The human body is made of trillions of human cells, comprising many different cell types and tissue types, each controlled by a single set of genes shared by all human cells. The full set of these human genes is called the human genome. But the human body also contains trillions of microbial cells, i.e. bacteria. Together, these microbial cells form the human ‘microbiome’ and play an important role in human health. Scientists now recognize that the human microbiome may be responsible for various metabolic and developmental processes, such as food digestion, vitamin synthesis, and even brain function.1
The human body has a hypothesized “Gut-Brain Axis,” a two-way pathway in which microorganisms living in the body affect the nervous system including the brain, through various mechanisms including direct effects on the immune system, hormone production, and metabolism, .2 When an imbalance occurs in a gluten sensitive person, elevated blood pressure, elevated blood sugar levels, altered cholesterol levels, and effect on the nervous system and immune system may occur. These changes may last for decades.
Researchers are continually evaluating the interrelationships of the various systems of the human body and the human microbiome. This article reviews the literature regarding the interrelationships between the microbiota in the human gut and other conditions in the human body. The review identifies that the microbial organisms in the human gut are mainly symbiotic. However, sometimes a ‘dysbiosis’ occurs, which is a change in the body’s microbial community that diminishes the essential population of good bacteria and allows pathogenic (bad) bacteria that are normally present in low amounts to flourish.
One of the major functions of the normal human microbiome is to protect against colonization by pathogens (disease-causing organisms) and overgrowth of organisms that can result from the disruption of the healthy microbial community. The mechanisms that regulate the ability of the microbiota to restrain pathogen growth are complex and include competitive metabolic interactions and immune responses. The gut microbiota that cause infection is known to upregulate gut-inflammation and systemic inflammation. These pathogenic gut microbiota enhance energy harvest, cause obesity, insulin resistance, and dysfunctional vago-vagal gut-brain axis.
Non-celiac gluten sensitivity is a hot topic associated with this subject. Daulatzai reports that non-celiac gluten sensitivity is a chronic functional gastrointestinal disorder which is very common across the world. When dysbiosis occurs in an individual with non-celiac gluten sensitivity, they may experience symptoms of gut inflammation, diarrhea, constipation, and abdominal pain. Also, during non-celiac gluten sensitivity dysbiosis, visceral hypersensitivity, dysfunctional metabolic state, and peripheral immune and neuro-immune communication are occurring. These immune-mediated gut and extra-gut dysfunctions may last for decades.
The neural, immunological, endocrine and metabolic pathways by which the microbiota influences the brain, and the proposed brain-to-microbiota component of this axis comprises the bidirectional “Gut-Brain Axis”. In the review, Daulatzai reports that a significant proportion of non-celiac gluten sensitive patients may chronically consume alcohol, non-steroidal anti-inflammatory drugs, and fatty diet, as well as suffer from various other disorders. Daulatzai reports that the above functional changes and dysbiosis are underpinned by a dysfunctional bidirectional “Gut-Brain Axis” pathway. It is conceivable that the above cascade of pathology may promote various pathophysiological mechanisms, neuroinflammation, and cognitive dysfunction; and the mechanisms of dysbiosis, gut inflammation, and chronic dyshomeostasis are of great clinical relevance.
Daulatzai explains that we need to be aware of non-celiac gluten sensitivity and its chronic pathophysiological impact. Daulatzai also explains that therapeutic measures including probiotics, vagus nerve stimulation, antioxidants, alpha 7 nicotinic receptor agonists, and corticotropin-releasing factor receptor 1 antagonist may reduce neuroinflammation and oxidative stress in non-celiac gluten sensitivity, which may in turnimprove cognitive function and reduce vulnerability to Alzheimer’s disease.
- American Society for Microbiology. FAQ: Human Microbiome, January 2014. http://academy.asm.org/index.php/faq-series/5122-humanmicrobiome. Accessed September 1, 2016.
- Daulatzai MA. Non-celiac gluten sensitivity triggers gut dysbiosis, neuroinflammation, gut-brain axis dysfunction, and vulnerability for dementia. CNS and Neurological Disorders Drug Targets. 2015;14(1):110-31. Review.