The effect of diet on oxidative stress and metabolic diseases—Clinically controlled trials

Abstract

Oxidative stress is associated with several chronic diseases. It is acknowledged that molecules damaged by reactive oxygen species activate the inflammatory process and that this response increases the production of free radicals. Modifications in a diet can improve or decrease redox state markers. The aim of this revision was to provide an update of clinical controlled trials, to assess changes in diet and markers of oxidative stress in subjects with metabolic diseases. They were investigated randomized controlled intervention studies (RCTs) published in MEDLINE (U.S. National Library of Medicine, National Institutes of Health) that were conducted in subjects with obesity, hypertension, diabetes, or dyslipidemia; with dietary intervention; where markers of oxidative stress have been evaluated and published in the last 5 years. Food antioxidants, hypocaloric diets with loss of adipose tissue, substitution of animal protein by vegetable, and changes in the microbiota improve antioxidant status in people with chronic disease. Practical applications Hyperglycemia in diabetes mellitus and adipose tissue in obesity are known to trigger oxidative stress. Oxidative stress, in turn, decreases insulin sensitivity and favors an inflammatory state producing adhesion molecules. Oxidative stress and adhesion molecules, can increase blood pressure and oxidation of lipoproteins, that ultimately could lead to a cerebrovascular event. Consumption of high‐antioxidant and polyphenol foods increases plasma antioxidant capacity and decreases oxidative stress markers in people with diabetes, obesity, hypertension, and hypertriglyceridemia. In addition, weight loss caused by caloric restriction with or without exercise increases the endogenous antioxidant capacity. Therefore, it is likely that the combination of a hypocaloric diet with a high content of antioxidants and polyphenols will have a greater effect. Other dietary changes with antioxidant effect, such as the substitution of animal for vegetable protein or the addition of fiber, might be mediated by changes in the microbiota. However, this aspect requires further study.

Iron Metabolism in Obesity and Metabolic Syndrome

“…Chronic diseases, also known as non-communicable diseases (NCDs), are the result of a combination of behavioral, environmental, genetic and physiological factors, being responsible for the 75% of deaths in low- and middle-income countries. Among them, obesity, along with cancer, cardiovascular diseases and diabetes, is one of the main NCDs worldwide [ 1 ]. Obesity is defined as an excessive fat accumulation that may have detrimental effects on health.…”

Interaction between dietary total antioxidant capacity and BDNF Val66Met polymorphism on lipid profiles and atherogenic indices among diabetic patients

“…Environmental factors, such as dietary consumption, genetic variations, and their interactions, have an impact on blood lipid levels 12 – 15 . Dietary changes could impact the oxidation profile of patients with various clinical diseases including diabetes, dyslipidemia, and CVDs, which are affected by foods and diets including polyphenols, flavonoids, PUFAs, and the Mediterranean diet 16 , 17 . The influence of antioxidants alone in decreasing oxidative stress has been identified; however, combining antioxidants is shown to have a synergistic activity; the perfect way to demonstrate this is to estimate the cumulative function and complex effects of all antioxidants in body fluids; total antioxidant capacity (TAC) is characterized as the moles of a given free radical removed by a test solution 16 , 18 , 19 .…”

Myron Gordon Award paper: Microbes, T‐cell diversity and pigmentation

“…Several healthy lifestyle measures can support beta‐hydroxybutyrate synthesis and block NLRP3‐mediated inflammation (Youm et al., 2015). The primary outcome to strive for is reducing reactive oxygen species (ROS) that promote inflammation (Ávila‐Escalante et al., 2020; Doroftei et al., 2020). A commonly proposed mechanism is the molecular damage derived from ROS excess, resulting in perturbed epithelial homeostasis and altered biodiversity of the (skin) microbiome.…”