Short Communication - Journal of Gastroenterology and Digestive Diseases (2024) Volume 9, Issue 5
Obesity and Microbiome Dysbiosis: Causes, Consequences, and Treatments
Emeran Frank *
Department of Ophthalmology, Bern University Hospital, Switzerland
- *Corresponding Author:
- Emeran Frank
Department of Ophthalmology, Bern University Hospital, Switzerland
E-mail: femeran@bu.swis.co
Received: 23-Aug-2024, Manuscript No. JGDD-24-148636; Editor assigned: 24-Aug-2024, PreQC No. JGDD-24-148636(PQ); Reviewed: 07-Sep-2024, QC No. JGDD-24-148636; Revised: 12-Sep-2024, Manuscript No. JGDD-24-148636(R); Published: 19-Sep-2024, DOI: 10.35841/jgdd-9.5.227
Citation: : Frank E. Obesity and Microbiome Dysbiosis: Causes, Consequences, and Treatments. J Gastroenterol Dig Dis.2024;9(5):227
Introduction
Obesity has become a major global health concern, closely linked to various metabolic disorders, including type 2 diabetes, cardiovascular diseases, and certain cancers [1]. Recent research has highlighted the role of the gut microbiome in the development and management of obesity, suggesting that microbiome dysbiosis—an imbalance in the microbial communities in the gut—may contribute to the onset and progression of obesity. Understanding the causes and consequences of this dysbiosis, as well as potential treatment strategies, is essential for addressing obesity effectively [2].
The human gut microbiome comprises trillions of microorganisms, including bacteria, archaea, viruses, and fungi, which play critical roles in digestion, metabolism, and immune function. Factors such as diet, lifestyle, genetics, and environmental influences can affect the composition of the microbiome [3]. Diet, in particular, has been shown to significantly impact microbial diversity and abundance. Diets high in sugars and unhealthy fats can promote the growth of pathogenic bacteria while reducing beneficial species, leading to dysbiosis [4].
Dysbiosis can contribute to obesity through several mechanisms. One key pathway is the alteration of energy metabolism. Certain gut bacteria are known to extract more energy from food, which can lead to increased fat storage [5]. Additionally, dysbiosis may disrupt the production of short-chain fatty acids (SCFAs), which are beneficial metabolites produced by the fermentation of dietary fibers. SCFAs play a vital role in regulating metabolism and maintaining gut health. A reduction in SCFA production has been linked to increased appetite and fat accumulation, further exacerbating obesity [6].
The inflammatory response associated with dysbiosis is another significant factor. An imbalanced microbiome can lead to increased intestinal permeability, often referred to as "leaky gut [7]. This condition allows bacterial endotoxins to enter the bloodstream, triggering systemic inflammation. Chronic inflammation has been implicated in the development of insulin resistance and metabolic syndrome, both of which are closely related to obesity [8].
The consequences of microbiome dysbiosis extend beyond metabolic disorders. Research has suggested connections between dysbiosis and mood disorders, including anxiety and depression. The gut-brain axis—a bidirectional communication system between the gut and the brain—plays a crucial role in this relationship. Dysbiosis may influence neuroinflammation and neurotransmitter levels, potentially affecting mental health [9].
Addressing obesity and microbiome dysbiosis requires a multifaceted approach. Dietary modifications are among the most effective strategies. Increasing the intake of fiber-rich foods, such as fruits, vegetables, whole grains, and legumes, can promote the growth of beneficial gut bacteria. Probiotics and prebiotics are also gaining attention for their potential to restore microbial balance. Probiotics are live beneficial bacteria that can be taken as supplements, while prebiotics are non-digestible food components that nourish these bacteria [10].
Conclusion
The interplay between obesity and microbiome dysbiosis is complex and multifactorial. Dysbiosis contributes to the development of obesity through alterations in energy metabolism, inflammation, and gut-brain interactions. Addressing this issue requires a comprehensive approach, including dietary modifications, lifestyle changes, and potential therapeutic interventions. By focusing on restoring microbial balance and promoting gut health, we can make significant strides in combating obesity and its associated health risks.
References
- Lee CJ, Sears CL, Maruthur N. Gut microbiome and its role in obesity and insulin resistance. Ann N Y Acad Sci. 2020;1461(1):37-52.
- Janeiro MH, Ramírez MJ, Solas M. Dysbiosis and alzheimer’s disease: cause or treatment opportunity?. Cell Mol Neurobiol. 2022;42(2):377-87.
- Kumavath R, Pavithran H, Paul S, et al. Effects of gut microbiome and obesity on the development, progression and prevention of cancer. Int J Oncol. 2023;64(1):4.
- Choi BS, Daoust L, Pilon G, et al, Tremblay A. Potential therapeutic applications of the gut microbiome in obesity: From brain function to body detoxification. Int J Obes (Lond). 2020;44(9):1818-31.
- Singer-Englar T, Barlow G, Mathur R. Obesity, diabetes, and the gut microbiome: an updated review. Expert Rev Gastroenterol Hepatol. 2019;13(1):3-15.
- Lee P, Yacyshyn BR, Yacyshyn MB. Gut microbiota and obesity: An opportunity to alter obesity through faecal microbiota transplant (FMT). Diabetes Obes Metab. 2019;21(3):479-90.
- Slyepchenko A, Maes M, Machado-Vieira R, et al. Intestinal dysbiosis, gut hyperpermeability and bacterial translocation: missing links between depression, obesity and type 2 diabetes. Curr Pharm Des. 2016;22(40):6087-106.
- Gupta A, Singh V, Mani I. Dysbiosis of human microbiome and infectious diseases. Prog Mol Biol Transl Sci. 2022;192(1):33-51.
- Fayfman M, Flint K, Srinivasan S. Obesity, motility, diet, and intestinal microbiota—connecting the dots. Curr Gastroenterol Rep. 2019;21:1-1.
- Sehgal K, Khanna S. Gut microbiota: a target for intervention in obesity. Expert Rev Gastroenterol Hepatol. 2021;15(10):1169-79.
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