CCSVI came along as a FAD treatment and we (academics) were kicking ourselves for not getting into the social media space to counter the claims going round the web about the wonder cure.
It started off with a bit of science and mushroomed into something different. However, we can’t blame Social Media for the the Microbiome fad. This is something that we have created and people are buying into the hype we have created.
There are loads of clinical trials that have now been initiated and I would say… wait and see if they show anthing remotely useful before splashing the cash for some potty (baby talk for toilet) pampering. Because the chances are there is no wonder cure. Why say that in the face of the academic steamroller that says the microbiome is the next best thing since sliced bread
Because our furry friends may put the writing on the wall.
Gut microbiota depletion from early adolescence alters adult immunological and neurobehavioral responses in a mouse model of multiple sclerosis. Zeraati M, Enayati M, Kafami L, Shahidi SH, Salari AA. Neuropharmacology. 2019:107685
Emerging evidence indicates that gut microbiota interacts with immune and nervous systems in the host and plays a critical role (critical means dependent for the problem to occur so science says deal with this at all costs!!!) in the pathogenesis of multiple sclerosis (MS) and many psychiatric disorders such as depression and anxiety. (So we have gone from MS to deperession and anxiety-what else doesn’t the microbiome do? No wonder we have a trial in every condition where someone will fund it.) The aim of this study was to explore the influence of gut bacterial depletion from early adolescence on adult immunological and neurobehavioral responses in mice with experimental-autoimmune-encephalomyelitis (EAE) (So we would stick a teenager on antibiotics for years for this study to have any meaning…Thats really how we should use antibiotics? The dutch in me says “Schtop”). We used an animal model of gut microbiota depletion induced by antibiotics from weaning to adulthood to assess clinical signs, cognitive function and depression-and anxiety-related symptoms in non-EAE and EAE-induced mice. We measured levels of interferon (IFN)-γ, interleukin (IL)-17A and IL-10 in serum, and BDNF, IL-1β and tumor necrosis factor (TNF)-α) in the hippocampus (There are few if any lesions in the hippocampus in mouse EAE . Why not look in the spinal cord where the action is occurring?). Antibiotic-treated mice displayed a significant delay in the onset of clinical symptoms of EAE. However, a higher severity of EAE was found between days 19-22 post-immunization in antibiotics-treated mice, while a reduction in the clinical signs of MS was observed at days 24-25 post-immunization. (So the results would suggest don’t go anywhere near these antibotics as a treatment for your MS. But don’t wory as you won’t remember how rubbish the effects are as your memory is impaired). Antibiotic administration decreased IFN-γ and IL-17A levels and increased IL-10 in serum of EAE-induced mice. Antibiotic treatment significantly decreased hippocampal BDNF and enhanced learning and memory impairments in EAE-induced mice. However, no significant changes were found in non-EAE mice. Non-EAE and EAE mice treated with antibiotics exhibited increased anxiety-related behaviors (So implying that using antibotics like sweets is not good for you..We know that. Use them sparingly and properly), whereas depression-related symptoms and increased hippocampal TNF-α and IL-1β were only observed in EAE-induced mice treated with antibiotics. This study supports the view that depletion of gut microbiota by antibiotics from weaning profoundly impacts adult immunological and neurobehavioral responses. (Profond indeed, so off you go to the pampering clinic for the new wonder treatment. Read through these results those mice still got EAE so is it the wonder cure we have been hyping.