Gut-brain axis in chronic fatigue syndrome – Complete Phd and Masters Thesis

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Introduction

Chronic fatigue syndrome (CFS) is a complex, debilitating condition characterized by persistent fatigue that is not relieved by rest, along with a range of other symptoms such as cognitive dysfunction, sleep disturbances, and muscle pain. Despite extensive research efforts, the underlying causes of CFS remain poorly understood.

One emerging area of interest is the gut-brain axis, a bidirectional communication system between the gastrointestinal tract and the central nervous system. The gut-brain axis plays a crucial role in regulating various physiological processes, including immune function, neurotransmitter production, and inflammation. Disruption of the gut-brain axis has been implicated in a variety of conditions, including irritable bowel syndrome, depression, and anxiety disorders.

This thesis aims to investigate the role of the gut-brain axis in the pathogenesis of CFS. By examining the interactions between the gut microbiota, intestinal permeability, and neuroinflammation in individuals with CFS, this study seeks to provide valuable insights into the underlying mechanisms of this complex disorder.

Table of Contents

Chapter 1: Introduction
1.1 Introduction
1.2 Background of study
1.3 Problem Statement
1.4 Objective of study
1.5 Limitation of study
1.6 Scope of study
1.7 Significance of study
1.8 Structure of the Thesis
1.9 Definition of terms

Chapter 2: Literature Review
2.1 Overview of Chronic Fatigue Syndrome
2.2 Gut Microbiota and Its Role in Health
2.3 Gut-Brain Axis: Concept and Mechanisms
2.4 Gut-Brain Axis in Neurological Disorders
2.5 Gut-Brain Axis in Psychiatric Disorders
2.6 Gut-Brain Axis in Immune Function
2.7 Gut-Brain Axis in Inflammation
2.8 Gut-Brain Axis and Chronic Fatigue Syndrome
2.9 Current Research on Gut-Brain Axis in CFS
2.10 Gaps in the Literature

Chapter 3: Research Methodology
3.1 Research Design
3.2 Participants Selection
3.3 Data Collection Methods
3.4 Measurement Tools
3.5 Data Analysis
3.6 Ethical Considerations
3.7 Validity and Reliability
3.8 Limitations of the Methodology

Chapter 4: Discussion of Findings
4.1 Gut Microbiota Composition in CFS
4.2 Intestinal Permeability in CFS
4.3 Neuroinflammation in CFS
4.4 Interaction Between Gut Microbiota, Intestinal Permeability, and Neuroinflammation in CFS
4.5 Implications for Understanding CFS Pathogenesis
4.6 Clinical Relevance of Gut-Brain Axis in CFS
4.7 Future Directions for Research
4.8 Conclusion

Chapter 5: Conclusion and Summary
5.1 Summary of Findings
5.2 Implications of the Study
5.3 Contributions to the Field
5.4 Recommendations for Future Research
5.5 Conclusion

Thesis Overview

Chronic fatigue syndrome (CFS) is a complex and debilitating condition that affects millions of individuals worldwide. Despite being recognized as a legitimate medical condition by major health organizations, the exact cause of CFS remains unclear. The gut-brain axis, a bidirectional communication system between the gut and the brain, has gained attention in recent years as a potential factor in the development and progression of CFS.

This thesis aims to explore the role of the gut-brain axis in CFS by investigating the interactions between the gut microbiota, intestinal permeability, and neuroinflammation in individuals with the condition. By conducting a comprehensive review of the existing literature, analyzing the findings of previous studies, and presenting new data from our research, this study seeks to shed light on the complex mechanisms underlying CFS and provide valuable insights for future research and clinical practice.

Through a multidisciplinary approach that integrates knowledge from the fields of microbiology, immunology, neuroscience, and psychology, this thesis aims to advance our understanding of CFS and pave the way for new treatment strategies and interventions. By elucidating the connections between the gut and the brain in individuals with CFS, this study has the potential to transform the way we diagnose, treat, and ultimately prevent this debilitating condition.

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