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Inflammation is a controlled process with an initiation, resolution and termination phase. After microbial invasion, lesion or chemical injury, the initiation phase starts with the production of pro-inflammatory mediators like LTB4 and PG2. These mediators increase inflammation until the Eicosanoid Switch, the end of the initiation phase, takes place. This occurs when the level of PGE2 plus PGD2 is equal to the LTB4 level. The resolution phase is entered, triggering the generation of anti-inflammatory mediators like LK, resolvins, protectins, maresins, PGD2 and PGF2a. When the total level of anti-inflammatory mediators exceeds the level of LTB4 the Stop Signal takes place. This is the last phase, the inflammation will be terminated by clearing the affected area [11]. The stress hormones produced by the systemic stress axes have a direct effect on the inflammation phases. A microbial invasion, lesion or injury sends off an alarm in the body, setting off the systemic stress system which produces NE as response and tunes the system to insulin and cortisol resistance [12]. The Eicosanoids Switch to resolution can only take place when NE is equal to the level of cortisol plus insulin and when cortisol sensitivity is recovered. The Stop Signal requires a low level of NE and normalized cortisol sensitivity. The termination phase is entered when the stress axes are switched off.

Inflammation is a controlled process with an initiation, resolution and termination phase. After microbial invasion, lesion or chemical injury, the initiation phase starts with the production of pro-inflammatory mediators like LTB4 and PG2. These mediators increase inflammation until the Eicosanoid Switch, the end of the initiation phase, takes place. This occurs when the level of PGE2 plus PGD2 is equal to the LTB4 level. The resolution phase is entered, triggering the generation of anti-inflammatory mediators like LK, resolvins, protectins, maresins, PGD2 and PGF2a. When the total level of anti-inflammatory mediators exceeds the level of LTB4 the Stop Signal takes place. This is the last phase, the inflammation will be terminated by clearing the affected area [11]. The stress hormones produced by the systemic stress axes have a direct effect on the inflammation phases. A microbial invasion, lesion or injury sends off an alarm in the body, setting off the systemic stress system which produces NE as response and tunes the system to insulin and cortisol resistance [12]. The Eicosanoids Switch to resolution can only take place when NE is equal to the level of cortisol plus insulin and when cortisol sensitivity is recovered. The Stop Signal requires a low level of NE and normalized cortisol sensitivity. The termination phase is entered when the stress axes are switched off.

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Serhan and colleagues introduced the term "Resoleomics" in 1996 as the process of inflammation resolution. The major discovery of Serhan's work is that onset to conclusion of an inflammation is a controlled process of the immune system (IS) and not simply the consequence of an extinguished or "exhausted" immune reaction. Resoleomics can be consider...

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... The SSBs could affect mental health by their sugary components; indeed, sugar can induce chronic systematic inflammation by activating the innate immune system, thus affecting psychological disorders [59]. Animal studies have shown that sugar could increase depression incidence by activating the hypothalamic-pituitaryadrenal (HPA) axis and inducing elevation in glucocorticoids [60]. ...
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... As reported, high intakes of starch and sugars can lead to hypoglycaemia because of an acute response to insulin; thus, this could induce central dysfunction and depressive disorder by influencing hormone levels [6]. Moreover, high intakes of starch and sugars and subsequent insulin secretion could increase the levels of circulating inflammatory markers, which may be associated with the risk of depression [7][8][9][10]. Circulating inflammatory markers reduce the expression of serum brain-derived neurotrophic factor [11], the lower level of which is suggested to reduce neurogenesis and lead to hippocampal atrophy in depression [12]. ...
... Meanwhile, the associations of starch intake (negative), lactose (no significant associations), and total fructose (positive) with depressive symptoms in the present population of young Japanese women differed from those in the US prospective study on menopausal women with no significant associations for starch and fructose and a negative association for lactose [21]. The associations of total and free sugars, sucrose, and glucose intakes with depressive symptoms could be a result of insulin secretion induced by an elevated blood glucose level and subsequent changes in hormone [6] and circulating inflammatory marker [7][8][9][10] levels, as well as the expression of serum brain-derived neurotrophic factor [11,12]. For total fructose, the association with depressive symptoms could be due to the increase in basal corticosterone concentration via hypothalamic-pituitary-adrenal axis stimulation [13]. ...
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... The combination of prolonged exposure to a non-healthy diet, low levels of physical activity (PA), and/or sedentary behavior (SED), induce the activation of the stress axis and the subsequent inflammatory response. 2 It is well established that low-grade chronic inflammation is a prospective risk factor linking several physio-pathological processes in the etiology of NCDs. 3 Potential mediators of the systemic inflammation include reactive oxygen species and a variety of inflammatory cytokines as a part of the complex interplay of immunometabolism 4 that amplify inflammation through stimulation of pro-inflammatory mediators, such as C-reactive protein (CRP). 5 In addition, an association between autonomic dysfunction and metabolic deregulation has been suggested 6,7 with sympathovagal imbalance being an independent risk factor for CVDs, 8 whereas a higher vagal activity is related to reduced expression of inflammatory cytokines. ...
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Sufficient amount of minerals, vitamins, and proteins in human diet play indispensable role in maintaining the active metabolism for better human health. All the essential nutrients that are requisite for an individual's survival are acquired from plants as well as animals. Micronutrients and macronutrients directly influence the metabolic pathways and their deficiencies play a substantial role in development of manifold disorders. In addition to environmental factors, quality and quantity of foods are key factors in maintaining the human health. Transition from healthy to diseased state is concurrent with the pattern of gene expression that is largely influenced by nutrition and environment. A combined approach to study the influence of nutrition on expression of numerous genes can be well explored through nutrigenomic studies. Nutrigenomics includes studies wherein applied genomics is used to investigate nutritional science to understand the compartmentalization of genes that influence the cause of diet-related complications. This review describes the role of underutilized crops as frontline foods to circumvent the health complications through the nutrigenomic studies. Further dynamics of nutrigenomic tools to study the impact of nutrition on the changing pattern of genome stability and gene expression for developing precise safety measures against wide range of health ailments linked to metabolic networks. Additionally, this review provides detailed information on nutrigenomic studies undertaken to unravel the potential of underutilized crops to augment the human health and to carry the agronomic/genomic approaches to enhance nutritional profile of underutilized crops to overcome diet-related disorders.
... The potential protective effects of adherence to an aMed diet against GDM may be due to the main components of the aMed diet, including high intakes of fruits, vegetables, nuts, and fish. These food items are associated with lower inflammation and less oxidative stress, which are associated with the risk of developing GDM (Bosma-den Boer et al. 2012). Further studies with a larger sample size of Mediterranean populations are required to confirm our results and to examine the relationship between adherence to the aMed diet and the risk of GDM. ...
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