1  Introduction
Non-communicable diseases (NCDs), the silent epidemic, are responsible for the majority of deaths in developed countries and their prevalence at a younger age was observed increasingly in the last years (WHO, 2013, 2018). Cardiovascular disease (CVD), diabetes, obesity, cancer, Alzheimer's and Parkinson's disease, arthritis, non-alcoholic fatty liver disease (NAFLD) and chronic obstructive disease are some of the most common NCDs sharing common features. Research shows that redox impairments and chronic low-grade inflammation generate a vicious biochemical self-propagating cycle, constituting the molecular pathological root of these diseases. In the context of modern lifestyle, stress factors including malnutrition/overnutrition, smoking or sedentary routine are initiating factors for the impairment of inflammatory pathways contributing to the development of NCDs. Furthermore, in real-life scenarios, people experience uncontrolled simultaneous exposure to many environmental chemicals, hence novel methodological approaches simulating real-life exposures are being developed under the name real life risk simulation (RLRS) with the aim to assess the potential adverse health effects of long-term exposure to chemical mixtures (Hernandez et al., 2019; Hernandez and Tsatsakis, 2017; Tsatsakis et al., 2016, 2019a). According to WHO, 80% of NCDs-related deaths could be prevented by changes in these modifiable risk factors, and recent evidence identified unhealthy diet as the biggest risk factor for NCDs-related deaths (Collaborators, 2019; WHO, 2018).
Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 2008).
Mitigating the pathological pathways associated with chronic low-grade inflammation through pharmacological agents but, more importantly, through diet and lifestyle changes might constitute an effective strategy in the prevention of NCD and NCD-related deaths. In the current review, we overview recent facts from molecular and animal studies to human clinical reports regarding the intricate pathways that are affected by some of our dietary habits, also discussing the next steps that ought to be taken in addressing these parameters.