A Significant Hidden Truth Concerning the Leaky Gut Syndrome: It Might Be a Small Intestinal Enteropathy Rather than a Gluten-Induced Intestinal Dehiscence

Introduction

Most of the world’s scientific efforts dealing with the hot topic of the leaky gut (LG) challenge are locked upon repair of gut permeability due to a chronic inflammatory disease, damage of intestinal barrier due to non-inflammatory stress-associated conditions, gluten and gluten sensitivity, intestinal dysbiosis and auto-immunity, misbehavior of gut microbiota and endorsing dietary exclusion; most of them are indefinite and unsupported by truly clear evidences [1-6]. Those investigators who are searching for a link between the LG syndrome and a microbiome-related potential intestinal inflammatory states, the link of the syndrome with microbiota and Alzheimer disease, a combined link between LG disease with microbiota and autism even those who are suggesting an association with colorectal cancer are possibly approaching indirectly very close to a real truth as concerns this conflicting medical challenge [1,7-10]. Employment of a probiotic cocktail though is not sufficiently decisive per its own yet it could be an intelligent idea enough to touching the roots of this truth [11]. The journey of this truth might have a bit long history since nearly 170 years before with sinificant stops before nearly 90 years, 30 years later and further 20 years after where an investigator has reported in 1853 that there is ammonia that exists in gastric lumen, in 1930s it was reported that the source of ammonia in the stomach is due to the activity of a urease enzyme, in 1960s a scientist has confirmed that the urease activity in the stomach is not a property of the stomach but of a bacterial origin and as early as the beginning of 1980s where it was illustrated that the amounts of ammonia existing in the stomach are not toxic but even beneficial [12]. That is until 1985 and 1986 where a biological bacterium (Helicobacter pylori) has been forced via antibiotic aggression to migrate outside the stomach with an associated world’s disease flare up; the LG challenge could be among these diseases. H. pylori while in the stomach could function to protect from acid reflux, significantly it also helps to protect the gastric wall from its acid if it goes in excess and protects from absence of the acid during abscece of food [12-14]. Its traces while in the stomach helps digestion, absorption and intestinal motility. If it is forced to migrate from its natural habitat and occupies the small intestine for nutrition during the process of digestion, its products in profuse amounts would definitely cause indigestion, malabsorption and intestinal delay with subsequent excess fermentation, even putrefaction and production of toxins [14]. Absorption of these toxins could explain the adverse symptoms encountered in the LG syndrome.

Aim

Demonstration of a hidden fact concerning the LG challenge due to a natural gut bacterium non-intentional misbehavior.

Motive of Study

In spite of all the extensive therapeutic efforts a successful achievement for the management of the LG disease is indefinite. Although some investigators emphasized an aging-related LG disorder [11], yet newly-developed gluten allergy betwwen 60-70 years of age was not enough convincing. The successful trials to develop a happy gut via dietary exclusion of some elements of food for some temporary periods then returning to them infrequently without developing any gut problems might signify that a permamant gut pathology is not a constant cell damage related to the disease but it could be a sort of constitutional dysfunction. These observational findings were sufficiently motivating this study to search for a temporary definite patho-physiological dysfunction that could explain the symptoms encountered in the LG syndrome.

Design

A prospective multiple-case clinical study has been done in Zaitona medical cupping center during 2019-2021 in Medina, Saudi Arabia.

Methods

Nine male patients known with LG disease on symptomatic medications were included in the study, they were in three age groups, each group included three patints and the age range was 16-25, 34-50 and 61-72 years. Their symptoms varied from mild to moderate while one of them aged 40 years used to develop sometimes severe symptoms. They were given a side dish of chickpea flour béchamel or puree during or between the attacks of symptoms for 6-9 weeks. They were also given a dried dates powder as an alternative sweetener when required when they feel craving for sweets. They tolerated both stuffs without problems as concerns their disease condition and they liked both of them. A specific test for existence of H. pylori in the colon (H. pylori fecal antigen) was done for all patients [12,14]. All patients were allowed and instructed to employ their own symptomatic medications when required.

Results

All patients were found positive for existence of colonic H. pylori strains. All patients have tolerated both food stuffs used in the study and they mostly preferred and enjoyed the chickpea béchamel or puree. All patients demonstrated obvious improvement and decreased frequency of symptoms even most of them did not find any need to use their own symptomatic medications during the period of study. Follow up of patients for further six months showed similar observations.

Ethical Considerations

All patients were re-assured about safety of the food stuffs used in the study as concerns their disease condition and it is just a dietary stuff. Patients were allowed to lead their own style of life and they were free to quit the study whenever they like. An informed signed consent was taken from all patients.

Discussion

The challenge of the LG is a hot world’s topic that has been extensively studied, great scientific and psophisticated efforts have been dealing with this problem but without definite cure outcomes. The literature reports include attempts to cure disorders in gut permeability barrier related to chronic inflammatory or stress conditions [1,2], management of gluten/food sensitivity and auto-immunity via dietary exclusion [3-6], and further efforts to rectify dysbiosis whether it is abnormal existence or misbehavior of natural microbiomes within its natural habitat [4,7,8]. However, all these great efforts were unsupported by clear evidences. Those investigators who are searching for a link of the syndrome with microbiota and Alzheimer disease, a combined link between LG disease with microbiota and autism and even those who are suggesting an association with colorectal cancer are possibly approaching indirectly very close to a real truth as concerns this conflicting medical challenge as all these pathologies could be a result of the same reason which is translocation or mal-existence of a natural microbiome where it does the proper good function in an improper site [7-10,15-17]. Employment of a probiotic cocktail though is not sufficiently decisive per its own yet it could be an intelligent idea touching the roots of this truth which could be dysbiosis [11].

The interest of the investigator of this study with the LG challenge started since 2017 through suggesting meals for LG disease patients as alternatives for wheat, milk products and sugars. Whereas his attention towards the hot world’s topic of H. pylori began as early since 2003; whether H. pylori is guilty, not guilty or innocent; whether it is biologic or pathologic; whether its antibiotic eradication is necessary and possible or un-necsssary because impossible; whether the antibiotic eradication therapies are effective or ineffective; whether H. pylori is eradicated or forced to migrate and should we fight and kill or save H. pylori!! It has been found that H. pylori colonized the stomach since an immemorial time as if both the gastric wall and the bacterium used to live together in peace harmless to each other, it has been also reported that recurrence of H. pylori in the stomach is unavoidable and it was further emphasized that H. pylori has got huge defense talents for survival within the hell fire of the gastric acid [12,14,17]. Could these criteria altogether suggest that H. pylori might be a natural bacterium!!

Physiological intelligence has been praised for juxta-mucosal ammonia of the stomach as the ammonia adjacent to the gastric mucosa is responsible for the endothelial-derived nitric oxide (NO) liberation from micro-capillaries of gastric mucosa via a shear stress effect whereas NO is entitled for the control of mucus secretion from gastric mucosa and mcus thickening; hence ammonia and NO are responsible for the formation of the thick viscid alkaline gastric mucus layer that constitutes the main gastric wall protection from its strong acid meanwhile H. pylori is lying safe under this mucus shield and protected by a sheath of ammonia at its immediate vicinity which helps to buffer any acidity that penetrates the mucus shield [12,14,18,19]. Then what is the nutrition of H. pylori and how it could gain it!! H. pylori eats organic urea to produce its ammonia and pyruvate in order to gain energy, it picks up its food from the remnants of gastric lumen contents in a blink after travel of the meal and drop of the acid to low residual level but still protected by a jacket of ammonia thus leaving before returning traces of ammonia in the gastric lumen that excites back the acid secretion [12,14]. Accordingly, H. pylori helps to protect the gastric wall from its acid if it goes in excess and helps to protect the gut and the human body from absence of the acid during absence of food as the gastric acid is the major defense line against bacteria invading the gut with food and drinks. This biological competitive buffering phemomena between ammonia of H. pylori and the gastric acid is constant leaving all the time residual traces of ammonia in gastric lumen that assists to maintain the integrity of the gastro-esophageal sphincter as ammonia is smooth muscle tonic helping in turn to protect from acid reflux [13,20-23]. If H. pylori is natural it should have a function, and if it plays these wonderful functions in only one area of the gut it should be natural and hugely biologic. It has been emphasized that H. pylori is not essentially pathologic in attitude by its own but it is mostly forced to its pathologic sequels either due to misbehavior in food habits or the antibiotic violence towards it. It has been further realized that misconception and misbehavior towards H. pylori was leading to major spread of illness during the latest three decades [14,17]; the leaky gut disease could be among these diseases.

NO is a cure and poison in the meantime; that is in normal levels it is cure while in overdoses it is toxic. As ammonia in the gut liberates NO via a shear stress effect, accordingly; ammonia in the gut is a cure and poison at the same time meaning that ammonia in low residual levels is healthy whereas in profuse amounts it could be toxic and pathologic [18,19,24]. Therefore; while H. pylori exists in the stomach, travel of few traces of its ammonia from gastric lumen to the small intestine is supposed to assist digestion, absorption and intestinal motility. If H. pylori is forced to migrate from the stomach and it comes to occupy the small intestinal mucosa for nutrition, it would definitely cause indigestion, malabsorption and intestinal delay with excess fermentation in turn, even putrefaction and production of toxins [14]. Absorption of these toxins could explain the adverse symptoms related to the LG syndrome without existence of a damage in gut barrier or constant pathologic change in intestinal permeability.

The chickpea flour béchamel was selected in this study for satiety as an alternative for wheat products while the dried date’s powder was chosen as a sweetener alternative for sugars and both of them are also suitable for the patient’s disease condition. It was interesting to observe apparent improvement and decreased frequency of symptoms among all patients upon using these two food stuffs even during the symptom attacks. It has been realized that the chickpea flour and the dried fibers contained in the date’s powder are known fluid absorbents and bulk formatives that could turn the liquid indigested gut contents into formed stuff which is less fermetable and travels better in the gut resulting in less production and less absorption of toxins. This could explain the improvement of symptoms among patients of this study upon adding the chickpea flour recepies and the dried date’s fibers to their diet. Further investigators have also emphasized that dietary fibers could impact a protective effect on gut barrier integrity being poorly fermented by gut microbes and likely promote the gut transit rate thus reduce the time available for bacterial fermentation of non-digested food stuff [25].

It was not scientifically sound then to suggest that any of these two food stuffs employed in this study would instantly correct a permanent pathologic dehiscence in the gut barrier. It is also scientifically silly to imagine that the gut bacteria change its behavior to cause anaerobic fermentation of the gut contents. It is better logic to consider that the fault in the LG disease is not a permanent gut permeability damage but it could simply be a potential inflammatory error. As all patients were found positive for H. pylori strains, thus; the assumption that the migrating H. pylori strains could come to occupy the mucosa of small intestine simply for nutrition seems logic whereas its produced ammonia which would be entrapped within the gut mucosa in excess amounts in this situation as being unbuffered by any acidity would be then toxic leading to indigestion, malabsorption and intestinal delay with excess fermentation particularly for fermentable food products containing gluten. Hence; could the challenge of the LG disease be a potential small intestinal enteropathy rather than it is a gluten-induced intestinal dehiscence!! Could a big compromise be as simple as such!! Could the challenge of the LG syndrome be just small intestinal enteropathy rather than it is true gut barrier damage!! Could the matter be a non-intentional misbehavior of a natural bacterium due to the antibiotic violence towards it and would correction of the antibiotic use alleviate the problem!!

Acknowledgement

This study appreciates the effort and clinical support offered by Zaitona Medical Cupping Center.

Conflict of Interest

No conflict of interest is existing.

Conclusion

The challenge of the LG syndrome might be a small intestinal enteropathy rather than it is a gluten-induced intestinal dehiscence. Scientific efforts should be better directed towards control of environmental chemicals and the antibiotic abuse which could lead to misbehavior of natural gut microbiota. Natural specific potent measures should be employed to correct abnormal behavior/existence of gut microbiota.

References