Benutzer:Teddet123/Darm-Hirn-Achse
Das Modell der Darm-Hirn-Achse oder Bauch-Hirn-Achse (engl. gut-brain axis) beschreibt den funktionellen Zusammenhang zwischen Gastrointestinaltrakt und Zentralem Nervensystem.[2] Der erweiterte Begriff Mikrobiom-Darm-Hirn-Achse weist explizit auf den dazugehörigen Einfluss von Darmbakterien hin.[2][3][4] Prinzipiell umfasst die Darm-Hirn-Achse das Zentrale Nervensystem, das neuroendokrine System, das Immunsystem, Bestandeile des sympathischen und parasympathischen Systems, das enterische Nervensystem, Teile des peripheren Systems (insb. N. vagus) sowie das Darmmikrobiom.[2][4]
As of October 2016, most of the work done on the role of gut flora in the gut–brain axis had been conducted in animals, or on characterizing the various neuroactive compounds that gut flora can produce. Studies with humans – measuring variations in gut flora between people with various psychiatric and neurological conditions or when stressed, or measuring effects of various probiotics (dubbed "psychobiotics" in this context) – had generally been small and were just beginning to be generalized.[5] Whether changes to gut flora are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut–brain axis, remained unclear.[6][2]
Enteric nervous system
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.[7]
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.[8][9][10]
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.[11][12]
Gut–brain integration
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).[2] That term has been expanded to include the role of the gut flora as part of the "microbiome-gut-brain axis", a linkage of functions including the gut flora.[2][4][3]
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.[2]
The gut flora 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.[13] Changes in the composition of the gut flora due to diet, drugs, or disease correlate with changes in levels of circulating cytokines, some of which can affect brain function.[13] The gut flora also release molecules that can directly activate the vagus nerve, which transmits information about the state of the intestines to the brain.[13]
Likewise, chronic or acutely stressful situations activate the hypothalamic–pituitary–adrenal axis, causing changes in the gut flora and intestinal epithelium, and possibly having systemic effects.[13] Additionally, the cholinergic anti-inflammatory pathway, signaling through the vagus nerve, affects the gut epithelium and flora.[13] 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 flora.[13]
That said, most of the work that has been done on the role of gut flora 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 flora in response to stress, or measuring effects of various probiotics, have generally been small and cannot be generalized; whether changes to gut flora 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.[6]
The concept is of special interest in autoimmune diseases such as Multiple Sclerosis .[14] Nutrition and microbiota can influence both each other as well as the immune system, for example by modifying the Th17, Th1 and Treg cell frequencies and activity in animal models and preliminary trial in humans.[15][16]
The history of ideas about a relationship between the gut and the mind dates from the nineteenth century. The concepts of dyspepsia and neurasthenia gastrica referred to the influence of the gut on human emotions and thoughts.[17][18]
Darmflora
Die Darmflora ist die Gesamtheit der im Verdauungstrakt eines Menschen oder anderen Tieres lebenden Bakterien. Das Darm-Mikrobiom ist die von diesen Bakterien gebildete genetische Information.[19][20]
Beim Menschen wird der Darmflora die größte Gesamtmasse und höchste Anzahl unterschiedlicher Bakterien-Spezies im Vergleich zu anderen Körperteilen zugeschrieben.[21] Sie entwickelt sich typischerweise über die ersten Lebensjahre; diese Zeit wird von der Darmschleimhaut benötigt, um sich sowohl auf die Toleranz als auch die symbiotische Unterstützung der Darmbakterien einzustellen. Daneben entwickelt sich auch ein Schutz vor pathologischen Mikroorganismen.[22][23]
Der bakterielle Stoffwechsel unterstützt die menschliche Verdauung, insbesondere bei der Fermentation unverdaulicher Pflanzenfasern und die Bereitstellung kurzkettiger Fettsäuren wie Aceton- und Proprionsäure.[21][24] Die Bakterien können wiederum auf ein breites Nährstoffangebot zurückgreifen. Darmbakterien spielen auch bei der Synthese von Vitamin B und Vitamin K sowie der Metabolisierung von Gallensäuren, Sterolen und Xenobiotika eine Rolle.[20][24] Die systemische Rolle von kurzkettigen Fettsäuren und anderer Metabolite kann Hormon-ähnlich begriffen werden, die Darmflora wurde daher auch mit einem endokrinen Organ verglichen.[24] Dysregulation der Darmflora wird insbesondere mit Autoimmunerkrankungen wie etwa Multiple Sklerose in Verbindung gebracht.[21][25]
Die Zusammensetzung der Darmflora verändert sich mit der Zeit, durch veränderte Essensgewohnheiten, sowie durch gesundheitliche Einflüsse.[21][25] Durchschnittlich besteht die humane Darmflora aus über 1000 im Mikrobiom detektierten Spezies. Ernährungsgewohnheiten können die Zusammensetzung verändern, so wird ein hoher Anteil industriell verarbeiteter Nahrungsbestandteile sowie eine hohe Salzbelastung mit negativen Veränderungen in Verbindung gebracht.[15] Auch Antibiotika und Probiotika wirken sich auf die Darmflora aus. Antibiotika können sowohl pathogene als auch vorteilhafte Spezies depletieren. Probiotika können eingesetzt werden, um als vorteilhaft angesehene Spezies zu stärken und die Wiederherstellung einer ausgeglichenen Darmflora nach Antibiose zu fördern. Hierbei sollte das verwendete Präparat sich an den individuellen Bedürfnissen des Patienten orientieren, da hiervon die Wirksamkeit und Sicherheit abhängen .[26]
Einzelnachweise
- ↑ Yin-Xia Chao, Muhammad Yaaseen Gulam, Nicholas Shyh Jenn Chia, Lei Feng, Olaf Rotzschke, Eng-King Tan: Gut–Brain Axis: Potential Factors Involved in the Pathogenesis of Parkinson's Disease. In: Frontiers in Neurology. 11, 2020, ISSN 1664-2295, S. 849. doi:10.3389/fneur.2020.00849.
- ↑ a b c d e f g N Sudo, Y Chida, Y Aiba: Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice. In: J Physiol. 558, Nr. 1, 2004, S. 263–275. doi:10.1113/jphysiol.2004.063388. PMID 15133062. PMC 1664925 (freier Volltext). cited in: Y Wang, LH Kasper: The role of microbiome in central nervous system disorders. In: Brain Behav Immun. 38, May 2014, S. 1–12. doi:10.1016/j.bbi.2013.12.015. PMID 24370461. PMC 4062078 (freier Volltext).
- ↑ a b EA Mayer, R Knight, SK Mazmanian: Gut microbes and the brain: paradigm shift in neuroscience. In: J Neurosci. 34, Nr. 46, 2014, S. 15490–15496. doi:10.1523/JNEUROSCI.3299-14.2014. PMID 25392516. PMC 4228144 (freier Volltext).
- ↑ a b c T.G Dinan, 2015 Cryan: The impact of gut microbiota on brain and behavior: implications for psychiatry. In: Curr Opin Clin Nutr Metab Care. 18, Nr. 6, 2015, S. 552–558. doi:10.1097/MCO.0000000000000221. PMID 26372511.
- ↑ Huiying Wang, In-Seon Lee, Christoph Braun, Paul Enck: Effect of Probiotics on Central Nervous System Functions in Animals and Humans: A Systematic Review. In: J Neurogastroenterol Motil. 22, Nr. 4, October 2016, S. 589–605. doi:10.5056/jnm16018. PMID 27413138. PMC 5056568 (freier Volltext).
- ↑ a b J Schneiderhan, T Master-Hunter, A Locke: Targeting gut flora to treat and prevent disease. In: J Fam Pract. 65, Nr. 1, 2016, S. 34–8. PMID 26845162.
- ↑ Musings on the Wanderer: What's New in Our Understanding of Vago-Vagal Reflexes? V. Remodeling of vagus and enteric neural circuitry after vagal injury. In: American Journal of Physiology. Gastrointestinal and Liver Physiology. 285, Nr. 3, September 2003, S. G461–9. doi:10.1152/ajpgi.00119.2003. PMID 12909562.
- ↑ Pankaj Jay Pasricha: Stanford Hospital: Brain in the Gut – Your Health.
- ↑ I Martinucci: Genetics and pharmacogenetics of aminergic transmitter pathways in functional gastrointestinal disorders. In: Pharmacogenomics. 16, Nr. 5, 2015, S. 523–39. doi:10.2217/pgs.15.12. PMID 25916523.
- ↑ K Smitka: The role of "mixed" orexigenic and anorexigenic signals and autoantibodies reacting with appetite-regulating neuropeptides and peptides of the adipose tissue-gutbrain axis: relevance to food intake and nutritional status in patients with anorexia nervosa and bulimia nervosa. In: Int J Endocrinol. 2013, 2013. doi:10.1155/2013/483145. PMID 24106499. PMC 3782835 (freier Volltext).
- ↑ L Filaretova, T Bagaeva: The Realization of the Brain–Gut Interactions with Corticotropin-Releasing Factor and Glucocorticoids.. In: Current Neuropharmacology. 14, Nr. 8, 2016, S. 876–881. doi:10.2174/1570159x14666160614094234. PMID 27306034. PMC 5333583 (freier Volltext).
- ↑ PA Smeets, A Erkner, C de Graaf: Cephalic phase responses and appetite.. In: Nutrition Reviews. 68, Nr. 11, November 2010, S. 643–55. doi:10.1111/j.1753-4887.2010.00334.x. PMID 20961295.
- ↑ a b c d e f AI Petra: Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation. In: Clin. Ther.. 37, Nr. 5, May 2015, S. 984–95. doi:10.1016/j.clinthera.2015.04.002. PMID 26046241. PMC 4458706 (freier Volltext).
- ↑ Benedetta Parodi, Nicole Kerlero de Rosbo: The Gut-Brain Axis in Multiple Sclerosis. Is Its Dysfunction a Pathological Trigger or a Consequence of the Disease?. In: Frontiers in Immunology. 12, 21. September 2021, ISSN 1664-3224, S. 718220. doi:10.3389/fimmu.2021.718220. PMID 34621267. PMC 8490747 (freier Volltext).
- ↑ a b Nicola Wilck, Mariana G. Matus, Sean M. Kearney, Scott W. Olesen, Kristoffer Forslund, Hendrik Bartolomaeus, Stefanie Haase, Anja Mähler, András Balogh, Lajos Markó, Olga Vvedenskaya: Salt-responsive gut commensal modulates TH17 axis and disease. In: Nature. 551, Nr. 7682, November 2017, ISSN 1476-4687, S. 585–589. doi:10.1038/nature24628.
- ↑ Alexander Duscha, Barbara Gisevius, Sarah Hirschberg, Nissan Yissachar, Gabriele I. Stangl, Eva Eilers, Verian Bader, Stefanie Haase, Johannes Kaisler, Christina David, Ruth Schneider: Propionic Acid Shapes the Multiple Sclerosis Disease Course by an Immunomodulatory Mechanism. In: Cell. 180, Nr. 6, 19. März 2020, ISSN 1097-4172, S. 1067–1080.e16. doi:10.1016/j.cell.2020.02.035. PMID 32160527.
- ↑ Manon Mathias and Alison M. Moore (eds), Gut Feeling and Digestive Health in Nineteenth-Century Literature, History and Culture. New York: Palgrave, 2018. Vorlage:ISBN
- ↑ Alison M. Moore, Manon Mathias and Jørgen Valeur, Microbial Ecology in Health and Disease, Volume 30 (1), Special issue on the Gut–Brain Axis in History and Culture, 2019
- ↑ R. Saxena, V.K Sharma: A Metagenomic Insight Into the Human Microbiome: Its Implications in Health and Disease. In: Medical and Health Genomics. Elsevier Science, 2016, ISBN 978-0-12-799922-7, S. 117, doi:10.1016/B978-0-12-420196-5.00009-5.
- ↑ a b Linda Sherwood, Joanne Willey, Christopher Woolverton: [[[:Vorlage:Google books]] Prescott's Microbiology], 9th. Auflage, McGraw Hill, New York 2013, ISBN 978-0-07-340240-6, S. 713–721, OCLC 886600661.
- ↑ a b c d EM Quigley: Gut bacteria in health and disease. In: Gastroenterol Hepatol (N Y). 9, Nr. 9, 2013, S. 560–9. PMID 24729765. PMC 3983973 (freier Volltext).
- ↑ F Sommer, F Bäckhed: The gut microbiota--masters of host development and physiology. In: Nat Rev Microbiol. 11, Nr. 4, Apr 2013, S. 227–38. doi:10.1038/nrmicro2974. PMID 23435359.
- ↑ M Faderl: Keeping bugs in check: The mucus layer as a critical component in maintaining intestinal homeostasis. In: IUBMB Life. 67, Nr. 4, Apr 2015, S. 275–85. doi:10.1002/iub.1374. PMID 25914114.
- ↑ a b c G Clarke: Minireview: Gut microbiota: the neglected endocrine organ. In: Mol Endocrinol. 28, Nr. 8, Aug 2014, S. 1221–38. doi:10.1210/me.2014-1108. PMID 24892638. PMC 5414803 (freier Volltext).
- ↑ a b S Shen, CH Wong: Bugging inflammation: role of the gut microbiota. In: Clin Transl Immunol. 5, Nr. 4, Apr 2016. doi:10.1038/cti.2016.12. PMID 27195115. PMC 4855262 (freier Volltext).
- ↑ Peera Hemarajata, James Versalovic: Effects of probiotics on gut microbiota: mechanisms of intestinal immunomodulation and neuromodulation. In: Therapeutic Advances in Gastroenterology. Band 6, Nr. 1, Januar 2013, ISSN 1756-2848, S. 39–51, doi:10.1177/1756283X12459294, PMID 23320049, PMC 3539293 (freier Volltext) – (sagepub.com [abgerufen am 4. Dezember 2021]).
