8 ms·
This has been my experience more-or-less as well. Any graduate student that does anything even alzheimer's adjacent at the school I used to work at absolutely h
by el_cujo 7y ago
This has been my experience more-or-less as well. Any graduate student that does anything even alzheimer's adjacent at the school I used to work at absolutely had to have a certain two researchers on their dissertation committee and they would 100% not let you progress without throwing a bone to beta-amyloid in your proposal (along with heavily pushing you to pander to some of their personal pet theories).
It's a sunken cost fallacy at this point, people have build entire careers on the beta-amyloid stuff and they will NEVER accept an alternative because it would make them irrelevant. These same people hold a lot of power in the field.
- nextos 7y agoIt's the same with autoimmunity. Some researchers are obsessed with genetics. But it's mostly about self misclassification due to infections and dysbiosis. Luckily, some top journals have started accepting this, but it's still an uphill battle against the establishment: * Type 1 diabetes: https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1 https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1 * Multiple sclerosis: https://stm.sciencemag.org/content/10/462/eaat4301 https://stm.sciencemag.org/content/10/462/eaat4301 * Lupus: https://stm.sciencemag.org/content/10/434/eaan2306 https://stm.sciencemag.org/content/10/434/eaan2306 * Sjogren's: https://www.sciencedirect.com/science/article/abs/pii/S1521661614000412 https://www.sciencedirect.com/science/article/abs/pii/S15216... * Anti-phospholipid: https://www.sciencedirect.com/science/article/abs/pii/S1931312819302483 https://www.sciencedirect.com/science/article/abs/pii/S19313... * Parkinson's: https://onlinelibrary.wiley.com/doi/full/10.1002/mds.27105 https://onlinelibrary.wiley.com/doi/full/10.1002/mds.27105 * Alzheimer's: https://advances.sciencemag.org/content/5/1/eaau3333?intcmp=trendmd-adv https://advances.sciencemag.org/content/5/1/eaau3333?intcmp=... It's like the old joke that science progresses one funeral at a time.
- darkerside 7y agoAre you saying many diseases we believe to be autoimmune may be caused by infections?
- nextos 7y agoYes. Or dysbiosis, i.e. your own commensal bacteria, fungi and phages going out of control in different ways. The consequence of this in both cases is that your immune system mis-classifies some of your own tissues as non-self and attacks them (autoimmunity). See introduction in: https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1 https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1 The reason is that both pathogens and your own microbiome mimic your tissue components. Especially proteins. They want to avoid being recognized as non-self, either to infect you or to keep their symbiotic relationship. Hence, in some scenarios it's hard for the immune system to classify a virus or a commensal as foreign and the mimicked tissue in your own body as self at the same time. The first reference in my previous post explains it well. Viral mimicry is quite old and well established in the literature both as an infection strategy and as a cause of autoimmunity [1-3]. But microbiome (commensal) mimicry is surprisingly unexplored, except for a few recent studies. Some are those I referred to in my previous post. Note in many ways tumors are also an immune problem. They should have been caught by the immune system. There is growing evidence that this is also related to mimicry and dysbiosis. [1] https://link.springer.com/chapter/10.1007/978-3-642-74594-2_11 https://link.springer.com/chapter/10.1007/978-3-642-74594-2_... [2] https://www.nejm.org/doi/full/10.1056/NEJM199912303412707 https://www.nejm.org/doi/full/10.1056/NEJM199912303412707 [3] https://science.sciencemag.org/content/279/5355/1344 https://science.sciencemag.org/content/279/5355/1344
- gavinray 7y agoI have subscribed to the theory that humans are first and foremost a host for bacteria, and that whether that relationship is symbiotic or dysbiotic is largely a factor of how happy your bacteria are. Happy microbiome, happy human. Unhappy microbiome, unhappy human. It seems like more research is published every day that links the microbiome to common disorders and diseases. Do you have any solid resources for someone without an academic background who has an interest in this area?
- nextos 7y agoI'm afraid we still know little about dysbiosis, but most decent findings are in the literature. I'd encourage you to take a look at good recent papers. Once you get used to the jargon, you will start learning a lot. Quick entry point, take a look at references in the introduction section of: https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1.full https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1.... Some other entry points: * Commensals in hunter gatherers: https://advances.sciencemag.org/content/1/3/e1500183.short https://advances.sciencemag.org/content/1/3/e1500183.short * Commensal extinction: https://www.sciencedirect.com/science/article/pii/S0960982215006144 https://www.sciencedirect.com/science/article/pii/S096098221... * Fiber, metabolites and the microbiome: https://www.nature.com/articles/nature12726 https://www.nature.com/articles/nature12726 * Leaky gut and immune responses: https://www.pnas.org/content/116/30/15140 https://www.pnas.org/content/116/30/15140 If you are not affiliated with an academic institution, use Sci-hub to get access to any paper behind a paywall.
- treeman79 7y agoOld Nero-ophthalmologist diagnosed me with Sjogrens because I mentioned my symptoms always improved for several weeks following a round of antibiotics. He has noticed that’s a common trend in Sjogrens patients. He’s never heard of the marshal protocol, just something He had noticed. Can’t find a single doctor that will take the infection theory seriously. a Year later I can’t get a prescription to even try it. My vit D is very low. Modern med just say take supplement. Mars shall protocol says that’s just feeding the infection. Supposedly bacteria loves vit D. Love to find a doctor that doesn’t automatically dismiss me for bringing it up.
- nextos 7y agoAs shown in my references above, Ro60, a potentially causal autoantigen for Lupus and Sjogren's has been linked to commensal bacteria. The study is published in Science Translational Medicine, which is a high end journal, and quite conservative. Plus other studies have reproduced equivalent results. So these doctors should both update their knowledge and also give you the benefit of doubt. There is a growing network of doctors that treat multiple sclerosis with high vitamin D doses. Look for the Coimbra Protocol. They also deal with other autoimmune patients. While their protocol is quite experimental, and it poses some safety concerns, it might be helpful to get in touch with more open minded MDs. Vitamin D influences so many immune pathways. I tend to think most of the effect comes from altering T regulatory / effector ratios. Others argue for regulation of HLA elements. Irrespective of that, low vitamin D is a big risk factor for many autoimmune disorders so I would question that statement.
- treeman79 7y agoHmm. Been avoiding vit D. But really unsure if that’s a good idea or not. Have a bottle of it on counter. Thanks for the information. Will research that protocol.
- atombender 7y agoAlso, psoriasis: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6369634/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6369634/ https://www.ncbi.nlm.nih.gov/pubmed/30222202 https://www.ncbi.nlm.nih.gov/pubmed/30222202 https://www.ncbi.nlm.nih.gov/pubmed/29908580 https://www.ncbi.nlm.nih.gov/pubmed/29908580 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881942/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881942/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6048199/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6048199/ etc.
- Itsdijital 7y agoI went on a soylent-like diet a few years ago and my psoriasis completely went away for the first time ever. I also felt better than ever. Eventually I went back to just eating regular food and within a month it was coming back along with not feeling as great. I have still never been able to nail it down, and my dermatologist is pretty dismissive of it.
- atombender 7y agoYour dermatologist doesn't know any better than you in this case, though I think he's wrong to be dismissive. This stuff about the gut-skin axis has only been coming out the last 2-3 years, although there are a few lone researchers who have been thinking this for decades. For myself, I experienced roughly 80% reduction in symptoms after switching to a strict vegetarian diet two years ago, and it's stayed that way.
- rurp 7y agoYou might want to look into trying an elimination diet. There are quite a few resources online for this and gist of it is that you cut out a whole bunch of food types that have been known to cause issues with some people. After a few weeks of that you add back in a single group of food every few days and check if any symptoms return. Some people have had luck using this method to find issues that doctor visits weren't able to surface.
- ubertoop 7y agoPosts like this one are exactly why I keep coming back day after day to this forum. Thank you for this amazing informational share. I've long wondered if infections are behind many of the unexplained mid and late life disorders. It's exciting to see that it's finally being recognized as a credible explanation in the literature. As someone with a family member suffering from autoimmune, I'm hopeful that this trend will continue and result in antigen mediation therapies that can help. Worth mentioning that the family member I am thinking of developed these symptoms within a year after getting a bad stomach/GI infection.
- nextos 7y agoThanks for your kind reply. Just to clarify, it's both infections OR dysbiosis (your own commensal bacteria, fungi and virus going out of control). The infection + molecular mimicry theory of autoimmunity was already quite well established in the 80s, but commensal dysbiosis + molecular mimicry is only starting to emerge now, and it's likely to be even more important. See section 1 (introduction) of this paper for a whole overview: https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1.full https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1....