Hey, There’s a Second Brain in Your Gut

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Scientists have known for years that there’s a “second brain” of autonomous neurons in your long, winding human digestive tract—but that’s about where their knowledge of the so-called abdominal brain ends. Now, research published in 2020 shows that scientists have catalogued 12 different kinds of neurons in the enteric nervous system (ENS) of mice.

This “fundamental knowledge” unlocks a huge number of paths to new experiments and findings. The gut brain greatly affects on how you body works. Your digestive system has a daily job to do as part of your metabolism, but it’s also subject to fluctuations in functionality, and otherwise related to your emotions.

Digestive symptoms and anxiety can be comorbid, and your gut is heavily affected by stress. So scientists believe having a better understanding of what happens in your ENS could lead to better medicines and treatments for a variety of conditions, as well as improved knowledge of the connection between the ENS and central nervous system..…Continue reading…

By: Caroline Delbert

Source: Hey, There’s a Second Brain in Your Gut

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The enteric nervous system is one of the main divisions of the nervous system and consists of a mesh-like system of neurons that governs the function of the gastrointestinal system; it has been described as a “second brain” for several reasons. The enteric nervous system can operate autonomously.

It normally communicates with the central nervous system (CNS) through the parasympathetic (e.g., via the vagus nerve) and sympathetic (e.g., via the prevertebral ganglia) nervous systems. However, vertebrate studies show that when the vagus nerve is severed, the enteric nervous system continues to function.

In vertebrates, the enteric nervous system includes efferent neurons, afferent neurons, and interneurons, all of which make the enteric nervous system capable of carrying reflexes in the absence of CNS input. The sensory neurons report on mechanical and chemical conditions. Through intestinal muscles, the motor neurons control peristalsis and churning of intestinal contents.

Other neurons control the secretion of enzymes. The enteric nervous system also makes use of more than 30 neurotransmitters, most of which are identical to the ones found in CNS, such as acetylcholine, dopamine, and serotonin. More than 90% of the body’s serotonin lies in the gut, as well as about 50% of the body’s dopamine; the dual function of these neurotransmitters is an active part of gut–brain research.

The first of the gut–brain interactions was shown to be between the sight and smell of food and the release of gastric secretions, known as the cephalic phase, or cephalic response of digestion. The gut–brain axis, a bidirectional neurohumoral communication system, is important for maintaining homeostasis and is regulated through the central and enteric nervous systems and the neural, endocrine, immune, and metabolic pathways, and especially including the hypothalamic–pituitary–adrenal axis (HPA axis).

That term has been expanded to include the role of the gut microbiota as part of the “microbiome-gut-brain axis”, a linkage of functions including the gut microbiota. Interest in the field was sparked by a 2004 study (Nobuyuki Sudo and Yoichi Chida) showing that germ-free mice (genetically homogeneous laboratory mice, birthed and raised in an antiseptic environment) showed an exaggerated HPA axis response to stress, compared to non-GF laboratory mice.

The gut microbiota can produce a range of neuroactive molecules, such as acetylcholine, catecholamines, γ-aminobutyric acid, histamine, melatonin, and serotonin, which are essential for regulating peristalsis and sensation in the gut. Changes in the composition of the gut microbiota due to diet, drugs, or disease correlate with changes in levels of circulating cytokines, some of which can affect brain function.

 The gut microbiota also release molecules that can directly activate the vagus nerve, which transmits information about the state of the intestines to the brain. Likewise, chronic or acutely stressful situations activate the hypothalamic–pituitary–adrenal axis, causing changes in the gut microbiota and intestinal epithelium, and possibly having systemic effects.

Additionally, the cholinergic anti-inflammatory pathway, signaling through the vagus nerve, affects the gut epithelium and microbiota. Hunger and satiety are integrated in the brain, and the presence or absence of food in the gut and types of food present also affect the composition and activity of gut microbiota. Most of the work that has been done on the role of gut microbiota in the gut–brain axis has been conducted in animals, including the highly artificial germ-free mice.

As of 2016, studies with humans measuring changes to gut microbiota in response to stress, or measuring effects of various probiotics, have generally been small and cannot be generalized; whether changes to gut microbiota are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut–brain axis, remains unclear.

The concept is of special interest in autoimmune diseases such as multiple sclerosis. This process is thought to be regulated via the gut microbiota, which ferment indigestible dietary fibre and resistant starch; the fermentation process produces short chain fatty acids (SCFAs) such as propionate, butyrate, and acetate. The history of ideas about a relationship between the gut and the mind dates from the nineteenth century.

A unifying theory that tied gastrointestinal mechanisms to anxiety, depression, and skin conditions such as acne was proposed as early as 1930. In a paper in 1930, it was proposed that emotional states might alter normal intestinal microbiota which could lead to increased intestinal permeability and therefore contribute to systemic inflammation. Many aspects of this theory have been validated since then.

Gut microbiota and oral probiotics have been found to influence systemic inflammation, oxidative stress, glycemic control, tissue lipid content, and mood. Microbial derived secondary bile acids produced in the gut may influence cognitive function. Altered bile acid profiles occur in cases of mild cognitive impairment and Alzheimer’s disease with an increase in cytotoxic secondary bile acids and a decrease in primary bile acids.

These findings suggest a role of the gut microbiome in the progression to Alzheimer’s disease. In contrast to the cytotoxic effect of secondary bile acids, the bile acid tauroursodeoxycholic acid may be beneficial in the treatment of neurodegenerative diseases.

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