Search

Abstract Background Weight re-gain (which is also known as re-obesity) is an overwhelming challenge many dieters face in their pursuit to maintain consistent results following successful weight loss. This frustrating pattern of weight cycling can have various mental and physical implications, which further puts another roadblock in any weight reduction program. Main body of the abstract A comprehensive analysis of the causes behind the phenomenon of re-obesity has been widely conducted in literature, exploring the importance of creating the right mindset for weight loss maintenance and identifying the hormonal role, specifically of insulin–leptin resistance and ghrelin enhanced affinity, on appetite and food intake regulation. Insulin–Leptin resistance, due to circulating prostaglandins and prostaglandin metabolites, along with a decline in leptin-producing adipocytes following body mass reduction, cuts off leptin’s satiety signals to the brain. The persistence of this hormonal dysregulation after weight loss is collectively called obesogenic memory, and it seems to be largely mediated by dysbiosis. Short conclusion In conclusion, understanding of the influence of hormonal dysbiosis on re-obesity is fundamental in targeting the culprits behind ineffective attempts at weight loss sustenance, optimization of diet duration, use of synbiotics. Fecal and oral microbial transplantation hold high potential in improving long-term management interventions in obesity patients.

Background: Weight re-gain (which is also known as re-obesity) is an overwhelming challenge many dieters face in their pursuit to maintain consistent results following successful weight loss. This frustrating pattern of weight cycling can have various mental and physical implications, which further puts another roadblock in any weight reduction program. A comprehensive analysis of the causes behind the phenomenon of re-obesity has been widely conducted in literature, exploring the importance of creating the right mindset for weight loss maintenance and identifying the hormonal role, specifically of insulin–leptin resistance and ghrelin enhanced affinity, on appetite and food intake regulation. Insulin–Leptin resistance, due to circulating prostaglandins and prostaglandin metabolites, along with a decline in leptin-producing adipocytes following body mass reduction, cuts off leptin's satiety signals to the brain. The persistence of this hormonal dysregulation after weight loss is collectively called obesogenic memory, and it seems to be largely mediated by dysbiosis. Short conclusion: In conclusion, understanding of the influence of hormonal dysbiosis on re-obesity is fundamental in targeting the culprits behind ineffective attempts at weight loss sustenance, optimization of diet duration, use of synbiotics. Fecal and oral microbial transplantation hold high potential in improving long-term management interventions in obesity patients. [ABSTRACT FROM AUTHOR]