Applied nutritional investigationEffects of different dietary approaches on inflammatory markers in patients with metabolic syndrome: A systematic review and meta-analysis
Introduction
Metabolic syndrome (MetS) is a major health issue of Western and westernized modern societies [1]. Here, lifestyle is often characterized by stress, fast food, and little exercise. The World Health Organization states obesity and overweight as the fifth leading risk for global deaths [2]. MetS is defined by the simultaneous occurrence of at least three of the following criteria: central obesity, elevated blood pressure, elevated plasma glucose, and dyslipidemia [3]. Obesity is common among patients suffering from MetS, which is associated with serious comorbidities [3]; obesity is a critical risk factor for cardiovascular diseases, diabetes mellitus 2, and arterial diseases [4]. These symptoms of MetS interact with and exacerbate each other.
The primary mediators of Mets may be excess accumulation of abdominal fats and mature adipocytes [5]. Insulin resistance correlates with a state of chronical subclinical inflammation and endothelial dysfunction. Furthermore, MetS is thought to be a low-grade inflammatory disease [5].
Adipose tissue itself can be seen as an endocrine organ that plays a critical role in the immune homeostasis. It produces and releases a variety of adipokines and cytokines, including leptin, adiponectin, resistin, and visfatin, as well as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and others [6], [7]. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of metabolic disease [5]. Furthermore, adipose tissue macrophages are a prominent source of proinflammatory cytokines, which can block insulin action in adipose tissue, skeletal muscle, and liver autocrine/paracrine signaling and cause systemic insulin resistance via endocrine signaling, providing a potential link between inflammation and insulin resistance [6]. Dietary approaches are thought to positively influence the immune responses by decreasing its predominant proinflammatory milieu [8].
Several trials and reviews have documented the potential benefits of different dietary approaches on immune functions [5], [8], [9], [10], [11]. However, just a few studies about different dietary approaches for patients with MetS were conducted.
A primary goal of low-carbohydrate diets is weight loss. Weight loss leads to reductions in inflammatory biomarkers in overweight men [12]. Experimental studies have provided evidence that, independent from weight gain, high intake levels of refined or simple carbohydrates are associated with proinflammatory effects [13].
Low-fat diets may simultaneously change macronutrient intake and quality that can increase intake of natural anti-inflammatory foods, such as fruits and vegetables, which may ultimately lower C-reactive protein (CRP) [14]. Another proposed mechanism involves low-fat foods limiting postprandial glucose response, thereby inhibiting cytokine release into the bloodstream [15] and subsequent CRP release from the endothelium [16].
Refined grains are able to induce short-term acute hyperglycemia and thus trigger proinflammatory cytokines. Switching to a diet rich in whole grains may decrease circulating levels of free radicals and proinflammatory cytokines, such as IL-6, IL-18, and TNF-α [8]. Intervention studies found a decrease in markers of inflammation in subjects with MetS who consume Mediterranean diets and/or adhere to national dietary guidelines [9]. By contrast, diets high in refined starches, sugars, and saturated and trans-fatty acids and poor in natural antioxidants and fiber from fruits, vegetables, and whole grains may cause an activation of the innate immune system. This is most likely caused by the excessive production of proinflammatory cytokines associated with a reduced production of anti-inflammatory cytokines. Thus, it seems likely that dietary adjustments have the potential to mediate a major effect on different components of MetS.
This systematic review was conducted to assess whether dietary interventions can positively modulate the immune system in MetS and help to improve favorable conditions, thus reducing the severity of the metabolic disorders in MetS.
Section snippets
Methods
This review was constructed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines for systematic reviews and meta-analyses [17] and the recommendations of the Cochrane Collaboration [18].
Literature search
Literature search retrieved 686 records; 194 of them were duplicates. We screened 492 abstracts, and 13 full-text articles [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31], [32], [59] with a total of 2017 patients were assessed for eligibility and all of them were eligible for qualitative analysis (Fig. 1).
We had to exclude studies by abstracts when no NCEP ATP III criteria were used or the intervention involved no dietary pattern or if none of our primary outcome (see
Summary of evidence
The meta-analysis of 10 RCTs provides small evidence that modifying dietary patterns can improve immunologic properties, serum insulin, and weight loss in people with MetS. Low-fat diets reduced levels of CRP significantly compared with control diets (SMD: −0.98; 95% CI: −1.6 to −0.35, P = 0.002). Low-fat diets restrict fat to less than 30% of daily energy intake. Because we found no between-group difference for CRP after sensitivity analyses, we assume that decrease of CRP was dependent on
Conclusions
Dietary approaches have a positive effect on immune markers. This meta-analysis revealed that low-fat diets can reduce CRP, though this seems to be dependent on weight loss. However, low-carbohydrate diets had the effect of reducing weight and fasting insulin effectively. Although low-carbohydrate diets are convenient to achieve weight control, reducing saturated fatty acids and enriching immunoactive biosubstances (vitamins, flavonoids, and unsaturated fatty acids) seems to be the best
Acknowledgments
This review was supported by a grant from the Corona-Foundation, Germany. The funding source had no influence on the design or conduct of the review; the collection, management, analysis, or interpretation of the data; or in the preparation, review, or approval of the manuscript. The authors would like to express their appreciation to Dr. R. Stange, Berlin, Germany, for critically revising the manuscript. The authors declare that they have no competing interests.
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