Obesity is a multifactorial disease resulting in excessive accumulation of adipose tissue. Over the last decade, growing evidence has identified the gut microbiota as a potential factor in the pathophysiology of both obesity and the related metabolic disorders. The gut microbiota is known to protect gastrointestinal mucosa permeability and to regulate the fermentation and absorption of dietary polysaccharides, perhaps explaining its importance in the regulation of fat accumulation and the resultant obesity. The proposed mechanisms by which the gut microbiota could contribute to the pathogenesis of obesity and the related metabolic diseases include: (a) a high abundance of bacteria that ferment carbohydrates, leading to increased rates of short-chain fatty acid (SCFA) biosynthesis, providing an extra source of energy for the host, that is eventually stored as lipids or glucose; (b) increased intestinal permeability to bacterial lipopolysaccharides (LPS), resulting in elevated systemic LPS levels that aggravate low-grade inflammation and insulin resistance; (c) increased activity of the gut endocannabinoid system. Fecal transplantation studies in germ-free mice have provided crucial insights into the potential causative role of the gut microbiota in the development of obesity and obesity-related disorders. Diet +/− bariatric surgery have been reported to modulate the gut microbiota, leading to lean host phenotype body composition. This review aims to report clinical evidence for a link of the gut microbiota with human obesity and obesity-related diseases, to provide molecular insights into these associations, and to address the effect of diet and bariatric surgery on the gut microbiota, including colonic microbiota, as a potential mechanism for promoting weight loss.

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At present, googling the search terms "COVID-19" and "Functional foods" yields nearly 500,000,000 hits, witnessing the growing interest of the scientific community and the general public in the role of nutrition and nutraceuticals during the COVID-19 pandemic. Many compounds have been proposed as phytotherapics in the prevention and/or treatment of COVID-19. The extensive interest of the general public and the enormous social media coverage on this topic urges the scientific community to address the question of whether which nutraceuticals can actually be employed in preventing and treating this newly described coronavirus-related disease. Recently, the Canadian biotech pharma company "FSD Pharma" received the green light from the Food and Drug Administration to design a proof-of-concept study evaluating the effects of ultramicronized palmitoylethanolamide (PEA) in COVID-19 patients. The story of PEA as a nutraceutical to prevent and treat infectious diseases dates back to the 1970s where the molecule was branded under the name Impulsin and was used for its immunomodulatory properties in influenza virus infection. The present paper aims at analyzing the potential of PEA as a nutraceutical and the previous evidence suggesting its anti-inflammatory and immunomodulatory properties in infectious and respiratory diseases and how these could translate to COVID-19 care.

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Summary Background There is evidence that idiopathic achalasia has an autoimmune component and a significant association with several autoimmune comorbidities has been described. However, data regarding the prevalence of autoimmune diseases in achalasia are not well established, and few studies have explored this association. Objective Our primary aim was to prospectively investigate the type and frequency of autoimmune comorbidities in a large cohort of consecutive achalasia patients. Our secondary aim was to investigate the effects of autoimmune comorbidities on achalasia phenotype (clinical features and manometric pattern). Methods The study population consisted of 375 consecutive patients (215 females—median age 55 ± 17 years), referred at our tertiary referral center from January 2008 to January 2018, with clinical and instrumental (EGDS, barium esophagogram, and manometry) diagnosis of idiopathic achalasia. Gender- and age-matched subjects undergoing manometry and pH-impedance monitoring for typical gastroesophageal reflux (GERD) complaints served as controls. In all patients a detailed history taking was carried out, recording the presence and type of autoimmune comorbidities. Results The overall prevalence of autoimmune comorbidities was two times higher in achalasia than in control patients (12.3 vs. 5%, respectively). The presence of comorbidities did not significantly affect disease’s phenotype, as the age of disease onset was similar in achalasia patients with and without comorbidities (50.13 ± 14.47 and 48.3 ± 18.71, respectively, P = NS). Conclusions Although larger epidemiologic studies are needed to confirm our data, our findings likely suggest that achalasia has a complex multifactorial pathophysiology with an autoimmune component.