholar
  112. Guevara-Cruz M, Tovar AR, Aguilar-Salinas CA et al (2012) A dietary pattern including nopal, chia seed, soy protein, and oat reduces serum triglycerides and glucose intolerance in patients with metabolic syndrome. J Nutr 142:64–69PubMedCrossRefGoogle Scholar
  113. Gylling H, Simonen P (2015) Phytosterols, phytostanols, and lipoprotein metabolism. Nutrients 7:7965–7977PubMedPubMedCentralCrossRefGoogle Scholar
  114. Gylling H, Plat J, Turley S et al (2014) Plant sterols and plant stanols in the management of dyslipidaemia and prevention of cardiovascular disease. Atherosclerosis 232:346–360PubMedCrossRefGoogle Scholar
  115. Hajer GR, van der Graaf Y, Olijhoek JK et al (2007) Levels of homocysteine are increased in metabolic syndrome patients but are not associated with an increased cardiovascular risk, in contrast to patients without the metabolic syndrome. Heart 93:216–220PubMedCrossRefGoogle Scholar
  116. Hannum SM (2004) Potential impact of strawberries on human health: a review of the science. Crit Rev Food Sci Nutr 44:1–17PubMedCrossRefGoogle Scholar
  117. Hautaniemi EJ, Tikkakoski AJ, Tahvanainen A et al (2015) Effect of fermented milk product containing lactotripeptides and plant sterol esters-a randomized, double-blind, placebo-controlled study. Br J Nutr 114:376–386PubMedCrossRefGoogle Scholar
  118. Heinemann T, Axtmann G, von Bergmann K (1993) Comparison of intestinal absorption of cholesterol with different plant sterols in man. Eur J Clin Invest 23:827–831PubMedCrossRefGoogle Scholar
  119. Hernandez-Mijares A, Banuls C, Jover A et al (2011) Low intestinal cholesterol absorption is associated with a reduced efficacy of phytosterol esters as hypolipemic agents in patients with metabolic syndrome. Clin Nutr 30:604–609PubMedCrossRefGoogle Scholar
  120. Higashikawa F, Noda M, Awaya T et al (2012) Reduction of serum lipids by the intake of the extract of garlic fermented with Monascus pilosus: a randomized, double-blind, placebo-controlled clinical trial. Clin Nutr 31:261–266PubMedCrossRefGoogle Scholar
  121. Hino A, Adachi H, Enomoto M et al (2007) Habitual coffee but not green tea consumption is inversely associated with metabolic syndrome. An epidemiological study in a general Japanese population. Diabetes Res Clin Pract 76:383–389PubMedCrossRefGoogle Scholar
  122. Holligan SD, West SG, Gebauer SK et al (2014) A moderate-fat diet containing pistachios improves emerging markers of cardiometabolic syndrome in healthy adults with elevated LDL levels. Br J Nutr 112:744–752PubMedCrossRefGoogle Scholar
  123. Holt EW, Wei EK, Bennett N et al (2014) Low skin carotenoid concentration measured by resonance Raman spectroscopy is associated with metabolic syndrome in adults. Nutr Res 34:821–826PubMedCrossRefGoogle Scholar
  124. Hosoda K, Wang MF, Liao ML et al (2003) Antihyperglycemic effect of oolong tea in type-2 diabetes. Diabetes Care 26:1714–1718PubMedCrossRefGoogle Scholar
  125. Hosseini A, Hosseinzadeh H (2015) A review on the effects of Allium sativum (Garlic) in metabolic syndrome. J Endocrinol Invest 38:1147–1157PubMedCrossRefGoogle Scholar
  126. Hosseinpour-Niazi S, Mirmiran P, Fallah-Ghohroudi A et al (2015) Combined effect of unsaturated fatty acids and saturated fatty acids on the metabolic syndrome: Tehran lipid and glucose study. J Health, Population and Nutr 33:5. doi: 10.1186/s41043-015-0015-z/ CrossRefGoogle Scholar
  127. Hursel R, Westerterp-Plantenga MS (2013) Catechin- and caffeine-rich teas for control of body weight in humans. Am J Clin Nutr 98:1682S–1698SPubMedCrossRefGoogle Scholar
  128. Imai K, Nakachi K (1995) Cross sectional study of effects of drinking green tea on cardiovascular and liver diseases. BMJ 310:693–696PubMedPubMedCentralCrossRefGoogle Scholar
  129. Isomaa B, Almgren P, Tuami T et al (2001) Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 24:683–689PubMedCrossRefGoogle Scholar
  130. Jaceldo-Siegl K, Haddad E, Oda K et al (2014) Tree nuts are inversely associated with metabolic syndrome and obesity: the Adventist Health Study-2. PLoS ONE 9:e85133. doi: 10.1371/journal.pone.0085133 PubMedPubMedCentralCrossRefGoogle Scholar
  131. Jia L, Liu XA, Bai YY et al (2010) Short-term effect of cocoa product consumption on lipid profile: a meta-analysis of randomized controlled trials. Am J Clin Nutr 92:218–225PubMedCrossRefGoogle Scholar
  132. Jones JL, Comperatore M, Barona J et al (2012) A Mediterranean-style, low-glycemic diet decreases atherogenic lipoproteins and reduces lipoprotein(a) and oxidized low-density lipoprotein in women with metabolic syndrome. Metabolism 61:366–372PubMedCrossRefGoogle Scholar
  133. Jung ES, Park SH, Choi EK et al (2014) Reduction of blood lipid parameters by a 12-wk supplementation of aged black garlic: a randomized controlled trial. Nutrition 30:1034–1039PubMedCrossRefGoogle Scholar
  134. Jurenka JS (2009) Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical and clinical research. Altern Med Rev 14:141–153PubMedGoogle Scholar
  135. Kabat GC, Heo M, Ochs-Balcom HM et al (2015) Longitudinal association of measures of adiposity with serum antioxidant concentration in postmenopausal women. Eur J Clin Nutr. doi: 10.1038/ejcn.2015.74 PubMedCrossRefGoogle Scholar
  136. Kaplan NM (1989) The deadly quartet. Upper-body obesity, glucose intolerance, hypertriglyceridemia and hypertension. Arch Intern Med 149:1514–1520PubMedCrossRefGoogle Scholar
  137. Katz DL, Davidhi A, Ma Y et al (2012) Effects of walnuts on endothelial function in overweight adults with visceral obesity: a randomized, controlled, crossover trial. J Am Coll Nutr 31:415–423PubMedCrossRefGoogle Scholar
  138. Kaur G, Mukundan S, Wani V et al (2015) Nutraceuticals in the management and prevention of metabolic syndrome. Austin J Pharmacol Ther 3:1063Google Scholar
  139. Kendall CWC, Josse AR, Esfahani A et al (2010) Nuts, metabolic syndrome and diabetes. Br J Nutr 104:465–473PubMedCrossRefGoogle Scholar
  140. Keske MA, Ng HL, Premilovac D et al (2015) Vascular and metabolic actions of the green tea polyphenol epigallocatechin gallate. Curr Med Chem 22:59–69PubMedPubMedCentralCrossRefGoogle Scholar
  141. Khan A, Safdar M, Kahn A et al (2003) Cinnamon improves glucose and lipids of people with type 2 diabetes. Diabetes Care 26:3215–3218PubMedCrossRefGoogle Scholar
  142. Khan N, Monagas M, Andres-Lacueva C et al (2012) Regular consumption of cocoa powder with milk increases HDL cholesterol and reduces oxidized LDL levels in subjects at high-risk of cardiovascular disease. Nutr Metab Cardiovasc Dis 22:1046–1053PubMedCrossRefGoogle Scholar
  143. Khan MI, Anjum FM, Sohaib M et al (2013) Tackling metabolic syndrome by functional foods. Rev Endocr Metab Disord 14:287–297PubMedCrossRefGoogle Scholar
  144. Khorsan R, Crawford C, Ives JA et al (2014) The effect of omega-3 fatty acids on biomarkers of inflammation: a rapid evidence assessment of the literature. Mil Med 179:2–60PubMedCrossRefGoogle Scholar
  145. Kim HJ, Cho S, Jacobs DR Jr et al (2014) Instant coffee consumption may be associated with higher risk of metabolic syndrome in Korean adults. Diabetes Res Clin Pract 106:145–153PubMedCrossRefGoogle Scholar
  146. Kolehmainen M, Mykkänen O, Kirjavainen PV et al (2012) Bilberries reduce low-grade inflammation in individuals with features of metabolic syndrome. Mol Nutr Food Res 56:1501–1510PubMedCrossRefGoogle Scholar
  147. Koster A, Stenholm S, Alley DE et al (2010) Body fat distribution and inflammation among obese older adults with and without metabolic syndrome. Obesity 18:2354–2361PubMedPubMedCentralCrossRefGoogle Scholar
  148. Kowalska K, Olejnik A (2016) Current evidence on the health-beneficial effects of berry fruits in the prevention and treatment of metabolic syndrome. Curr Opin Clin Nutr Metab Care 19:446–452PubMedCrossRefGoogle Scholar
  149. Lakka HM, Laaksonen DE, Lakka TA et al (2002) The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA 288:2709–2716PubMedCrossRefGoogle Scholar
  150. Lann D, LeRoith D (2007) Insulin resistance as the underlying cause for the metabolic syndrome. Med Clin North Am 91:1063–1077PubMedCrossRefGoogle Scholar
  151. Lee IT, Lee WJ, Tsai CM et al (2012) Combined extractives of red yeast rice, bitter gourd, chlorella, soy protein, and licorice improve total cholesterol, low-density lipoprotein cholesterol, and triglycerides in subjects with metabolic syndrome. Nutr Res 32:85–92PubMedCrossRefGoogle Scholar
  152. Lee YJ, Nam GE, Seo JA et al (2014) Nut consumption has favorable effects on lipid profiles of Korean women with metabolic syndrome. Nutr Res 34:814–820PubMedCrossRefGoogle Scholar
  153. Leermakers ETM, Kiefte-de Jong JC, Hofman A et al (2015) Lutein intake at the age of 1 year and cardiometabolic health at the age of 6 years: the Generation R study. Br J Nutr 114:970–978PubMedCrossRefGoogle Scholar
  154. Leermakers ETM, Darweesh SKL, Baena CP et al (2016) The effects of lutein on cardiometabolic health across the life course: a systematic review and meta-analysis. Am J Clin Nutr 103:481–494PubMedCrossRefGoogle Scholar
  155. Legeay S, Rodier M, Fillon L et al (2015) Epigallocatechin gallate: a review of its beneficial properties to prevent metabolic syndrome. Nutrients 7:5443–5468PubMedPubMedCentralCrossRefGoogle Scholar
  156. Lehtonen H-M, Suomela J-P, Tahvonen R et al (2010) Berry meals and risk factors associated with metabolic syndrome. Eur J Clin Nutr 64:614–621PubMedCrossRefGoogle Scholar
  157. Lehtonen HM, Suomela JP, Tahvonen R et al (2011) Different berries and berry fractions have various but slightly positive effects on the associated variables of metabolic diseases on overweight and obese women. Eur J Clin Nutr 65:394–401PubMedCrossRefGoogle Scholar
  158. Lerman RH, Minich DM, Darland G et al (2008) Enhancement of a modified Mediterranean-style, low glycemic load diet with specific phytochemicals improves cardiometabolic risk factors In subjects with metabolic syndrome and hypercholesterolemia in a randomized trial. Nutr Metab 5:29. doi: 10.1186/1743-7075-5-29
  159. Lerman RH, Minich DM, Darland G et al (2010) Subjects with elevated LDL cholesterol and metabolic syndrome benefit from supplementation with soy protein, phytosterols, hops rho iso-alpha acids, and Acacia nilotica proanthocyanidins. J Clin Lipidol 4:59–68PubMedCrossRefGoogle Scholar
  160. Li Y, Guo H, Wu M et al (2013) Serum and dietary antioxidant status is associated with lower prevalence of the metabolic syndrome in a study in Shanghai, China. Asia Pac J Clin Nutr 22:60–68PubMedGoogle Scholar
  161. Lila MA (2011) Impact of bioflavonoids from berry fruits on biomarkers of metabolic syndrome. Functional Foods Health and Dis 2:13–24Google Scholar
  162. Liu J, Shi WQ, Cao Y et al (2014) High serum carotenoid concentrations associated with a lower prevalence of the metabolic syndrome in middle-aged and elderly Chinese adults. Br J Nutr 112:2041–2048PubMedCrossRefGoogle Scholar
  163. Lopez-Miranda J, Perez-Jiminez F, Ros E et al (2008) Olive oil and health: summary of the II International conference on olive oil and healthy consensus report, Jaen and Cordoba (Spain). Nutr Metab Cardiovasc Dis 20:284–294CrossRefGoogle Scholar
  164. Lopez-Uriarte P, Nogues R, Saez G et al (2010) Effect of nut consumption on oxidative stress and endothelial function in metabolic syndrome. Clin Nutr 29:373–380PubMedCrossRefGoogle Scholar
  165. Lorenz M (2013) Cellular targets for the beneficial actions of tea polyphenols. Am J Clin Nutr 98:1642S–1650SPubMedCrossRefGoogle Scholar
  166. Lukaczer D, Liska DJ, Lerman RH et al (2006) Effect of low glycemic index diet with soy protein and phytosterols on CVD risk factors in postmenopausal women. Nutrition 22:104–113PubMedCrossRefGoogle Scholar
  167. Machowetz A, Gruendel S, Garcia AL et al (2008) Effect of olive oil consumption on serum resistin concentrations in healthy men. Horm Metab Res 40:697–701PubMedCrossRefGoogle Scholar
  168. Mansoub S, Chan MK, Adeli K (2006) Gap analysis of pediatric reference intervals for risk biomarkers of cardiovascular disease and the metabolic syndrome. Clin Biochem 39:569–587PubMedCrossRefGoogle Scholar
  169. Maranhao PA, Kraemer-Aguiar LG, de Oliveira CL et al (2011) Brazil nuts intake improves lipid profile, oxidative stress and microvascular function in obese adolescents: a randomized controlled trial. Nutr Metab 8:32.
  170. Martinez-Gonzalez MA, Martin-Calvo N (2013) The major European dietary patterns and metabolic syndrome. Rev Endocr Metab Disord 14:265–271PubMedCrossRefGoogle Scholar
  171. Marventano S, Salomone F, Godos J et al (2016) Coffee and tea consumption in relation with non-alcoholic fatty liver and metabolic syndrome: a systematic review and meta-analysis of observational studies. Clin Nutr. doi: 10.1016/j.clnu.2016.03.012 PubMedCrossRefGoogle Scholar
  172. Masella R, Giovannini C, Vari R et al (2001) Effects of dietary virgin olive oil phenols on low density lipoprotein oxidation in hyperlipidemic patients. Lipids 36:1195–1202PubMedCrossRefGoogle Scholar
  173. Masquio DC, de Piano-Ganen A, Oyama LM et al (2016) The role of free fatty acids in the inflammatory and cardiometabolic profile in adolescents with metabolic syndrome engaged in interdisciplinary therapy. J Nutr Biochem 33:136–144PubMedCrossRefGoogle Scholar
  174. Matsuuraa H, Mure K, Nishio N et al (2012) Relationship between coffee consumption and prevalence of metabolic syndrome among Japanese civil servants. J Epidemiol 22:160–166CrossRefGoogle Scholar
  175. Matthan NR, Jalbert SM, Ausman LM et al (2007) Effect of soy protein from differently processed products on cardiovascular disease risk factors and vascular and endothelial function in hypercholesterolemic subjects. Am J Clin Nutr 85:960–966PubMedCrossRefGoogle Scholar
  176. Maury E, Brichard SM (2010) Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome. Mol Cell Endocrinol 314:1–16PubMedCrossRefGoogle Scholar
  177. Mayanglambam A, Dangelmaier CA, Thomas D et al (2010) Curcumin inhibits GPVI-mediated platelet-activation by interfering with the kinase activity of syk and the subsequent activation of PLC2. Platelets 21:211–220PubMedCrossRefGoogle Scholar
  178. Mayneris-Perxachs J, Sala-Vila A, Chisaguano M et al (2014) Effects of 1-year intervention with a Mediterranean diet on plasma fatty acid composition and metabolic syndrome in a population at high cardiovascular risk. PLoS 9:e85202. doi: 10.1371/journal.pone.0085202 CrossRefGoogle Scholar
  179. McVeigh BL, Dillingham BL, Lampe JW et al (2006) Effect of soy protein varying in isoflavone content on serum lipids in healthy young men. Am J Clin Nutr 83:244–251PubMedCrossRefGoogle Scholar
  180. Mellor DD, Sathyapalan T, Kilpatrick ES et al (2010) High cocoa polyphenol-rich chocolate improves HDL cholesterol int type 2 diabetes patients. Diabet Med 27:1318–1321PubMedCrossRefGoogle Scholar
  181. Mendez-del Villar M, Gonzalez-Ortiz M, Martinez-Abundis E et al (2014) Effect of resveratrol administration on metabolic syndrome, insulin sensitivity, and insulin secretion. Metab Syndr Relat Disord 12:497–501PubMedCrossRefGoogle Scholar
  182. Mielgo-Ayuso J, Barrenechea L, Alcorta P et al (2014) Effects of dietary supplementation with epigallocatechin-3-gallate on weight loss, energy homeostasis, cardio-metabolic risk factors and liver function in obese women: randomized, double-blind, placebo-controlled clinical trial. Br J Nutr 111:1263–1271PubMedCrossRefGoogle Scholar
  183. Minich DM, Bland JS (2008) Dietary management of the metabolic syndrome beyond macronutrients. Nutr Rev 66:429–444PubMedCrossRefGoogle Scholar
  184. Mtjavila MT, Fandos M, Salas-Salvado J et al (2013) The Mediterranean diet improves the systemic lipid and DNA oxidative damage in metabolic syndrome individuals. A randomized controlled, trial. Clin Nutr 32:172–178CrossRefGoogle Scholar
  185. Mukuddem-Petersen J, Stonehouse W, Jerling JC et al (2007) Effects of a high walnut and high cashew nut diet on selected markers of the metabolic syndrome: a controlled feeding trial. Br J Nutr 97:1144–1153PubMedCrossRefGoogle Scholar
  186. Mulero J, Bernabé J, Cerda B et al (2012) Variations on cardiovascular risk factors in metabolic syndrome after consumption of a citrus-based juice. Clin Nutr 31:372–377PubMedCrossRefGoogle Scholar
  187. Mulvihill EE, Allister EM, Sutherland BG et al (2009) Naringenin prevents dyslipidemia, apoB overproduction and hyperinsulinemia in LDL-receptor null mice with diet-induced insulin resistance. Diabetes 58:2198–2210PubMedPubMedCentralCrossRefGoogle Scholar
  188. Muniyappa R, Hall G, Kolodziej TL et al (2008) Cocoa consumption for 2 wk enhances insulin-mediated vasodilatation without improving blood pressure or insulin resistance in essential hypertension. Am J Clin Nutr 88:1685–1696PubMedPubMedCentralCrossRefGoogle Scholar
  189. Mure K, Maeda S, Mukoubayashi C et al (2013) Habitual coffee consumption inversely associated with metabolic syndrome-related biomarkers involving adiponectin. Nutrition 29:982–987PubMedCrossRefGoogle Scholar
  190. Mursu J, Voutilainen S, Nurmi T et al (2004) Dark chocolate consumption increases HDL cholesterol concentration and chocolate fatty acids may inhibit lipid peroxidation in healthy humans. Free Radic Biol Met 37:1351–1359CrossRefGoogle Scholar
  191. Nakachi K, Matsuyama S, Miyake S et al (2000) Preventive effects of drinking green tea on cancer and cardiovascular disease: epidemiological evidence for multiple targeting prevention. BioFactors 13:49–54PubMedCrossRefGoogle Scholar
  192. Nelson KM, Dahlin JL, Bisson J et al (2017) The essential medicinal chemistry of curcumin. J Med Chem 60:1620–1637PubMedPubMedCentralCrossRefGoogle Scholar
  193. Nordestgaard AT, Thomsen M, Nordestgaard BG (2015) Coffee intake and risk of obesity, metabolic syndrome and type 2 diabetes: a Mendelian randomization study. Int J Epidemiol. doi: 10.1093/ije/dyv083 CrossRefPubMedGoogle Scholar
  194. Normen L, Dutta P, Lia A et al (2000) Soy sterol esters and β-sitostanol ester as inhibitors of cholesterol absorption in human small bowel. Am J Clin Nutr 71:908–913PubMedCrossRefGoogle Scholar
  195. Novotny JA, Baer DJ, Khoo C et al (2015) Cranberry juice consumption lowers markers of cardiometabolic risk, including blood pressure and circulating C-reactive protein, triglyceride, and glucose concentrations in adults. J Nutr 145:1185–1193PubMedCrossRefGoogle Scholar
  196. Nuefingerl N, Zebregs YEMP, Schuring EAH et al (2013) Effect of cocoa and theobromine consumption on serum HDL-cholesterol concentrations: a randomized controlled trial. Am J Clin Nutr 97:1201–1209CrossRefGoogle Scholar
  197. O’Neil CE, Nicklas TA, Rampersaud GC et al (2012a) 100% orange juice consumption is associated with better diet quality, improved nutrient adequacy, decreased risk for obesity, and improved biomarkers of health in adults: National Health and Nutrition Examination Survey, 2003-2006. Nutr J 11:107. doi: 10.1186/1475-2891-11-107 PubMedPubMedCentralCrossRefGoogle Scholar
  198. O’Neil CE, Deast DR, Nicklas TA et al (2012b) Out-of-hand nut consumption is associated with improved nutrient intake and health risk markers in US children and adults: National Health and Nutrition Examination Survey 1999-2004. Nutr Res 32:185–194PubMedCrossRefGoogle Scholar
  199. O’Neil CE, Fulgoni VL, Nicklas TA (2015) Tree nut consumption is associated with better adiposity measures and cardiovascular and metabolic syndrome health risk factors in U.S. adults: NHANES 2005-2010. Nutr J 14:64. doi: 10.1186/s12937-015-0052-x PubMedPubMedCentralCrossRefGoogle Scholar
  200. Oh J-E, Lee YJ, Kim Y-W et al (2009) The effect of black tea on biomarkers of metabolic syndrome in high fat diet fed rats. J Korean Soc Appl Chem 52:193–197CrossRefGoogle Scholar
  201. Oliveras-Lopez MJ, Berna G, Jurado-Ruiz E et al (2014) Consumption of extra-virgin olive oil rich in phenolic compounds has beneficial antioxidant effects in healthy human adults. J Funct Foods 10:475–484CrossRefGoogle Scholar
  202. Onakpoya I, Spencer E, Heneghan C et al (2014) The effect of green tea on blood pressure and lipid profile: a systematic review and meta-analysis of randomized clinical trials. Nutr Metab Cardiovasc Dis 24:823–836PubMedCrossRefGoogle Scholar
  203. Onat A, Uyarel H, Hergenç G et al (2006) Serum uric acid is a determinant of metabolic syndrome in a population-based study. Am J Hypertens 19:1055–1062PubMedCrossRefGoogle Scholar
  204. Ooi EM, Watts GF, Barrett PH et al (2007) Dietary plant sterols supplementation does not alter lipoprotein kinetics in men with the metabolic syndrome. Asia Pac J Clin Nutr 16:624–631PubMedGoogle Scholar
  205. Ozen AE, Pons A, Tur JA (2012) Worldwide consumption of functional foods: a systematic review. Nutr Rev 40:472–481CrossRefGoogle Scholar
  206. Padiya R, Khatua TN, Bagul PK et al (2011) Garlic improves insulin sensitivity and associated metabolic syndromes in fructose fed rats. Nutr and Metabol 8:53.
  207. Pan A, Franco OH, Ye J et al (2008) Soy protein intake has sex-specific effects on the risk of metabolic syndrome in middle-aged and elderly Chinese. J Nutr 138:2413–2421PubMedCrossRefGoogle Scholar
  208. Panahi Y, Khalili N, Hosseini MS et al (2014) Lipid-modifying effects of adjunctive therapy with curcumoids-piperine combination in patients with metabolic syndrome: results of a randomized controlled trial. Complement Ther Med 22:851–857PubMedCrossRefGoogle Scholar
  209. Panahi Y, Hosseini MS, Khalili N et al (2016) Effects of supplementation with curcumin on serum adipokine concentrations: a randomized controlled trial. doi: 10.1016/J.Nutr.2016.03.018 CrossRefGoogle Scholar
  210. Panchai SK, Poudyal H, Waanders J et al (2012a) Coffee extract attenuates changes in cardiovascular and hepatic structure and function without decreasing obesity in high-carbohydrate, high-fat diet-fed male rats. J Nutr 142:690–697CrossRefGoogle Scholar
  211. Panchai SK, Wong W-Y, Kauter K et al (2012b) Caffeine attenuates metabolic syndrome in diet-induces obese rats. Nutrition 28:1055–1062CrossRefGoogle Scholar
  212. Park S, Ham JQ, Lee BK (2015) Effects of total vitamin A, vitamin C, and fruit intake on risk for metabolic syndrome in Korean women and men. Nutrition 31:111–118PubMedCrossRefGoogle Scholar
  213. Patel S (2016) Functional food red yeast rice (RYR) for metabolic syndrome amelioration: a review on pros and cons. World J Microbiol Biotechnol 32:87. doi: 10.1007/s11274-016-2035-2 PubMedCrossRefGoogle Scholar
  214. Pearson DA, Frankel EN, Aeschbach R et al (1998) Inhibition of endothelial cell mediated low-density lipoprotein oxidation by green tea extracts. J Agric Food Chem 46:1445–1449CrossRefGoogle Scholar
  215. Perez-Martinez P, Garcia-Rios A, Delgado-Lista J et al (2011) Mediterranean diet rich in olive oil and obesity, metabolic syndrome and diabetes mellitus. Curr Pharm Des 17:769–777PubMedCrossRefGoogle Scholar
  216. Perez-Torres I, Ruiz-Ramirez A, Banos G et al (2013) Hibiscus sabdariffa Linnaeus (Malvaceae), curcumin and resveratrol as alternative medicinal agents against metabolic syndrome. Cardiovasc Hematol Agents Med Chem 11:25–37PubMedCrossRefGoogle Scholar
  217. Perveen R, Suleria HAR, Anjum FM et al (2015) Tomato (Solanum lycopersicum) carotenoids and lycopenes chemistry; metabolism, absorption, nutrition, and allied health claims–a comprehensive review. Crit Rev Food Science Nutr 55:919–929CrossRefGoogle Scholar
  218. Phillips KM, Ruggio DM, Ashraf-Khorassani M (2005) Phytosterol composition of nuts and seeds commonly consumed in the United States. J Agric Food Chem 53:9436–9445PubMedCrossRefGoogle Scholar
  219. Pieters M, Oosthuizen W, Jerling JC et al (2005) Clustering of haemostatic variables and the effect of high cashew and walnut diets on these variables in metabolic syndrome patients. Blood Coagul Fibrinol 16:429–437CrossRefGoogle Scholar
  220. Pirillo A, Catapano AL (2013) Omega-3 polyunsaturated fatty acids in the treatment of atherogenic dyslipidemia. Atheroscler Suppl 14:237–242PubMedCrossRefGoogle Scholar
  221. Plat J, Mensink RP (2009) Plant stanol esters lower serum triacylglycerol concentration via a reduced hepatic VLDL-1 production. Lipids 44:1149–1153PubMedPubMedCentralCrossRefGoogle Scholar
  222. Plat J, Brufau G, Dallinga-Thie GM et al (2009) A plant stanol yogurt drink alone or combined with a low-dose statin lowers serum triacylglycerol and non-HDL cholesterol in metabolic syndrome patients. J Nutr 139:1143–1149PubMedCrossRefGoogle Scholar
  223. Platt DE, Ghassibe-Sabbagh M, Salameh P et al (2016) Caffeine impact on metabolic syndrome components is modulated by a CYP1A2 variant. Ann Nutr Metab 68:1–11PubMedCrossRefGoogle Scholar
  224. Potter SM (1998) Soy protein and cardiovascular disease: the impact of bioactive components in soy. Nutr Rev 56:231–235PubMedCrossRefGoogle Scholar
  225. Power M, Pratley R (2011) Alternative and complementary treatments for metabolic syndrome. Curr Diab Rep 11:173–178PubMedCrossRefGoogle Scholar
  226. Princen HM, van Duyvenvoorde W, Buytenhek R et al (1998) No effect of consumption of green and black tea on plasma lipid and antioxidant levels and on LDL-oxidation in smokers. Arterioscler Thromb Vasc Biol 18:833–841PubMedCrossRefGoogle Scholar
  227. Pulido-Moran M, Moreno-Fernandez J, Ramirez-Tortosa C et al (2016) Curcumin and health. Molecules 21:264. doi: 10.3390/molecules21030264 PubMedCrossRefGoogle Scholar
  228. Qin B, Panickar KS, Anderson RA (2010) Cinnamon: potential role in the prevention of insulin resistance, metabolic syndrome, and type 2 diabetes. J Diabetes Sci Technol 4:685–693PubMedPubMedCentralCrossRefGoogle Scholar
  229. Ramaswammi G, Chai H, Yao Q et al (2004) Curcumin blocks homocysteine-induced endothelial dysfunction in porcine coronary arteries. J Vasc Surg 40:1216–1222CrossRefGoogle Scholar
  230. Reaven GM (1988) Role of insulin resistance in human disease. Diabetes 37:1595–1607PubMedCrossRefGoogle Scholar
  231. Reinwald S, Akabas SR, Weaver CM et al (2010) Whole versus piecemeal approach to evaluating soy. J Nutr 40:2335S–2343SCrossRefGoogle Scholar
  232. Rigacci S, Stefani M (2016) Nutraceutical properties of olive oil polyphenols. An itinerary from cultured cells through animal models of humans. Int J Mol Sci 17:E434. doi: 10.3390/ijms17060843 CrossRefGoogle Scholar
  233. Rizza S, Muniyappa R, Iantorno M et al (2011) Citrus polyphenol hesperidin stimulates production of nitric oxide in endothelial cells while improving endothelial function and reducing inflammatory markers in patients with metabolic syndrome. J Clin Endocrinol Metab 96:E782–E792PubMedPubMedCentralCrossRefGoogle Scholar
  234. Robberecht H, Hermans N (2016) Biomarkers of the metabolic syndrome: biochemical background and clinical significance. Metab Syndr and Relat Dis 14:1–47. doi: 10.1089/met.2015:0113 CrossRefGoogle Scholar
  235. Robberecht H, De Bruyne T, Hermans N (2016a) Effect of various diets on biomarkers of the metabolic syndrome. Int J Food Sci Nutr. doi: 10.1080/09637486.2016.1269726 PubMedCrossRefGoogle Scholar
  236. Robberecht H, De Bruyne T, Hermans N (2016b) Biomarkers of the metabolic syndrome: influence of minerals, oligo and trace elements. J Trace Elem in Med Biol. doi: 10.1016/j.temb.2016.10.005 CrossRefGoogle Scholar
  237. Robberecht H, De Bruyne T, Hermans N (2017) Biomarkers of the metabolic syndrome: influence of caloric intake and various food groups and vitamins. J Food Nutr Res 5:101–109Google Scholar
  238. Rocha VZ, Ras RT, Gagliardi AC et al (2016) Effects of phytosterols on markers of inflammation: a systematic review and meta-analysis. Atherosclerosis. doi: 10.1016/j.atherosclerosis.2016.01.035 CrossRefPubMedGoogle Scholar
  239. Rondanelli M, Monteferrario F, Faliva MA et al (2013) Key points for maximum effectiveness and safety for cholesterol-lowering properties of plant sterols and use in the treatment of metabolic syndrome. J Sci Food Agric 93:2605–2610PubMedCrossRefGoogle Scholar
  240. Ros E (2009) Nuts and novel biomarkers of cardiovascular disease. Am J Clin Nutr 89:1649S–1656SPubMedCrossRefGoogle Scholar
  241. Ros E, Martinez-Gonzalez MA, Estruch R et al (2014) Mediterranean diet and cardiovascular healthy: teachings of the PREDIMED study. Adv Nutr 14:330S–336SCrossRefGoogle Scholar
  242. Rubio-Ruiz ME, El Hafidi M, Perez-Torres I et al (2013) Medicinal agents and metabolic syndrome. Curr Med Chem 120:2626–2640CrossRefGoogle Scholar
  243. Ruidavets JB, Bongard V, Dallongeville J et al (2007) High consumption of grain, fish, dairy products and combinations of these are associated with a low prevalence of metabolic syndrome. J Epidemiol Community Health 61:810–817PubMedPubMedCentralCrossRefGoogle Scholar
  244. Rungseesantivanon S, Thenchaisri N, Ruangvejvorachai P et al (2010) Curcumin supplementation could improve diabetes-induced endothelial dysfunction associated with decreased vascular superoxide production and PKC inhibition. BMC Complement Altern Med 10:57. doi: 10.1186/1472-6882-10-57 PubMedPubMedCentralCrossRefGoogle Scholar
  245. Sahebkar A (2013) Why it is necessary to translate curcumin into clinical practice for the prevention and treatment of metabolic syndrome ? BioFactors 39:197–208PubMedCrossRefGoogle Scholar
  246. Sahebkar A (2014) A systematic review and meta-analysis of randomized controlled trials investigating the effects of curcumin on blood lipid levels. Clin Nutr 33:406–414PubMedCrossRefGoogle Scholar
  247. Salas-Salvado J, Fernandez-Ballart J, Ros E et al (2008) Effect of a Mediterranean diet supplemented with nuts on metabolic syndrome status. One-year results of the PREDIMED randomized trial. Arch Intern Med 168:2449–2458PubMedCrossRefGoogle Scholar
  248. Salas-Salvado J, Guasch-Ferré M, Bullo M et al (2014) Nuts in the prevention and treatment of metabolic syndrome. Am J Clin Nutr 100:399S–407SPubMedCrossRefGoogle Scholar
  249. Sano J, Inami S, Seimiya K et al (2004) Effects of green tea intake on the development of coronary artery disease. Circ J 68:665–670PubMedCrossRefGoogle Scholar
  250. Sarria B, Martinez-Lopez S, Sierra-Cinos JL et al (2016) Regularly consuming a green-roasted coffee blend reduces the risk of metabolic syndrome. Eur J Nutr. doi: 10.1007/s00394-016-1316-8 PubMedCrossRefGoogle Scholar
  251. Sasazuki S, Kodama H, Yoshimasu K et al (2000) Relation between green tea consumption and the severity of coronary atherosclerosis among Japanese men and women. Ann Epidemiol 10:401–408PubMedCrossRefGoogle Scholar
  252. Segura R, Javierre C, Lizarraga MA et al (2006) Other relevant components of nuts: phytosterols, folate and minerals. Br J Nutr 96:S36–S44PubMedCrossRefGoogle Scholar
  253. Serafini M, Laranjinha JA, Almeida LM et al (2000) Inhibition of human LDL lipid peroxidation by phenol-rich beverages and their impact on plasma antioxidant capacity in humans. J Nutr Biochem 11:585–590PubMedCrossRefGoogle Scholar
  254. Shah BH, Nawaz Z, Pertani SA et al (1999) Inhibitory effect of curcumin, a food spice from turmeric, on platelet-activating factor- and arachidonic acid-mediated platelet aggregation through inhibition of thromboxane formation and Ca2+ signaling. Biochem Pharmacol 58:1167–1172PubMedCrossRefGoogle Scholar
  255. Shang F, Li X, Jiang X (2016) Coffee consumption and risk of the metabolic syndrome: a meta-analysis. Diabetes Metab 42:80–87PubMedCrossRefGoogle Scholar
  256. Sharifi F, Sheikhi AK, Behdad M et al (2010) Effect of garlic on serum adiponectin and interleukin levels in women with metabolic syndrome. Int J Endocrinol Metab 8:68–73Google Scholar
  257. Shen L (2012) Beneficial effects of coffee consumption go beyond antioxidation. Nutr 28:1194–1195CrossRefGoogle Scholar
  258. Shen Y, Jia L-N, Honma N et al (2012) Beneficial effects of Cinnamon on the metabolic syndrome, inflammation, and pain, and mechanisms underlying these effects: a review. J Tradit Complement Med 2:27–32PubMedPubMedCentralCrossRefGoogle Scholar
  259. Shin JY, Kim JY, Kang HK et al (2015) Effect of fruits and vegetables on metabolic syndrome: a systematic review and meta-analysis of randomized controlled trials. Int J Food Sci Nutr 66:416–425PubMedCrossRefGoogle Scholar
  260. Shrime MG, Bauer SR, McDonald AC et al (2011) Flavonoid-rich cocoa consumption affects multiple cardiovascular risk factors in a meta-analysis of short-term studies. J Nutr 141:1982–1988PubMedCrossRefGoogle Scholar
  261. Sialvera TE, Pounis GD, Koutelidakis AE et al (2012) Phytosterols supplementation decreases plasma small and dense LDL levels in metabolic syndrome patients on a westernized type diet. Nutrition, Metab and Cardiovasc Dis 22:843–848CrossRefGoogle Scholar
  262. Sialvera TE, Koutelidakis AE, Richter DJ et al (2013) Phytosterol supplementation does not affect plasma antioxidant capacity in patients with metabolic syndrome. Int J Food Sci. doi: 10.3109/09637486.2012.706597 CrossRefGoogle Scholar
  263. Silveira JQ, Dourado GK, Cesar TB (2015) Red-fleshed sweet orange juice improves the risk factors for metabolic syndrome. Int J Food Sci Nutr 66:830–836PubMedCrossRefGoogle Scholar
  264. Simao AN, Lozovoy MA, Simao TN et al (2010) Nitric oxide enhancement and blood pressure decrease in patients with metabolic syndrome using soy protein or fish oil. Arq Bras Endocrinol Metabol 54:540–545PubMedCrossRefGoogle Scholar
  265. Simão ANC, Lozovoy MAB, Bahls LD et al (2012) Blood pressure decrease with ingestion of a soya product (kinako) or fish oil in women with the metabolic syndrome: role of adiponectin and nitric oxide. Br J Nutr 108:1435–1442PubMedCrossRefGoogle Scholar
  266. Simao TNC, Lozovoy MAB, Simao ANC et al (2013) Reduced-energy cranberry juice increases folic acid and adiponectin and reduces homocysteine and oxidative stress in patients with the metabolic syndrome. Br J Nutr 110:1885–1894PubMedCrossRefGoogle Scholar
  267. Simao AN, Lozovoy MA, Dichi I (2014) Effect of soy product kinako and fish oil on serum lipids and glucose metabolism in women with metabolic syndrome. Nutrition 30:112–115PubMedCrossRefGoogle Scholar
  268. Sirtori CR, Galli C, Anderson JW et al (2009) Functional foods for dyslipidaemia and cardiovascular risk prevention. Nutr Res Rev 22:244–261PubMedCrossRefGoogle Scholar
  269. Sluijs I, Beulens JW, Grobbee DE et al (2009) Dietary carotenoid intake is associated with lower prevalence of metabolic syndrome in middle-aged and elderly men. J Nutr 139:987–992PubMedCrossRefGoogle Scholar
  270. Smit HJ (2011) Theobromine and the pharmacology of cocoa. In: Fredholm BB (ed) Methylxanthines. Springer Verlag Berlin, Heidelberg, pp 201–234CrossRefGoogle Scholar
  271. Son Y, Lee JH, Chung H-T et al (2013) Therapeutic roles of heme oxygenase-1 in metabolic diseases: curcumin and resveratrol analogues as possible inducers of heme oxygenase-1. Oxidative Medicine and Cellular Longevity ID639541. doi:  10.1155/2013/639541
  272. Soni KB, Kuttan R (1992) Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers. Indian J Physiol Pharmacol 36:273–275PubMedGoogle Scholar
  273. Soriguer F, Rojo-Martinez G, de Fonseca FR et al (2007) Obesity and the metabolic syndrome in Mediterranean countries: a hypothesis related to olive oil. Mol Nutr Food Res 51:1260–1267PubMedCrossRefGoogle Scholar
  274. Srivastava R, Kikshit M, Srimal RC et al (1985) Anti-thrombotic effect of curcumin. Thromb Res 40:413–417PubMedCrossRefGoogle Scholar
  275. Stefanon B, Colitti M (2016) Hydroxytyrosol, an ingredient of olive oil, reduces triglyceride accumulation and promotes lipolysis in human primary visceral adipocytes during differentiation. Exp Biol Med (Epub ahead of print)Google Scholar
  276. Strat KM, Rowley TJ, Smithson AT et al (2016) Mechanisms by which cocoa flavonoids improve metabolic syndrome and related disorders. J Nutr Biochem 35:1–21PubMedCrossRefGoogle Scholar
  277. Sugiura M, Nakamura M, Ogawa K et al (2008) Associations of serum carotenoid concentrations with the metabolic syndrome: interactions with smoking. Br J Nutr 100:1297–1306PubMedCrossRefGoogle Scholar
  278. Sugiura M, Nakamura M, Ogawa K et al (2015) High serum carotenoids associated with lower risk for the metabolic syndrome and its components among Japanese subjects: Mikkabi cohort study. Br J Nutr 114:1674–1682PubMedCrossRefGoogle Scholar
  279. Suhaila M (2014) Functional foods against metabolic syndrome (obesity, diabetes, hypertension and dyslipidemia) and cardiovascular disease. Trends Food Sci Technol 35:114–128CrossRefGoogle Scholar
  280. Sung H, Min WK, Lee W et al (2005) The effects of green tea ingestion over 4 weeks on atherosclerotic markers. Ann Clin Biochem 42:292–297PubMedCrossRefGoogle Scholar
  281. Suriyaprom K, Phonrat B, Satitvipawee P et al (2014) Homocysteine but not serum amyloid A, vitamin A and E related to increased risk of metabolic syndrome in post-menopausal Thai women. Int J Vitam Nutr Res 84:35–44PubMedCrossRefGoogle Scholar
  282. Suzuki K, Ito Y, Inoue T et al (2011) Inverse association of serum carotenoids with prevalence of metabolic syndrome among Japanese. Clin Nutr 30:369–375PubMedCrossRefGoogle Scholar
  283. Swiderski F, Dabrowska M, Rusaczonek A et al (2007) Bioactive substances of garlic and their role in dietoprophylaxis and dietotherapy. Roczn Phz 58:41–46Google Scholar
  284. Takami H, Nakamoto M, Uemura H et al (2013) Inverse correlation between coffee consumption and prevalence of metabolic syndrome: baseline survey of the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study in Tokushima, Japan. J Epidemiol 23:12–20PubMedCrossRefGoogle Scholar
  285. Taku K, Umegaki K, Sato Y et al (2007) Soy isoflavones lower serum total and LDL cholesterol in humans: a meta-analysis of 11 randomized controlled trials. Am J Clin Nutr 85:1148–1156PubMedCrossRefGoogle Scholar
  286. Tardiva AP, Nahas-Neto J, Orsatti CL et al (2015) Effects of omega-3 on metabolic markers in postmenopausal women with metabolic syndrome. Climacteric 18:290–298CrossRefGoogle Scholar
  287. Teske M, Melges AP, de Souza FI et al (2014) Plasma concentrations of retinol in obese children and adolescents: relationship to metabolic syndrome components. Rev Paul Pediatr 32:50–54PubMedPubMedCentralCrossRefGoogle Scholar
  288. Thielecke F, Boschmann M (2009) The potential role of green tea catechin in the prevention of the metabolic syndrome-A review. Phytochemistry 70:11–24PubMedCrossRefGoogle Scholar
  289. Thomas S, Senthilkumar GP, Sivaraman K et al (2015) Effect of S-methyl-l-cysteine on oxidative stress, inflammation and insulin resistance in male Wistar rats fed with high fructose diet. Iran J Med Sci 40:45–50PubMedPubMedCentralGoogle Scholar
  290. Thomson CD, Chisholm A, McLachlan SK et al (2008) Brazil nuts: an effective way to improve selenium status. Am J Clin Nutr 87:379–384PubMedCrossRefGoogle Scholar
  291. Tokede OA, Gaziano JM, Djousse L (2011) Effects of cocoa products/dark chocolate on serum lipids: a meta-analysis. Eur J Clin Nutr 65:879–886PubMedCrossRefGoogle Scholar
  292. Tokede OA, Ellison CR, Pankow JS et al (2012) Chocolate consumption and prevalence of metabolic syndrome in the NHLBI Family Heart Study. Clin Nutr 7:e139–e143Google Scholar
  293. Tortosa-Caparros E, Navas-Carrillo D, Marin F et al (2016) Anti-inflammatory effects of omega-3 and omega-6 polyunsaturated fatty acids in cardiovascular disease and metabolic syndrome. Crit Rev Food Sci Nutr. doi: 10.1080/10408398.20151126549 CrossRefGoogle Scholar
  294. Tsuneki H, Ishizuka M, Terasawa M et al (2004) Effect of green tea on blood glucose levels and serum proteomic patterns in diabetic (db/db) mice and on glucose metabolism in healthy humans. BMC Pharmacol 4:18. doi: 10.1186/1471-2210-4-18 PubMedPubMedCentralCrossRefGoogle Scholar
  295. Udani JK, Singh BB, Barrett ML et al (2009) Evaluation of mangosteen juice blend on biomarkers of inflammation in obese subjects: a pilot, dose finding study. Nutr J 8:48. doi: 10.1186/1475-2891-8-48 PubMedPubMedCentralCrossRefGoogle Scholar
  296. Udani JK, Singh BB, Singh VJ et al (2011) Effects of açai (Euterpe oleracea Mart.) berry preparation on metabolic parameters in a healthy overweight population: a pilot study. Nutr J 10:45.
  297. Uemura H, Katsuura-Kamano S, Yamaguchi M et al (2013) Consumption of coffee, not green tea, is inversely associated with arterial stiffness in Japanese men. Eur J Clin Nutr 67:1109–1114PubMedCrossRefGoogle Scholar
  298. Urpi-Sarda M, Casas R, Chiva-Blanch G et al (2012) Virgin oil and nuts as key foods of the Mediterranean diet effects on inflammatory biomarkers related to atherosclerosis. Pharmacol Res 65:577–583PubMedCrossRefGoogle Scholar
  299. Van der Made SM, Plat J, Mensink RP (2015) Resveratrol does not influence metabolic syndrome risk markers related to cardiovascular health in overweight and slightly obese subjects: a randomized, placebo-controlled crossover trial. PLoS ONE 10:e0118393PubMedPubMedCentralCrossRefGoogle Scholar
  300. van Doorn MB, Espirito Santo SM, Meijer P et al (2006) Effect of garlic powder on C-reactive protein and plasma lipids in overweight and smoking subjects. Am J Clin Nutr 84:1324–1329PubMedCrossRefGoogle Scholar
  301. Venturini D, Simao AN, Urbano MR et al (2015) Effects of extra virgin olive oil and fish oil on lipid profile and oxidative stress in patients with metabolic syndrome. Nutrition 31:834–840PubMedCrossRefGoogle Scholar
  302. Vernarelli JA, Lambert JD (2013) Tea consumption is inversely associated with weight status and other markers for metabolic syndrome in US adults. Eur J Nutr 52:1039–1048PubMedCrossRefGoogle Scholar
  303. Vieira Senger AE, Schwanke CH, Gomes I et al (2012) Effect of green tea (Camelia sinensis) consumption on the components of metabolic syndrome in elderly. J Nutr Health Aging 16:738–742PubMedCrossRefGoogle Scholar
  304. Villaca Chaves G, Goncalves de Souza G, Cardoso de Matos A et al (2010) Serum retinol and β-carotene levels and risk factors for cardiovascular disease in morbid obesity. Int J Vitam Nutr Res 80:159–167PubMedCrossRefGoogle Scholar
  305. Virgili F, Marino M (2008) Regulation of cellular signals from nutritional molecules: a specific role for phytochemicals, beyond antioxidant activity. Free Radic Biol Med 45:1205–1216PubMedCrossRefGoogle Scholar
  306. Viscogliosi G, Cipriani E, Liguori ML et al (2013) Mediterranean dietary pattern adherence: associations with prediabetes, metabolic syndrome, and related microinflammation. Metab Syndr and Relat Disord 11:210–216CrossRefGoogle Scholar
  307. Vissers MN, Zock PL, Katan MB (2004) Bioavailability and antioxidant effects of olive oil phenols in humans: a review. Eur J Clin Nutr 58:955–965PubMedCrossRefGoogle Scholar
  308. Wan Y, Vinson JA, Etherton TD et al (2001) Effects of cocoa powder and dark chocolate on LDL oxidative susceptibility and prostaglandin concentrations in humans. Am J Clin Nutr 74:596–602PubMedCrossRefGoogle Scholar
  309. Wang-Polagruto JF, Villablanca AC, Polagruto JA et al (2006) Chronic consumption of flavanol-rich cocoa improves endothelial function and decreases vascular cell adhesion molecule in hyper-cholesterolemic postmenopausal women. J Cardiovasc Pharmacol 47:S177–S186PubMedCrossRefGoogle Scholar
  310. Wei J, Zeng C, Qy Gong et al (2015) Associations between dietary antioxidant intake and metabolic syndrome. PLoS ONE. doi: 10.1371/journal.pone.0130876 CrossRefPubMedPubMedCentralGoogle Scholar
  311. Wei X, Peng R, Cao J et al (2016) Serum vitamin A status is associated with obesity and the metabolic syndrome among school-age children in Chongqing, China. Asia Pac J Clin Nutr 25:563–570PubMedGoogle Scholar
  312. Williams SJ, Sutherland WH, McCormick MP et al (2005) Aged garlic extract improves endothelial function in men with coronary artery disease. Phytother Res 19:314–319PubMedCrossRefGoogle Scholar
  313. Wolfram S, Wang Y, Thielecke F (2006) Anti-obesity effects of green tea: from bedside to bench. Mol Nutr Food Res 50:176–187PubMedCrossRefGoogle Scholar
  314. Wong WW, Smith EO, Stuff JE et al (1998) Cholesterol-lowering effect of soy protein in normocholesterolemic and hypercholesterolemic men. Am J Clin Nutr 68:1385S–1389SPubMedCrossRefGoogle Scholar
  315. Wu L, Piotrowski K, Rau T et al (2014) Walnut-enriched diet reduces fasting non-HDL-cholesterol and apolipoprotein B in healthy Caucasian subjects: a randomized controlled cross-over clinical trial. Metab Clin Experim 63:382–391CrossRefGoogle Scholar
  316. Xu Y, Ku B, Cui L et al (2007) Curcumin reverses impaired hippocampal neurogenesis and increases serotonin receptor 1A mRNA and brain-derived neurotrophic factor expression in chronically stressed rats. Brain Res 1162:9–18PubMedCrossRefGoogle Scholar
  317. Yang YS, Su YF, Yang HW et al (2014a) Lipid-lowering effects of curcumin in patients with metabolic syndrome: a randomized, double-blind, placebo-controlled trial. Phytother Res 28:1770–1777PubMedCrossRefGoogle Scholar
  318. Yang X, Yin L, Li T et al (2014b) Green tea extracts reduce adipogenesis by decreasing expression of transcription factors C/EPBα and PPARϒ. Int J Clin Exp Med 15:4906–4914Google Scholar
  319. Yao Z, Zhang L, Ji G (2014) Efficacy of polyphenolic ingredients of Chinese herbs in treating dyslipidemia of metabolic syndromes. J Integr Med 12:135–146PubMedCrossRefGoogle Scholar
  320. Yesil A, Yilmaz Y (2013) Review article: coffee consumption, the metabolic syndrome and non-alcoholic fatty liver disease. Aliment Pharmacol Ther 38:1038–1044PubMedCrossRefGoogle Scholar
  321. Yoshida H, Yanai H, Ito K et al (2010) Administration of natural astaxanthin increases serum HDL-cholesterol and adiponectin in subjects with mild hyperlipidemia. Atherosclerosis 209:520–523PubMedCrossRefGoogle Scholar
  322. Yu S, Guo X, Yang H et al (2014) An update on the prevalence of metabolic syndrome and its associated factors in rural northeast China. BMC Public Health 14:877. doi: 10.1186/1471-2458-14-877 PubMedPubMedCentralCrossRefGoogle Scholar
  323. Zeba AN, Delisie HF, Rossier C et al (2013) Association of high-sensitivity C-reactive protein with cardiometabolic risk factors and micronutrient deficiencies in adults of Ouagadougou, Burkina Faso. Br J Nutr 109:1266–1275PubMedCrossRefGoogle Scholar
  324. Zhang W, Teng SP, Popovich DG (2009) Generation of group B soyasaponins I and III by hydrolysis. J Agric Food Chem 57:3620–3625PubMedCrossRefGoogle Scholar
  325. Zhang AL, Li BX, Li M et al (2012) Relationship between skin carotenoid level and metabolic syndrome related indices. Zhonghua Yi Xue Za Zhi 92:2865–2867PubMedGoogle Scholar
  326. Zheng T, Zhang CL, Zhao XL et al (2013) The roles of garlic on the lipid parameters: a systematic review of the literature. Crit Rev Food Sci Nutr 53:215–230CrossRefGoogle Scholar
  327. Zhong X, Zhang T, Liu Y et al (2015) Short-term weight-centric effects of tea or tea extract in patients with metabolic syndrome: a meta-analysis of randomized controlled trials. Nutr Diabetes 5:e160. doi: 10.1038/nutd.2015.10 PubMedPubMedCentralCrossRefGoogle Scholar
  328. Zhuo XG, Melissa KM, Shaw W (2004) Soy isoflavone intake lowers serum LDL-cholesterol: a meta-analysis of 8 randomized controlled trials in humans. J Nutr 134:2395–2400PubMedCrossRefGoogle Scholar
  329. Ziegenfuss TN, Hofheins JE, Mendel RW et al (2006) Effects of water-soluble cinnamon extract on body composition and features of the metabolic syndrome in pre-diabetic men and women. J Int Soc Sports Nutr 3:45–53PubMedPubMedCentralCrossRefGoogle Scholar
  330. Zimmermann MB, Aeberli I (2008) Dietary determinants of subclinical inflammation, dyslipidemia and components of the metabolic syndrome in overweight children: a review. Int J Obesity 32:S11–S18CrossRefGoogle Scholar
  331. Zulet MA, Puchau B, Hermsdorff HH et al (2008) Vitamin A intake is inversely related with adiposity in healthy young adults. J Nutr Sci Vitaminol 54:347–352PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media B.V. 2017

Authors and Affiliations

  • Harry Robberecht
    • 1
  • Tess De Bruyne
    • 1
  • Nina Hermans
    • 1
  1. 1.Department of Pharmaceutical Sciences, Laboratory of General and Functional Foods, NatuRA (Natural Products and Food-Research and Analysis)University of AntwerpWilrijkBelgium

Personalised recommendations