I was diagnosed with ALS in August 2013 while I was living in Germany. My symptoms actually started with left foot drop around February same year. Thanks to the horribly slow healthcare system in Germany, my diagnosis has been given quite late. I was initially diagnosed as probably ALS. Interested reader can download my German medical report from the bottom of this page.
That diagnosis changed my life, as it can change any person’s life, as a person with ALS usually dies within 2-3 years after diagnosis. When I was diagnosed, I was 28, had a 6 months old daughter, and so much to leave behind. At that point I stopped doing everything I have been doing and gave my whole attention to find out how I could treat this normally untreatable condition. Shortly after I found about the Deanne Protocol, sticked to it for two years. Unfortunately, my progression continued with the protocol, although I followed it to the point. I tried all sorts of other protocols, chelations, supplements and vitamins besides the Deanne protocol, which weren’t helping either. Actually my medical report from MGH ALS clinic attached at the bottom of this page has a good summary about the treatments I have tried so far.
After reading the posts at myalsremissionstory.blogspot.com and reading many publications showing the major role of inflammation on ALS progression, I used Dexamethasone for two months in the summer of 2014. My spasticity was significantly reduced, which had been my most prominent symptom. I could move my muscles much easier, climb up/down stairs faster. Life was much easier when compared to the previous months. I could also talk without any difficulty, which i have noticed in the first few days of my Dexamethasone usage. I was getting 4 mg Dexamethasone. After I started tapering the dosage to find a safer therapeutic dose, I felt that my ALS symptoms started to return again. Most notably, spasticity, hyperreflexia, fasicculations, hypertonia returned back shortly. After returning to the start dose, my symptoms were significantly reduced again. I find it very awkward that, although inflammation plays such a major role in ALS, supported by many scientific publications, there is no any recent study that test corticosteroids for ALS (at least I couldn’t find any). The only study I could find was from 60s, which tested corticosteroids in a very small group for other neurodegenerative conditions including ALS, and the study had mixed results.
If you try corticosteroids, you should see the improvements in the first week, if you don’t then they will probably not going to work. Surprisingly, it worked for most of the people I know who tried it so far. My neurologist went along with my request, but then he wanted me stop using them as he worried about the side effects, then I got worse, then I started again and felt much better. If you try corticosteroids for your condition, you should do it under the medical supervision of your healthcare provider, not your neurologist, as they are mostly prejudiced to try corticosteroids for ALS.
An ALS patient should also get his PVO2 levels monitored regularly. PVO2 (venous blood oxygen pressure) PVO2 is usually measured in a hospital environment. A healthy person should have a value like 30. Mine came 64. High PVO2 simply means your cells cannot utilize enough oxygen, which is vital for ATP production. You can lower this value by taking oxygen therapy daily, or some drugs, which forces oxygen into cells. Another thing that is typically ignored by neurologists is your ANA (anti- nuclear antibodies), which usually comes positive for ALS patients when there is autoimmunity involved. What confuses neurologists in the titer that those antibodies are found, which is usually much lower when compared to rheumatoid arthritis or systemic lupus, which should be expected as the number of motor neurons is always much less in numbers compared to other potentially inflammable nuclei (e.g. Total number of joint nuclei). But this is unfortunately again beyond neurologists understanding or comprehension, and positive ANA remain as a clear biomarker of your motor neurons are slowly being attacked and killed. As many of you do, I used all sorts of supplements. However, none of those together had any positive effect on me until I started corticosteroids again.
Unfortunately, while saving your neurons, long term use of corticosteroids may cause (non-neuronal death caused) muscle atrophy, if your liver is not able to synthesize enough protein. As was suggested to me by my friend Paul Aiken, which was also tested on mice on corticosteroids, boosting testosterone levels significantly attenuates such atrophies. I started getting testosterone injections in Turkey, My latest Creatine Kinase bloodwork came 69 U/L, which is even lower than most healthy people’s. In the past it was between 250-800. It means, no more muscle breakdown.
So, there is the obvious fact. Corticosteroids definitely work for an unknown percentage of ALS patients, thanks to the ignorant neurologists since the invention of corticosteroids (year 1944). I claim that those cases will be called autoimmune or inflammatory ALS in an unknown future. With that amount of ignorance, I assume it will take several more decades to realize that. My wife has used 40 mg prednisone for her nickel allergy. I have used it for tinnitus many years ago. Why do people are so afraid to try it on a death sentence named ALS at the symptom onset? While waiting for an official FDA approved treatment, people are dying or loosing their loved ones because of this treatable condition, which I find impossible to accept. My recommendation to any newly diagnosed ALS patient is to stop neuroinflammation either using my protocol, or any other appropriate immunesuppression protocol, whatever the cost is. I waited 1 year for that and unfortunately lost so much functionality just because of waiting.