Search

Western diets are rapidly spreading due to globalization, causing an increase in obesity and diseases of civilization. These Western diets are associated with changes in the gut microbiota related to intestinal inflammation. This review discusses the adverse effects of Western diets, which are high in fat and sugar and low in vegetable fiber, on the gut microbiota. This leads to gut dysbiosis and overgrowth of Candida albicans, which is a major cause of fungal infection worldwide. In addition to an unhealthy Western diet, other factors related to disease development and gut dysbiosis include smoking, excessive alcohol consumption, lack of physical activity, prolonged use of antibiotics, and chronic psychological stress. This review suggests that a diversified diet containing vegetable fiber, omega-3 polyunsaturated fatty acids, vitamins D and E, as well as micronutrients associated with probiotic or prebiotic supplements can improve the biodiversity of the microbiota, lead to short-chain fatty acid production, and reduce the abundance of fungal species in the gut. The review also discusses a variety of foods and plants that are effective against fungal overgrowth and gut dysbiosis in traditional medicine. Overall, healthy diets and lifestyle factors contribute to human well-being and increase the biodiversity of the gut microbiota, which positively modulates the brain and central nervous system. [ABSTRACT FROM AUTHOR]

Background Observational studies have linked Mediterranean Diets (MedDiets) and organic food consumption with positive health outcomes, which may be explained by higher mineral micronutrient and phenolic intake and lower dietary exposure to toxic compounds. Objectives We aimed to determine the effects of diet and food type (organic compared with conventional) on urinary excretion (UE) and/or plasma concentrations of mineral micronutrients, phenolics, and toxic metals. Methods Healthy adult participants were randomly allocated to a conventional (n  = 14) or an intervention (n  = 13) group. During a 2-wk period, the intervention group consumed a MedDiet made entirely from organic foods, whereas the conventional group consumed a MedDiet made from conventional foods. Before and after the intervention period, both groups consumed their habitual Western diets made from conventional foods. The primary outcome was UE and/or plasma concentrations of selected mineral micronutrients, toxic metals, and phenolic markers. In addition, we monitored diets using food diaries. The participants were aware of study group assignment, but the study assessors were not. Results Changing from a Western Diet to a MedDiet for 2 wk resulted in significant increases in UE of total phenolics and salicylic acid (by 46% and 45%, respectively), the mineral micronutrients Co, I, and Mn (by 211%, 70%, and 102%, respectively), and the toxic metal Ni (by 42%), and plasma Se concentrations (by 14%). However, no significant effects of food type (organic compared with conventional) were detected. Redundancy analysis identified vegetables, coffee, wine, and fruit as positive drivers for UE of phenolic markers and mineral micronutrients, and fish consumption as a positive driver for UE of Cd and Pb. Conclusions Although small effects of food type cannot be ruled out, our study suggests that only changing to a MedDiet with higher fruit and vegetable, and lower meat, consumption results in a large increase in phenolic and mineral micronutrient intakes. This trial was registered at clinicaltrials.gov as NCT03254537. [ABSTRACT FROM AUTHOR]

Western diets are rapidly spreading due to globalization, causing an increase in obesity and diseases of civilization. These Western diets are associated with changes in the gut microbiota related to intestinal inflammation. This review discusses the adverse effects of Western diets, which are high in fat and sugar and low in vegetable fiber, on the gut microbiota. This leads to gut dysbiosis and overgrowth of Candida albicans, which is a major cause of fungal infection worldwide. In addition to an unhealthy Western diet, other factors related to disease development and gut dysbiosis include smoking, excessive alcohol consumption, lack of physical activity, prolonged use of antibiotics, and chronic psychological stress. This review suggests that a diversified diet containing vegetable fiber, omega-3 polyunsaturated fatty acids, vitamins D and E, as well as micronutrients associated with probiotic or prebiotic supplements can improve the biodiversity of the microbiota, lead to short-chain fatty acid production, and reduce the abundance of fungal species in the gut. The review also discusses a variety of foods and plants that are effective against fungal overgrowth and gut dysbiosis in traditional medicine. Overall, healthy diets and lifestyle factors contribute to human well-being and increase the biodiversity of the gut microbiota, which positively modulates the brain and central nervous system.

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]

Background and Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) and its more advanced form, metabolic dysfunction-associated steatohepatitis, have emerged as the most prevalent liver diseases worldwide. Currently, lifestyle modification is the foremost guideline-recommended management strategy for MASLD. However, it remains unclear which detrimental signals persist in MASLD even after disease remission. Thus, we aimed to examine the persistent changes in liver transcriptomic profiles following this reversal., Methods: Male C57BL/6J mice were divided into three groups: Western diet (WD) feeding, chow diet (CD) feeding, or diet reversal from WD to CD. After 16 weeks of feeding, RNA sequencing was performed on the mice's livers to identify persistent alterations characteristic of MASLD. Additionally, RNA sequencing databases containing high-fat diet-fed P53-knockout mice and human MASLD samples were utilized., Results: WD-induced MASLD triggered persistent activation of the DNA damage response (DDR) and its primary transcription factor, P53, long after the resolution of the hepatic phenotype through dietary reversal. Elevated levels of P53 might promote apoptosis, thereby exacerbating metabolic dysfunction-associated steatohepatitis, as they strongly correlated with hepatocyte ballooning, an indicator of apoptosis activation. Moreover, P53 knockout in mice led to downregulated expression of apoptosis signaling in the liver. Mechanistically, P53 may regulate apoptosis by transcriptionally activating the expression of apoptosis-enhancing nuclease (AEN). Consistently, P53, AEN, and the apoptosis process all exhibited persistently elevated expression and showed a strong inter-correlation in the liver following dietary reversal., Conclusions: The liver demonstrated upregulation of DDR signaling and the P53-AEN-apoptosis axis both during and after exposure to WD. Our findings provide new insights into the mechanisms of MASLD relapse, highlighting DDR signaling as a promising target to prevent MASLD recurrence., Competing Interests: JGF has been an associate editor of the Journal of Clinical and Translational Hepatology since 2013. The other authors have no conflicts of interest related to this publication., (© 2024 Authors.)

Public health courses are emerging as popular undergraduate offerings, especially at universities with schools of public health. It is important to note that evolution has shaped the burden of disease in the modern world in which we practice and educate for public health. Human cultures and technologies have modified life on Planet Earth and have co-evolved with myriad other species, including microorganisms, plant and animal sources of food, invertebrate vectors of disease, and intermediate bird, mammal, and primate hosts. Molecular mechanisms of evolution have produced differential resistance or susceptibility to infectious agents, including malaria, plague, smallpox, TB, measles, and diarrheal and respiratory diseases. The domestication of sheep and cattle led to natural selection in favor of human populations able to digest milk throughout life through persistence into adulthood of lactase enzyme expression in the intestine, a major story of anthropology. The emergence of a 'Western diet' of dairy, refined cereal grains, refined sugars, vegetable oils, alcoholic beverages, salt, and omega-6-rich meats has dramatically altered glycemic load, fatty acid composition, macronutrients, acid-base balance, sodium/potassium ratio, and fiber content. This is a major story of nutrition and disease. The results include epidemics of atherosclerotic cardiovascular disease, obesity, diabetes, high blood pressure, osteoporosis, certain cancers, and bowel, inflammatory, and autoimmune disorders. Another interesting phenomenon is the selection of excessive hemostatic activity from platelets and the plasma clotting proteins; what was protective against death from bleeding after injuries among hunter-gatherers or from pregnancy-related hemorrhage now contributes to thrombosis underlying heart attacks and strokes. Conversely, there is little pressure against hemostasis and thrombosis since deaths from these causes occur mostly after the reproductive years of life. Learning about evolution over millennia for humans and over hours or days for microbes enlivens the experience of understanding evolutionary biology in public health context. [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]

Overnutrition and obesity have developed into a major public health problem across different parts of the world. Epidemiological studies have shown that excessive intake of dietary components, such as fatty acids and/or sugars, can promote obesity. In this context, the use of dietary intervention in animal models that respond to a diet similar to humans is useful to understand this preventable, multifactorial disease. The aim of this chapter is to aid researchers in choosing specific nutritional interventions and animal strains to induce obesity and obesity-related morbidities in experimental models.