**1. Introduction**

A famous ancient proverb states that "Eat breakfast like a king, lunch like a prince, and dinner like a pauper." In today's era, these words have long been discarded. The magnitude of obesity has reached in pandemic proportion due to new technology and modern life, which makes life easier and less active along with the intake of high energy dense food for better taste [1–3]. This is one of the biggest public health concerns of today's era, which affects the individual not only physically but also physiologically and psychologically.

The World Health Organization (WHO) has reported that obesity has been growing at an alarming rate worldwide and has nearly been tripled between 1975 and 2016. It was also reported by WHO in the year 2016 that more than 1.9 billion adults, 18 years and older, were overweight; of these over 650 million were obese (https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight) [4].

Nowadays, obesity is regarded as a complex dysfunctional neuroendocrine problem in which genetic makeup and environmental factors act in concert. The nongenetic risk factors encompass a wide range of social, physiological,

#### **Figure 1.**

*Overnutrition (overconsumption of high-fat and energy dense foods), lack of physical activity, sedentary lifestyle, and genetic susceptibility are the leading factors associated with the development of obesity. In addition to dysfunctional angiogenesis, an obese state is characterized by an abnormal inflammatory response, low antioxidant capacity, and reduced insulin sensitivity that may eventually lead to the generation of inflammation, oxidative stress, and insulin resistance. The figure was modified from the following review paper by Dludla et al. [6].*

environmental, and behavioral factors. Sedentary lifestyle and overconsumption of high-fat and energy dense foods are a major contributor to energy imbalance. The altered phenomenon of hunger and satiety, lack of physical activity, decreased thermogenesis, and resting metabolic rate over a long period of time may lead to the energy imbalance.

In addition, other external factors such as age, gender, food preference, breakfast skipping, medications, chemical toxicity, disorders of the endocrine system, socioeconomic status, and a psychological factor may give rise to weight gain problems. It is considered as a major contributor to the global burden of chronic diseases like hypertension, type 2 diabetes, hypercholesterolemia, heart diseases, insulin resistance, atherosclerosis, ischemic heart diseases, respiratory diseases, orthopedic disorders, several types of cancer, hormonal imbalance, disability, and many other diseases. Overweight and obesity also play a pivotal role in the development of low-grade inflammation, which contribute to the development of obesity-linked disorders, in particular to metabolic dysfunction [5]. However, a growing body of knowledge suggests that a possible convergence of an inflammatory state, which results in chronic inflammation and oxidative stress, is localized within adipose tissue [6] as shown in **Figure 1**. Adipose tissue inflammation plays a crucial role in promulgating obesity-related metabolic complications including the development of insulin resistance [6–8].

#### **2. Adipose tissue: manager of inflammation**

Over the past decades, it is well established that adipose tissue is not merely a fat storage depot but has been recognized as an endocrine organ capable of producing various bioactive substances. It then became evident that white adipose tissue (WAT) secretes ample of peptides. Few of them regulate the inflammatory

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**Figure 2.**

*Weight Management: Inflammation*

*DOI: http://dx.doi.org/10.5772/intechopen.92380*

classification of cytokines is depicted in **Figure 3**.

processes such as leptin and adiponectin, whereas others are well-known cytokines such as interleukin (IL)-6, IL-1 and its receptor antagonist (IL-1Ra), and tumor necrosis factor (TNF)-α [9]. As we know, obesity is one of the major causes of atherosclerosis, which is recognized as a chronic vascular inflammatory process in which cytokines and chemokines play a dramatic role [9–10]. White adipose tissue plays an important role in metabolism and inflammation as illustrated in **Figure 2**. Cytokines are categorized as interleukins, interferons, chemokines, hematopoietic factors, and growth factors. They are knotted in many biological processes such as growth, differentiation, cell division, apoptosis, immunity, and inflammation [9]. Cytokines are produced by numerous cell types of the hematopoietic lineage including T cells, B cells, mast cells, macrophages, dendritic cells, and natural killer cells. In spite of these, cytokines are also produced by nonhematopoietic cells such as epithelial cells, hepatocytes, and fibroblasts [9, 12]. Evidence revealed that IL-1, IL-6, and TNF-α are characterized as a proinflammatory cytokine that activates both acute and chronic inflammatory responses [9]. Inhibitors that control inflammation can be categorized as anti-inflammatory cytokines, soluble receptors to cytokines, and naturally occurring proteins. Types of antiinflammatory cytokines are IL-10, IL-4, and TGF-β; soluble receptors to cytokines are IL-1 and TNF-α; and naturally occurring proteins are IL-1Ra receptors. The

Chemokines are a type of cytokine that is a part of family molecules that are indulged in the chemotaxis of inflammatory cells via the generation of local concentration gradients. Chemokines play an important role in various physiological and pathological processes such as cell recruitment process and development of lymphoid organs or metastases. In spite of these, chemokines also participate in metabolic and inflammatory disorders such as rheumatoid arthritis, glomerulonephritis,

*Adipose tissue is a metabolically dynamic, highly active endocrine organ. White adipose tissue (WAT) produces a large variety of proteins regulating metabolism and inflammation, contributing to the maintenance of energy homeostasis and, probably, the pathogenesis of obesity-related metabolic and vascular complications. The figure was modified from the following research paper by Juge-Aubry et al. [9]. The following website was used for the* 

*extraction of image: https://scitechdaily.com/gc-1-turns-white-fat-brown-fat/ [11].*

#### *Weight Management: Inflammation DOI: http://dx.doi.org/10.5772/intechopen.92380*

processes such as leptin and adiponectin, whereas others are well-known cytokines such as interleukin (IL)-6, IL-1 and its receptor antagonist (IL-1Ra), and tumor necrosis factor (TNF)-α [9]. As we know, obesity is one of the major causes of atherosclerosis, which is recognized as a chronic vascular inflammatory process in which cytokines and chemokines play a dramatic role [9–10]. White adipose tissue plays an important role in metabolism and inflammation as illustrated in **Figure 2**.

Cytokines are categorized as interleukins, interferons, chemokines, hematopoietic factors, and growth factors. They are knotted in many biological processes such as growth, differentiation, cell division, apoptosis, immunity, and inflammation [9]. Cytokines are produced by numerous cell types of the hematopoietic lineage including T cells, B cells, mast cells, macrophages, dendritic cells, and natural killer cells. In spite of these, cytokines are also produced by nonhematopoietic cells such as epithelial cells, hepatocytes, and fibroblasts [9, 12]. Evidence revealed that IL-1, IL-6, and TNF-α are characterized as a proinflammatory cytokine that activates both acute and chronic inflammatory responses [9]. Inhibitors that control inflammation can be categorized as anti-inflammatory cytokines, soluble receptors to cytokines, and naturally occurring proteins. Types of antiinflammatory cytokines are IL-10, IL-4, and TGF-β; soluble receptors to cytokines are IL-1 and TNF-α; and naturally occurring proteins are IL-1Ra receptors. The classification of cytokines is depicted in **Figure 3**.

Chemokines are a type of cytokine that is a part of family molecules that are indulged in the chemotaxis of inflammatory cells via the generation of local concentration gradients. Chemokines play an important role in various physiological and pathological processes such as cell recruitment process and development of lymphoid organs or metastases. In spite of these, chemokines also participate in metabolic and inflammatory disorders such as rheumatoid arthritis, glomerulonephritis,

#### **Figure 2.**

*Adipose tissue is a metabolically dynamic, highly active endocrine organ. White adipose tissue (WAT) produces a large variety of proteins regulating metabolism and inflammation, contributing to the maintenance of energy homeostasis and, probably, the pathogenesis of obesity-related metabolic and vascular complications. The figure was modified from the following research paper by Juge-Aubry et al. [9]. The following website was used for the extraction of image: https://scitechdaily.com/gc-1-turns-white-fat-brown-fat/ [11].*

#### **Figure 3.**

*Classification of cytokines. (a) Classes of inflammatory cytokines. (b) Anti-inflammatory mediators. The figure was modified from the following research paper by Juge-Aubry et al. [9].*

and atherosclerosis via their innate ability to recruit and activate the inflammatory cells [9]. They are categorized into four subclasses according to the position of their cysteines (CXC, C, CX3C, and CC) [9, 13]. Chemokines that are produced from WAT are interferon-γ inducible protein 10 (IP-10 or CXCL10) and IL-8 (or CXCL8) belong to the CXC chemokines, while monocyte chemo-attractant protein-1 (MCP-1 or CCL2) and regulated upon activation normal T-cell express sequence (RANTES or CCL5) are CC chemokines [9, 13]. Previous studies showed that chemokines are paracrine rather than systemic factors, the significance of their secretion via adipose tissue may be seen in the context of fat depots found in close proximity to their target tissues, for example, subcutaneous fat in inflammatory skin diseases, perivascular adipose tissue in obesity-associated cardiovascular diseases, and perirenal fat in glomerulonephritis [9, 14].

In addition, several other metabolically important proteins with immunomodulatory actions are secreted by adipose tissue, including leptin, adiponectin, and resistin. The dysregulated expression of these factors, caused by excess adiposity and adipocyte dysfunction, has been linked to the pathogenesis of various disease processes through altered immune responses. As such, much attention has been paid to develop a better understanding of the immunoregulatory functions of adipose tissue. New factors secreted by adipose tissue have been identified that either promote inflammatory responses and metabolic dysfunction or contribute to the resolution of inflammation and have beneficial effects on obesity-linked metabolic disorders. These findings lend additional support to the notion that an imbalance of pro- and anti-inflammatory adipokines secreted by adipose tissue contributes to metabolic dysfunction [5].

### **3. Obesity: state of low-grade inflammation**

Obesity is associated with alterations in immunity, a chronic low-grade inflammation, which is characterized by abnormal secretion of adipokines, that is, there is an increment in circulating proinflammatory cytokines and a decrement in anti-inflammatory cytokines. It is also linked with alteration in immunity. However,

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enumerated below:

**4.1 Carbohydrates**

*Weight Management: Inflammation*

*DOI: http://dx.doi.org/10.5772/intechopen.92380*

with the reduction in body weight, these parameters may reverse or come to the normal level. Although, it is still debatable how obesity triggers inflammation. Earlier, several hypotheses were proposed regarding the inflammation of obesity. The first one stated that overburden of nutrients in the adipocytes leads to intracellular stress that results in the stimulation of inflammatory cytokines [15–17]. The excessive nutrients may lead to aggregation of unfolded proteins in the endoplasmic reticulum (ER) via activation of the unfolded protein response (UPR) pathway [15, 17]. The pathway of UPR depends on basically three main sensors of ER, that is, PKR-like eukaryotic initiation factor 2α kinase (PERK), inositolrequiring enzyme 1 (IRE-1), and activating transcription factor 6 (ATF-6) [15, 18]. The activity of the C-Jun amino-terminal kinase (JNK) and inhibitor of IκB (IKK-β), serine-phosphorylation of insulin-receptor substrate protein 1 (IRS-1), and the nuclear factor-κB (NF-κB) pathway may increase by the activated sensors of ER that

results in increased expression of proinflammatory cytokines [15–16, 19–21].

**4. Dietary components that affect obesity related to inflammation**

healthy immune balance of an individual [15] as shown in **Figure 4**.

The analysis of dietary intake is an approach to investigate a link between diet and overweight and obesity-related inflammation. Various studies reported that bioactive nutrients and dietary non-nutrients strongly influence health, metabolism, and progression of pathologic states that ultimately result in chronic degenerative diseases [26]. Many studies indicate that diet may affect body weight by controlling satiety and metabolic efficiency or by harmonizing insulin secretion and action [3, 27]. It is an essential key factor for immune response. Earlier, evidence revealed that undernutrition brings about immunosuppression due to susceptibility to infection. Whereas, overnutrition brings about immunoactivation due to susceptibility to inflammatory diseases. As a result, optimum nutrition is mandatory for a

Dietary components play an important role in obesity-related inflammation as

Carbohydrates are the main food source of a living organism and a major source

of energy. Carbohydrates are also known as energy giving foods. The source of energy was estimated based on their glycemic index (GI) or glycemic load (GL) values. GI is the value given to the foods on how quickly they increase the glucose level postprandially and measures the quality of carbohydrate. GL calculates both the quality and quantity of carbohydrates [15, 28]. Earlier studies reported that, positive correlation exists between dietary GI and GL and biomarkers of inflammation because a low GI diet decreases the rate of glucose absorption in the body that subsequently reduces hyperglycemia and hyperinsulinemia that results in the reduction of systemic inflammation. Earlier, it was also reported that weight loss

pathogen sensors that result in chronic inflammation [15, 25].

The second hypothesis enumerates that overburdened adipocytes with fat cells intensely increase the infiltration of macrophages, which may lead to subsequent differentiation and activation of cytotoxic T cells. As a result, initiation and propagation of inflammatory cytokines cascades occur [15, 22]. Third hypothesis proposes that as during obesity, enlargement of adipose tissue happens as a result tissue becomes relatively hypoxic. Hypoxia within the adipose tissues results in the activation of inflammatory pathways [15, 23–24]. Above all, the last hypothesis suggests that overburdened adipocytes themselves may directly activate immune

#### *Weight Management: Inflammation DOI: http://dx.doi.org/10.5772/intechopen.92380*

with the reduction in body weight, these parameters may reverse or come to the normal level. Although, it is still debatable how obesity triggers inflammation. Earlier, several hypotheses were proposed regarding the inflammation of obesity. The first one stated that overburden of nutrients in the adipocytes leads to intracellular stress that results in the stimulation of inflammatory cytokines [15–17].

The excessive nutrients may lead to aggregation of unfolded proteins in the endoplasmic reticulum (ER) via activation of the unfolded protein response (UPR) pathway [15, 17]. The pathway of UPR depends on basically three main sensors of ER, that is, PKR-like eukaryotic initiation factor 2α kinase (PERK), inositolrequiring enzyme 1 (IRE-1), and activating transcription factor 6 (ATF-6) [15, 18]. The activity of the C-Jun amino-terminal kinase (JNK) and inhibitor of IκB (IKK-β), serine-phosphorylation of insulin-receptor substrate protein 1 (IRS-1), and the nuclear factor-κB (NF-κB) pathway may increase by the activated sensors of ER that results in increased expression of proinflammatory cytokines [15–16, 19–21].

The second hypothesis enumerates that overburdened adipocytes with fat cells intensely increase the infiltration of macrophages, which may lead to subsequent differentiation and activation of cytotoxic T cells. As a result, initiation and propagation of inflammatory cytokines cascades occur [15, 22]. Third hypothesis proposes that as during obesity, enlargement of adipose tissue happens as a result tissue becomes relatively hypoxic. Hypoxia within the adipose tissues results in the activation of inflammatory pathways [15, 23–24]. Above all, the last hypothesis suggests that overburdened adipocytes themselves may directly activate immune pathogen sensors that result in chronic inflammation [15, 25].

#### **4. Dietary components that affect obesity related to inflammation**

The analysis of dietary intake is an approach to investigate a link between diet and overweight and obesity-related inflammation. Various studies reported that bioactive nutrients and dietary non-nutrients strongly influence health, metabolism, and progression of pathologic states that ultimately result in chronic degenerative diseases [26]. Many studies indicate that diet may affect body weight by controlling satiety and metabolic efficiency or by harmonizing insulin secretion and action [3, 27]. It is an essential key factor for immune response. Earlier, evidence revealed that undernutrition brings about immunosuppression due to susceptibility to infection. Whereas, overnutrition brings about immunoactivation due to susceptibility to inflammatory diseases. As a result, optimum nutrition is mandatory for a healthy immune balance of an individual [15] as shown in **Figure 4**.

Dietary components play an important role in obesity-related inflammation as enumerated below:

#### **4.1 Carbohydrates**

Carbohydrates are the main food source of a living organism and a major source of energy. Carbohydrates are also known as energy giving foods. The source of energy was estimated based on their glycemic index (GI) or glycemic load (GL) values. GI is the value given to the foods on how quickly they increase the glucose level postprandially and measures the quality of carbohydrate. GL calculates both the quality and quantity of carbohydrates [15, 28]. Earlier studies reported that, positive correlation exists between dietary GI and GL and biomarkers of inflammation because a low GI diet decreases the rate of glucose absorption in the body that subsequently reduces hyperglycemia and hyperinsulinemia that results in the reduction of systemic inflammation. Earlier, it was also reported that weight loss

#### **Figure 4.**

*Healthy immune balance between undernutrition and overnutrition. The figure was modified from the following research paper by Lee et al. [15].*

leads to improvement in insulin sensitivity and a reduction in the level of proinflammatory cytokines. Various health organization also reported that low GI diets help in managing diabetes and coronary heart diseases and considered as a weapon against obesity [29–30].

Neuhouser et al. [31] revealed from randomized, crossover feeding study that respondents with high-fat mass (>32.0% for male and >25.0% for female) showed reduced CRP (*P* = 0.02) and marginally increased adiponectin (*P* = 0.06). Therefore, it was concluded that the quality of carbohydrates independent of energy was very important as low-GL foods improve the inflammatory and adipokine profiles of overweight and obese individuals [31]. Another study done by Levitan et al., among women (*n* = 18,137, >45 years of age), reported that diets characterized by lower GI and GL were associated with somewhat more favorable lipid profiles and lower CRP [32]. Interestingly, one of the epidemiological studies done by Vrolix and Mensick found that consumption of a diet with decreased GL does not decrease the metabolic risk parameters in overweight subjects [33]. Another study done by Kelly et al. also supports the above findings, that is, it does not found any additional benefit of including a low glycemic diet with exercise on insulin sensitivity and adipokine concentrations [34]. Above all, it may be stated that observational studies showed a positive association between intake of GI/GL diet and markers of inflammation. However, interventional studies do not found such an association.

#### **4.2 Dietary fat**

Fat is also one of the important sources of energy that serves both structural and metabolic functions of living organisms. The excessive accumulation of fat in the body leads to impairment of the immune system. A number of fatty acids have been studied including saturated, trans-fatty acids, and polyunsaturated fatty acids (PUFA) for their effect on inflammatory status [15].

#### *4.2.1 Polyunsaturated fatty acids*

The omega-3 (n-3) and omega-6 (n-6) PUFA families are precursors of eicosanoids, which play a vital role in the immune response [15]. Simpoulos [35]

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*Weight Management: Inflammation*

inflammatory diseases [36].

*4.2.2 Trans and saturated fatty acids*

**4.3 Fruits and vegetables**

*DOI: http://dx.doi.org/10.5772/intechopen.92380*

stated that high omega-6 fatty acids increase leptin and insulin resistance, whereas omega-3 fatty acids lead to homeostasis and weight loss. This is so because the high omega-6/omega-3 ratio is associated with overweight/obesity, whereas a balanced ratio decreases obesity and weight gain [35]. Another study showed that an increase in the intake of n-6:n-3 PUFA potentiates the inflammatory processes that ultimately lead to many inflammatory diseases such as nonalcoholic fatty liver disease (NAFLD), cardiovascular disease, diabetes, obesity, inflammatory bowel disease (IBD), rheumatoid arthritis, and Alzheimer's disease. This change in the ratio of consumption of n-3/n-6 fatty acids changes the production of important mediators and regulators of inflammation and immune response that leads toward the proinflammatory state. Hence, it was concluded in the study that increasing the ratio of (n-3)/(n-6) PUFA in the diet may lead to a reduction in the incidence of chronic

A clinical trial and in-vitro experiment study reported that supplementation of fish oil delineates the expression of adipose inflammatory genes including inflammasome-associated IL-18 and IL-1b and circulating IL-18 levels. In spite of this, it was also stated that both eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) decrease the inflammasome gene expression in obese human adipose and human adipocyte and macrophages [37]. Above all, various studies concluded that omega-3 fatty acids, namely EPA and DHA, have an anti-inflammatory effect.

A review study was done by Rogero and Calder stated that saturated fatty acids induce inflammation by activating the TLR4 signaling pathway (TLR4 signaling pathway is recognized as the main pathway that triggers in obesity-induced inflammation) [38]. Another study revealed that the ingestion of excessive amounts of trans-fatty acids and saturated fatty acids is considered to be a risk factor for metabolic and degenerative diseases. It was also emphasized that saturated and trans-fatty acids favor a proinflammatory state leading to insulin resistance. These fatty acids can be indulged in several inflammatory pathways, contributing to disease progression in chronic inflammation, autoimmunity, allergy, cancer, atherosclerosis, hypertension, and heart hypertrophy as well as other metabolic and degenerative diseases. As a consequence, intake of dietary saturated and trans-fatty acids leads to lipotoxicity in several target organs by direct effects, represented by various inflammatory pathways, and through indirect effects, including an important alteration in the gut microbiota associated with endotoxemia process [39].

Fruits and vegetables comprise a myriad of nutrients, that is, vitamins, minerals, and many food compounds that have been inversely correlated with metabolic risk factors such as oxidative stress and inflammation. In a randomized controlled trial study, it was found that fruits and vegetables reduce the risk of metabolic disease that may be via modulation of gut microbiota. The study also revealed that fruits and vegetables decrease the secretion of interleukin-6 (IL-6) and lipopolysaccharide-binding protein (LBP) [40]. Another study done by Navarro et al. through factor analysis found that dietary patterns loaded with fruits and vegetables strongly negatively correlated with the secretion of hs-CRP among prepubertal girls [41]. An almost similar result was observed by Julia et al. that dietary pattern characterized by intake rich in vegetable and vegetable oil leads to the supply of essential fatty acids and antioxidant micronutrients showed a negative correlation with the risk of elevation of CRP [42]. Another cross-sectional study done on a group of 7574

#### *Weight Management: Inflammation DOI: http://dx.doi.org/10.5772/intechopen.92380*

stated that high omega-6 fatty acids increase leptin and insulin resistance, whereas omega-3 fatty acids lead to homeostasis and weight loss. This is so because the high omega-6/omega-3 ratio is associated with overweight/obesity, whereas a balanced ratio decreases obesity and weight gain [35]. Another study showed that an increase in the intake of n-6:n-3 PUFA potentiates the inflammatory processes that ultimately lead to many inflammatory diseases such as nonalcoholic fatty liver disease (NAFLD), cardiovascular disease, diabetes, obesity, inflammatory bowel disease (IBD), rheumatoid arthritis, and Alzheimer's disease. This change in the ratio of consumption of n-3/n-6 fatty acids changes the production of important mediators and regulators of inflammation and immune response that leads toward the proinflammatory state. Hence, it was concluded in the study that increasing the ratio of (n-3)/(n-6) PUFA in the diet may lead to a reduction in the incidence of chronic inflammatory diseases [36].

A clinical trial and in-vitro experiment study reported that supplementation of fish oil delineates the expression of adipose inflammatory genes including inflammasome-associated IL-18 and IL-1b and circulating IL-18 levels. In spite of this, it was also stated that both eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) decrease the inflammasome gene expression in obese human adipose and human adipocyte and macrophages [37]. Above all, various studies concluded that omega-3 fatty acids, namely EPA and DHA, have an anti-inflammatory effect.

#### *4.2.2 Trans and saturated fatty acids*

A review study was done by Rogero and Calder stated that saturated fatty acids induce inflammation by activating the TLR4 signaling pathway (TLR4 signaling pathway is recognized as the main pathway that triggers in obesity-induced inflammation) [38]. Another study revealed that the ingestion of excessive amounts of trans-fatty acids and saturated fatty acids is considered to be a risk factor for metabolic and degenerative diseases. It was also emphasized that saturated and trans-fatty acids favor a proinflammatory state leading to insulin resistance. These fatty acids can be indulged in several inflammatory pathways, contributing to disease progression in chronic inflammation, autoimmunity, allergy, cancer, atherosclerosis, hypertension, and heart hypertrophy as well as other metabolic and degenerative diseases. As a consequence, intake of dietary saturated and trans-fatty acids leads to lipotoxicity in several target organs by direct effects, represented by various inflammatory pathways, and through indirect effects, including an important alteration in the gut microbiota associated with endotoxemia process [39].

### **4.3 Fruits and vegetables**

Fruits and vegetables comprise a myriad of nutrients, that is, vitamins, minerals, and many food compounds that have been inversely correlated with metabolic risk factors such as oxidative stress and inflammation. In a randomized controlled trial study, it was found that fruits and vegetables reduce the risk of metabolic disease that may be via modulation of gut microbiota. The study also revealed that fruits and vegetables decrease the secretion of interleukin-6 (IL-6) and lipopolysaccharide-binding protein (LBP) [40]. Another study done by Navarro et al. through factor analysis found that dietary patterns loaded with fruits and vegetables strongly negatively correlated with the secretion of hs-CRP among prepubertal girls [41]. An almost similar result was observed by Julia et al. that dietary pattern characterized by intake rich in vegetable and vegetable oil leads to the supply of essential fatty acids and antioxidant micronutrients showed a negative correlation with the risk of elevation of CRP [42]. Another cross-sectional study done on a group of 7574

Koreans found that an inverse correlation exists between vegetable pattern and CRP and the association appeared to be more predominant in men having hypertensive blood pressure [43]. Surprisingly, the study done by Salas-Salvado et al. (*n* = 772, 55–80 years of age) and Freese et al. (*n* = 77, 19–52 years of age) did not found any association between a diet rich in vegetables and fruits with inflammatory markers [adiponectin, CRP, IL-6, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1)] [15, 44–45]. Another study done by Morand et al. (*n* = 24, mean age of 56 years) also showed a similar pattern of above finding that a single fruit supplementation (500 mL of orange juice/d for 4 weeks) did not change the levels of CRP, IL-6, ICAM-1, and VCAM-1 [15, 46].
