Exploring the Impact of Trauma and Eating Habits on Gastrointestinal Health

Seamy Graece^*
*Correspondence: Seamy Graece, Department of Surgery, University of Arkansas for Medical Sciences, Arkansas, USA, Email:

Introduction

The relationship between intestinal function and dysfunction has long been intertwined with emotional states, such as embarrassment, shame, and stress. In different populations, perceptions of gastrointestinal (GI) symptoms vary significantly. In some societies, GI disturbances may be dismissed as mere hallucinations, while in others, individuals from lower socioeconomic backgrounds may not even recognize these symptoms as indicative of a medical condition. However, contemporary research has illuminated the complex interplay between diet, emotional well-being, stress, anxiety, and GI health. It is now understood that these factors often work in concert to trigger GI symptoms, a phenomenon well-documented in the context of Functional GI Disorders (FGIDs). Studies have shown that emotional states, such as stress, can influence gut motility, particularly in conditions like Irritable Bowel Syndrome (IBS). For example, aggression has been linked with an increase in intestinal motility, while feelings of helplessness have been associated with its reduction. These findings, though valuable, have been limited by early methods that failed to account for the reciprocal nature of the interaction between gut physiology and mental health.

Description

The biopsychosocial model provides a comprehensive framework for understanding the pathogenesis and clinical manifestations of FGIDs, viewing gastrointestinal disturbances as the outcome of complex interactions between social, psychological, and biological subsystems. This model bridges the gap between clinical observations and biomedical findings by considering not only the physiological aspects of GI health but also the psychological and behavioral dimensions of the patient’s experience. By using multivariate statistical methods, the model offers a robust approach to assessing how chronic or acute GI symptoms can be influenced by social and psychological factors. It also highlights the need for a holistic approach to treatment that addresses all aspects of a patient’s life [1].

Neurogastroenterology, or the study of the brain-gut axis, complements the biopsychosocial model by delving into the physiological and structural components that influence gut health. This field of study explores the role of gut microbiota and how it is shaped by dietary habits, as well as its impact on both physical health and mental well-being. The gut microbiome plays a crucial role in regulating the immune system and neural pathways through the brain-gut axis, influencing a wide range of brain functions, including those related to emotion. Short-term dietary changes, whether plant- or animal-based, can rapidly alter the gut microbiome, which in turn affects the expression of microbial genes and the overall function of the gut-brain axis. Research has shown that these interactions have significant implications for mental health, as disruptions in the microbiota can contribute to the development or exacerbation of mood disorders, anxiety, and other psychiatric conditions [2].

The brain-gut axis is maintained through intricate neuronal communication between the Central Nervous System (CNS), Autonomic Nervous System (ANS), Enteric Nervous System (ENS), and various neuroimmune and neuroendocrine pathways. This system ensures the proper functioning of the gut and allows it to respond to both physical and emotional stimuli. In conditions like IBS, dysregulation of the brain-gut axis can lead to abnormal brain responses to visceral pain, which has been linked to changes in brain activity. For example, individuals with IBS often show abnormal brain activity in regions involved in pain modulation and processing. Cognitive function in these patients may also be affected, with deficits observed in non-emotional aspects like visuospatial memory, as well as in emotionally modulated cognitive functions related to the hippocampus and amygdala. Furthermore, IBS patients demonstrate attentional biases toward negative stimuli, particularly those related to GI symptoms, indicating a cognitive pattern consistent with a cognitive-behavioral framework.

Studies have also highlighted the role of the Hypothalamic-Pituitary-Adrenal (HPA) axis in IBS. Abnormalities in HPA-axis functioning, particularly with regards to cortisol levels, can have a profound impact on cognitive performance. For instance, Cortisol Awakening Response (CAR), a marker of HPA-axis activity, has been shown to correlate with cognitive performance in IBS patients. A blunted or exaggerated CAR has been linked to poorer memory test performance, and this dysregulation of cortisol may be one of the underlying mechanisms contributing to cognitive dysfunction in these patients. Other studies have suggested that increased levels of cytokines in patients with both IBS and depression can also negatively affect cognitive function, further linking the gut-brain axis to cognitive health.

The functional changes observed in IBS patients are not limited to local changes in the brain but also extend to global alterations in brain activity, as evidenced by functional Magnetic Resonance Imaging (fMRI) studies. These studies have revealed reduced amplitude in certain brain regions involved in pain processing and cognitive functions, such as the right middle frontal gyrus and the hippocampus. However, other regions, such as the left calcarine and median cingulate, show increased activity in IBS patients. Functional connectivity analyses have also demonstrated enhanced connectivity between the frontal and cingulate cortices in IBS patients, highlighting the complex network of brain regions involved in the gut-brain communication process. These findings suggest that IBS is not merely a local digestive issue but a condition that involves widespread changes in brain function.

Although the exact pathophysiology of IBS remains elusive, it is widely believed that it is triggered by dysregulation of the brain-gut axis, with the microbiota playing a central role. The gut microbiota, composed of bacteria, viruses, fungi, and other microorganisms, is influenced by both diet and stress, which can alter the microbial community and affect gut-brain interactions. Dietary factors, in particular, have been shown to have a rapid impact on the gut microbiota, leading to changes in microbial gene expression. These changes, in turn, can affect brain function and contribute to the development or exacerbation of IBS symptoms. Stress, too, has been shown to alter gut-brain axis functioning, leading to flare-ups or intensification of symptoms in IBS patients. Chronic stress can also affect the HPA axis, further disrupting the balance of the gut-brain interaction and exacerbating symptoms.

Conclusion

This study aims to explore the psycho-neurology of GI symptoms that may trigger IBS, with a focus on the correlation between GI symptoms, stress, and diet. By examining the interconnection between these factors and their impact on visuospatial memory, this research seeks to deepen our understanding of the complex relationships between gut health, emotional well-being, and cognitive function. Through this investigation, the goal is to provide insights into how stress and dietary habits contribute to the manifestation of GI symptoms and to explore potential therapeutic strategies to manage these symptoms in individuals with IBS.

Acknowledgement

None.

Conflict of Interest

There is no conflict of interest by author.

References

1. McKee, Ann C., Robert C. Cantu, Christopher J. Nowinski and E. Tessa Hedley-Whyte, et al. "Chronic traumatic encephalopathy in athletes: Progressive tauopathy after repetitive head injury." J Neuropathol Exp Neurol 68 (2009): 709-735.

Google Scholar, Crossref, Indexed at

2. Goldstein, Lee E., Andrew M. Fisher, Chad A. Tagge and Xiao-Lei Zhang, et al. “Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model.” Sci Transl Med 4 (2012).

Google Scholar, Crossref, Indexed at