Background: Antioxidant potential is defined as the ability to neutralize oxygen free radicals that are generated in excess due to environmental influences. The body’s defense mechanisms often require support in preventing the effects of oxidative stress. The literature data suggest that curcumin has antioxidant activity that can significantly reduce oxidative stress levels. The aim was to assess the impact of curcumin on oxidative stress markers. Methods: PubMed and Embase were searched from database inception until 27 September 2019 for randomized clinical trials in >20 patients treated with curcumin supplements and randomized to placebo/no intervention/physical activity to verify the antioxidant potential of curcumin. Results: Four studies were included in the meta-analysis, three of which were double-blind and one single-blind. A total of 308 participants took part in the research. A total of 40% of the respondents were men. The average age of participants was 27.60 ± 3.79 years. The average supplementation time was 67 days and the average dose of curcumin administered was 645 mg/24 h. Curcumin significantly increased total antioxidant capacity (TAC) (SMD = 2.696, Z = 2.003, CI = 95%, p = 0.045) and had a tendency to decrease malondialdehyde (MDA) concentration (SMD = −1.579, Z = −1.714, CI = 95%, p = 0.086). Conclusions: Pure curcumin has the potential to reduce MDA concentration and increase total antioxidant capacity.

Short chain fatty acids (SCFAs) being produced during fermentation of non-digestible polysaccharides are regulatory compounds with the potential to influence inflammatory, as well as emotional state and cognition through the gut–brain axis. We analyzed the association between stool concentration of SCFAs (acetic acid (C 2:0), propionic acid (C 3:0), isobutyric acid (C 4:0 i), butyric acid (C 4:0 n), isovaleric acid (C 5:0 i) valeric acid (C 5:0 n), isocaproic acid (C 6:0 i), caproic acid, and (C 6:0 n) heptanoic acid (C 7:0)) and depressive symptoms among women and looked for the potential confounders of microbiota byproduct synthesis. We enrolled 116 women aged 52.0 ± 4.7 years and recognized depression in 47 (40.52%). To analyze the emotional state, Beck’s Depression Inventory (BDI) was used. We assessed SCFAs content by means of gas chromatography. Fiber intake was estimated using parts of food frequency questionnaire. The content of acetic acid was significantly lowered compared to non-depressed women (median {IQR}: 29.49 {20.81} vs. 34.99 {19.55}, p = 0.04). A tendency toward decreased level of propionic acid was noticed (median {IQR}: 16.88 {9.73} vs. 21.64 {12.17}, p = 0.07), while the concentration of isocaproic acid was significantly increased in (median {IQR}: 0.89 {1.15} vs. 0.56 {0.95}, p < 0.01) comparison to matched healthy subjects. We found negative correlations between acetate, propionate, and Beck’s score (r = −0.2, p = 0.03; r = −0.21, p = 0.02, respectively). Statistically significant correlations between acetate and propionate and BDI somatic score (r = −0.21, p = 0.01; r = −0.17, p = 0.03), as well as correlations regarding isocaproic and both cognitive/affective (r = 0.37, p = 0.0001) and somatic (r = 9.37, p < 0.001) scores were found. Women who declared current usage of lipid-lowering and thyroid drugs in the past, had higher content of C6:0-i (Users; median {IQR}: 1.91 {3.62} vs. non-users; 0.55 {0.67}; p = 0.0048).and lower of C2:0 (Users; median {IQR}: 23.07 {12.80} vs. non users 33.73 {21.44}; p = 0.041), respectively. No correlations regarding SCFAs concentration and fiber intake were found. We concluded that SCFAs may potentially contribute to depression phenotype, however, due to the small size of groups suffering from moderately heavy (n = 5) and severe (n = 7) depression, the conclusion should be treated with caution. Pharmacotherapy of hyperlipidemia and thyroid disease might affect SCFAs synthesis. Studies with more participants are required.

Excessive training may limit physiological muscle adaptation through chronic oxidative stress and inflammation. Improper diet and overtraining may also disrupt intestinal homeostasis and in consequence enhance inflammation. Altogether, these factors may lead to an imbalance in the gut ecosystem, causing dysregulation of the immune system. Therefore, it seems to be important to optimize the intestinal microbiota composition, which is able to modulate the immune system and reduce oxidative stress. Moreover, the optimal intestinal microbiota composition may have an impact on muscle protein synthesis and mitochondrial biogenesis and function, as well as muscle glycogen storage. Aproperly balanced microbiome may also reduce inflammatory markers and reactive oxygen species production, which may further attenuate macromolecules damage. Consequently, supplementation with probiotics may have some beneficial effect on aerobic and anaerobic performance. The phenomenon of gut-muscle axis should be continuously explored to function maintenance, not only in athletes.

The central nervous system (CNS) and the human gastrointestinal (GI) tract communicate through the gut-brain axis (GBA). Such communication is bi-directional and involves neuronal, endocrine, and immunological mechanisms. There is mounting data that gut microbiota is the source of a number of neuroactive and immunocompetent substances, which shape the structure and function of brain regions involved in the control of emotions, cognition, and physical activity. Most GI diseases are associated with altered transmission within the GBA that are influenced by both genetic and environmental factors. Current treatment protocols for GI and non-GI disorders may positively or adversely affect the composition of intestinal microbiota with a diverse impact on therapeutic outcome(s). Alterations of gut microbiota have been associated with mood and depressive disorders. Moreover, mental health is frequently affected in GI and non-GI diseases. Deregulation of the GBA may constitute a grip point for the development of diagnostic tools and personalized microbiota-based therapy. For example, next generation sequencing (NGS) offers detailed analysis of microbiome footprints in patients with mental and GI disorders. Elucidating the role of stem cell–host microbiome cross talks in tissues in GBA disorders might lead to the development of next generation diagnostics and therapeutics. Psychobiotics are a new class of beneficial bacteria with documented efficacy for the treatment of GBA disorders. Novel therapies interfering with small molecules involved in adult stem cell trafficking are on the horizon.

Introduction: Metformin is the first choice drug in the treatment of type 2 diabetes mellitus but its administration may be linked to gastrointestinal adverse events limiting its use.Objectives: The objective of this systematic review and meta-analysis was to assess the risk of gastrointestinal adverse events related to metformin use in patients with type 2 diabetes treated with metformin.Methods: PUB MED/CINAHL/Web of Science/Scopus were searched from database inception until 08.11.2020 for articles in English and randomized controlled trials related to patients with type 2 diabetes treated with metformin were included.Results: From 5315 publications, we identified 199 potentially eligible full-text articles. Finally, 71 randomized controlled trials were included in the meta-analysis. In these studies, metformin use was associated with higher risk of abdominal pain, diarrhea and nausea comparing to control. The risks of abdominal pain and nausea were highest comparing to placebo. Bloating risk was only elevated when metformin treatment was compared to DPP4i.Conclusions: The risk of gastrointestinal adverse events such as abdominal pain, nausea and diarrhea is higher in type 2 diabetes patients treated with metformin compared to other antidiabetic drugs. There is a higher risk of bloating and diarrhea with metformin immediate-release than with metformin extended release formulation.Systematic Review Registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021289975, identifier CRD42021289975.