Abstract:As Antonio Damasio highlighted back in 1994, Descartes' division of mind and body slowed the full realization of the connectedness of the brain and the body by centuries. The simple fact that homeostasis in the brain was fully interconnected with the body has eluded researchers and clinicians even after the connection was well established. Recent studies reporting the central role in dysfunction of mental systems as a result of inflammation in the gut and the autonomic nervous system (ANS) was yet one more rem… Show more
“…Additionally, these aromatic amines can directly enter the brain when liver function is impaired, and generate pseudo-neurotransmitters including phenylethanolamine and β-hydroxytyramine. These pseudo-neurotransmitters cannot transmit nerve impulses [ 49 , 50 ] and, therefore, may cause brain dysfunction and liver coma. Research on the influence of gut microbiota-derived metabolites on the pathophysiological mechanisms of HE found that hyperammonemia plays an important role in the progression of HE.…”
Section: Bioactive Molecules As Mediators Of the Microbiome-gut-liver...mentioning
Hepatic encephalopathy (HE) is a clinical manifestation of neurological and psychiatric abnormalities that are caused by complications of liver dysfunction including hyperammonemia, hyperuricemia, and portal hypertension. Accumulating evidence suggests that HE could be reversed through therapeutic modifications of gut microbiota. Multiple preclinical and clinical studies have indicated that gut microbiome affects the physiological function of the liver, such as the regulation of metabolism, secretion, and immunity, through the gut-liver crosstalk. In addition, gut microbiota also influences the brain through the gut-brain crosstalk, altering its physiological functions including the regulation of the immune, neuroendocrine, and vagal pathways. Thus, key molecules that are involved in the microbiota-gut-liver-brain axis might be able to serve as clinical biomarkers for early diagnosis of HE, and could be effective therapeutic targets for clinical interventions. In this review, we summarize the pathophysiology of HE and further propose approaches modulating the microbiota-gut-liver-brain axis in order to provide a comprehensive understanding of the prevention and potential clinical treatment for HE with a microbiota-targeted therapy.
“…Additionally, these aromatic amines can directly enter the brain when liver function is impaired, and generate pseudo-neurotransmitters including phenylethanolamine and β-hydroxytyramine. These pseudo-neurotransmitters cannot transmit nerve impulses [ 49 , 50 ] and, therefore, may cause brain dysfunction and liver coma. Research on the influence of gut microbiota-derived metabolites on the pathophysiological mechanisms of HE found that hyperammonemia plays an important role in the progression of HE.…”
Section: Bioactive Molecules As Mediators Of the Microbiome-gut-liver...mentioning
Hepatic encephalopathy (HE) is a clinical manifestation of neurological and psychiatric abnormalities that are caused by complications of liver dysfunction including hyperammonemia, hyperuricemia, and portal hypertension. Accumulating evidence suggests that HE could be reversed through therapeutic modifications of gut microbiota. Multiple preclinical and clinical studies have indicated that gut microbiome affects the physiological function of the liver, such as the regulation of metabolism, secretion, and immunity, through the gut-liver crosstalk. In addition, gut microbiota also influences the brain through the gut-brain crosstalk, altering its physiological functions including the regulation of the immune, neuroendocrine, and vagal pathways. Thus, key molecules that are involved in the microbiota-gut-liver-brain axis might be able to serve as clinical biomarkers for early diagnosis of HE, and could be effective therapeutic targets for clinical interventions. In this review, we summarize the pathophysiology of HE and further propose approaches modulating the microbiota-gut-liver-brain axis in order to provide a comprehensive understanding of the prevention and potential clinical treatment for HE with a microbiota-targeted therapy.
“…It has been shown to have positive effects on conditions such as depression, schizophrenia, addiction, and various neurological diseases (22). Stress and anxiety in rats have been observed to alter the composition of intestinal microbiota and decrease the production of neurogenesis factors derived from the brain (23).…”
Section: Microbiota and Neurotransmittersmentioning
confidence: 99%
“…The intestinal microbiota also has the ability to regulate hormone release through the hypothalamus-pituitary-adrenal axis, which is involved in the body's response to stress. Additionally, corticosteroid hormones released by the hypothalamus-pituitary-adrenal axis can influence the composition of the intestinal microbiota (24). The colonization of Bifidobacterium infantis in the gut has been shown to improve behavioral and stress-related brain deficits.…”
Section: Microbiota and Neurotransmittersmentioning
Background: The human intestine harbors a collection of microorganisms known as intestinal microbiota, which encompasses bacteria, archaea, and eukaryotes. However, bacteria reign supreme as the most prevalent members of the intestinal microbiota. Notably, the gut microbiota plays a crucial role in regulating various physiological functions of the human body. In addition to its influence on digestion, the gut microbiota also exerts control over the function of the brain and central nervous system, earning the enteric nervous system the title of the "second brain." The behavior and mood, as well as the progression of nervous system diseases like multiple sclerosis, autism, Alzheimer's, schizophrenia, and Parkinson's, can potentially be regulated by the intestinal microbiota. Through the intestinal nervous system, production of metabolites, stimulation of entero-endocrine cells, and the immune system, the gut microbiota plays a role in regulating the function of the central nervous system. Disturbances caused by improper nutrition, indiscriminate use of antibiotics, stress, anxiety, and depression are significant factors that can worsen these diseases and disrupt the balance of gut microbiota.
“…However, with populations, that have established a stable homeostatic symbiosis with beneficial microbiome, now eating foods that challenge the established microbiome, are creating new gut microenvironments for new microbiome populations that might not be compatible for normal tissue health [82][83][84][85]. The consequences of these new microbiome secreted toxins might have all kinds of health effects along the gut/brain axis [86]. With the trillions of various populations of microbes in the gut, confronting all kinds of foods, grown and processed differently, together with medications, pollutants and supplements, it seems that the chemical sequelae of the signaling from this metabolism on the physiological responses of all the organs affected would be unpredictable.…”
Section: The Role Of Epigenetics In Food Safetymentioning
Nutrition and diet, which are fundamental to human development and health, in the context of food safety, can be major
determinants in the prevention and contributor to both acute and chronic diseases. While the predominant and legitimate
concern is to detect and eliminate microbial pathogens that can cause acute illnesses and deaths (estimated 3-5 thousand
deaths in the United States and millions of various acute disorders), food components (nutrients, pollutants, additives,
processing by-products, etc.) are major factors in chronic diseases (e.g., “metabolic diseases” of diabetes, cardiovascular
diseases, cancers). They contribute to millions of long-term health problems and deaths, globally. The objective of this
“Communication” is to integrate a shared underlying mechanism of toxicity between acute and chronic diseases. The
traditional separation of the strategy to understand “causes” of acute and chronic diseases, while for some practical tactics
is understandable (i.e. screening for food-associated pathogens), it fails to recognize that these microbial -associated toxins
work by exactly the same molecular/biochemical and cellular mechanisms as the toxicants- causing chronic diseases. Since all
chemicals work by mutagenic, cytotoxic or “epigenetic” alteration of gene expression at the transcriptional, translational or
post-translational levels, understanding characteristics of all three of these toxicological mechanisms is important so
that public policy- strategies for prevention of both these classes of food –related diseases can be made and that a solid
foundation for the concept of “functional foods” be made. A moral imperative has to be given to the critical role that safe
food can make during pregnancy in preventing long-term health effects later in life.
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