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In modern lifestyle, stress and Western diets are two major environmental risk factors involved in the etiology of neuropsychiatric disorders. Lifelong interactions between stress, Western diets, and how they can affect brain physiology, remain unknown. A possible relation between dietary long chain polyunsaturated fatty acids (PUFA), endocannabinoids, and stress is proposed. This review suggests that both Western diets and negative stress or distress increase n-6/n-3 PUFA ratio in the phospholipids of the plasma membrane in neurons, allowing an over-activation of the endocannabinoid system in the limbic areas that control emotions. As a consequence, an excitatory/inhibitory imbalance is induced, which may affect the ability to synchronize brain areas involved in the control of stress responses. These alterations increase vulnerability to neuropsychiatric disorders. Accordingly, dietary intake of n-3 PUFA would counter the effects of stress on the brain of stressed subjects. In conclusion, this article proposes that PUFA, endocannabinoids, and stress form a unique system which is self-regulated in limbic areas which in turn controls the effects of stress on the brain throughout a lifetime. [ABSTRACT FROM AUTHOR]

Food additives such as titanium dioxide (E171), iron oxides and hydroxides (E172), silver (E174), and gold (E175) are highly used as colorants while silicon dioxide (E551) is generally used as anticaking in ultra-processed foodstuff highly used in the Western diets. These additives contain nanosized particles (1–100 nm) and there is a rising concern since these nanoparticles could exert major adverse effects due to they are not metabolized but are accumulated in several organs. Here, we analyze the evidence of gastrotoxicity, hepatotoxicity and the impact of microbiota on gut-brain and gut-liver axis induced by E171, E172, E174, E175 and E551 and their non-food grade nanosized counterparts after oral consumption. Although, no studies using these food additives have been performed to evaluate neurotoxicity or alterations in animal behavior, their non-food grade nanosized counterparts have been associated with stress, depression, cognitive and eating disorders as signs of animal behavior alterations. We identified that these food additives induce gastrotoxicity, hepatotoxicity and alterations in gut microbiota and most evidence points out oxidative stress as the main mechanism of toxicity, however, the role of oxidative stress as the main mechanism needs to be explored further. The evidence of toxicity induced by oral consumption of E171, E172, E174, E175, E551 and their nanoparticles counterparts. Oral consumption of titanium dioxide (E171), iron oxide and hydroxides (E172), silver (E174), gold (E175) and silicon dioxide (E551) causes several signs of toxicity in the gastrointestinal tissues and liver (blue bullets) and oxidative stress in both (red bullets). However, the evidence of oxidative stress is restricted to description of increase in reactive oxygen species (ROS), decrease in antioxidant enzymes (catalase, superoxide dismutase and, glutathione reductase) and oxidative damage to biomolecules such as lipids, proteins and DNA. On the other hand, there is no available evidence of neurotoxicity of these five food-additives, however, their nanosized counterparts used in animal experimental models have induced clear signs of neurotoxicity and alterations in the behavior but scarce evidence of oxidative stress has been associated with. Image 1 • E171, E172, E174, E175 and E551 food additives contain a fraction of nanoparticles. • E171, E172, E174, E175 and E551 are accumulated inducing gastro and hepatotoxicity. • Microbiome is altered by oral consumption of E171, E172, E174, E175 and E551. • Neurotoxicity and alterations in behavior and cognition are potentials effects. • Oxidative stress is important in their toxicity but further studies are needed. [ABSTRACT FROM AUTHOR]