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#1 | |||
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Wisest Elder Ever
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a tight BBB only allows certain drugs thru..mostly a function of
lipid solubility. For example, alcohol and anesthetics pass the easiest. In the case of the Zonulin channels, these would allow bacteria thru, and large water soluble substances and peptides. This would be the CNS version of "leaky gut syndrome". Leaky gut was always pooh poohed by doctors and now with the new information, that is no longer that controversial. Some drugs like H2 antagonists, Zantac and Pepcid, pass the BBB more often in the elderly. They cause a delirium when that happens. That is one example of how the BBB changes with age.
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All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei ************************************ . Weezie looking at petunias 8.25.2017 **************************** These forums are for mutual support and information sharing only. The forums are not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider. Always consult your doctor before trying anything you read here.
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#2 | |||
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In Remembrance
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Do you have any info on things that might simultaneously increase permeability of both BBB and gut? Given our slow GI motility that would seem to dump toxins into the bloodstream at the worst possible time.
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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#3 | |||
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In Remembrance
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We already know that stress opens the BBB. It works both ends of the street, it seems,
1: Curr Mol Med. 2008 Jun;8(4):299-312. The effects of physical and psychological stress on the gastro-intestinal tract: lessons from animal models. Caso JR, Leza JC, Menchén L. Sección de Gastroenterología, Servicio de Aparato Digestivo, Hospital General Universitario "Gregorio Marañón", C/ Dr Esquerdo 46. 28007 Madrid, Spain. Physical and psychological stresses are widely accepted as triggers and / or modifiers of the clinical course of diverse gastrointestinal disorders such as peptic ulcer, irritable bowel syndrome or inflammatory bowel disease. Growing experimental evidence from a variety of models such as immobilization, thermal injury or early maternal deprivation in laboratory animals uniformly supports the ability of stress to induce the development of gastric ulcers, altered gastrointestinal motility and ion secretion, and increased intestinal permeability leading to the passage of antigens to the lamina propria and bacterial translocation. Stress can also synergize with other pathogenic factors such as Helicobacter pylori, non-steroidal anti-inflammatory drugs or colitis-inducing chemicals to produce gastrointestinal disease. The brain-gut axis provides the anatomical basis through emotions and environmental influences modulate the gastrointestinal function through the regulation of gastrointestinal immune system and mucosal inflammation; in this sense, mucosal mast cells - at cellular level - and corticotropin releasing factor (CRF) - at molecular level - seem to play a crucial role. On the other hand, an array of adaptive responses have been evolved in order to maintain the homeostasis and to ensure the survival of the individual. In the gut mucosa anti-inflammatory pathways counteract the deleterious effect of the stressful stimuli on the gastrointestinal homeostasis. In the present review we discuss the several experimental approaches used to mimic human stressful events or chronic stress in laboratory animals, the evidence of stress-induced gastrointestinal inflammation and dysfunction derived from them, and the involved cellular and molecular mechanisms that are being discovered during the last years. PMID: 18537637 [PubMed - indexed for MEDLINE]
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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#4 | |||
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Wisest Elder Ever
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a long time now, and have read the Celiac boards for years.
I can't recall finding out the "why" it is higher in some people than others. It just "is". If you Google it there are many hits, including the drug company who has a compound in trials. Here is an interesting Wiki, with illustrations: http://en.wikipedia.org/wiki/Tight_junction I think PD along with other CNS neuro problems, may have a connection to gluten intolerance. Here is the Gluten file: http://jccglutenfree.googlepages.com/ It is a huge collection of data, including neuro issues and very helpful. Going gluten free may be very helpful for some people here.
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All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei ************************************ . Weezie looking at petunias 8.25.2017 **************************** These forums are for mutual support and information sharing only. The forums are not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider. Always consult your doctor before trying anything you read here.
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