00000Right. ALS. Nerve degeneration may be genetic (0/0 of cases) but predominantly unknown. Autoimmune, but I tend to keep looking because I don't think autoimmune happens in a vacuum.  For other readers, I'm attaching the current status of treatments for ALS to get a sense of what you deal with and other options. But I think I may have something helpful.  Turns out your colleagues in Seattle already came across the same idea, but I don't think you're using it yet. It involves Clostridium difficile causing a portion of the ALS cases. I came across this idea when I was researching possible ALS support and I found a small study on stool analysis of ALS patients. About 0/0 had significant Clostridium overgrowth, but I can't find the study on medline listed under Clostridium. I assume the Seattle neurologists must have found the same study.  So here's the thought: if a portion of ALS patients (peripheral onset?) are genetically susceptible to the relatively mild Clostridium difficile toxins then a stool analysis would give a possible treatment option: systemic antibiotics and the addition of Sacchromyces boulardii. Previous trials with antibiotics and ALS haven't focused on the possibility of an antibiotic resistant organism causing the problem. I think the addition of S. boulardii is essential to provide competition to C. difficile regrowth.  So, trash away. But maybe have a discussion with Seattle about why they have the same crazy, quacky idea I do. If you don't want to put ALS patients through the systemic antibiotics, what about a simple trial of S. boulardii for patients? Keep patients on oral feeding and add S. boulardii with every meal. It has a good safety profile.  I've got some other ideas, but I want to get this one out to you quickly. Please at least talk to Seattle about it.  Department of Neurology, School of Medicine, University of Washington, Seattle, Washington, USA. wl@u.washington.edu 