My ALS Remission Story

Important Update

I am currently getting an 8 mg Dexamethasone every morning intramuscularly. Getting corticosteroids non-orally surprisingly have far less side effects. Most probably the first pass mechanism is largely skipped through the non-oral route, therefore far less liver related side effects. I would strongly suggest everyone using corticosteroids to combat ALS to try I.M. corticosteroids. Corticosteroids definitely HALTS ALS progression for the majority of ALS patients. If you haven’t tried them for your condition so far, you are either ill informed, or you are a coward, as simple as that, or you don’t have access to corticosteroids, which I find very unlikely. I tried every humanly possible way to raise awareness on the topic, but not surprisingly, all of my attempts are being continuously blocked. Thanks to the NIH, FDA, ALSTDI, ALS Association, ALS Research Institutes, Far too many dumb as fuck PALS, this disease will never see a cure ever.

My Story

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 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 the last two years. Unfortunately, my progression continued with the protocol, although I followed it to the point. I tried all sorts of 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 stories at myalsremissionstory.blogspot.com and nequals2.com and reading many publications showing the major role of inflammation on ALS progression, I used Dexamethasone for two months this summer. 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 4mg 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, supperted 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 everybody 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 unable to observe the positive changes I have been mentioning. Use insulin if your glucose levels rises too much, this will also boost your energy levels.

I would also like to thank to everyone in ALS.net forum for the vast amount of information they have shared there. While in USA, I corrected many things that might be worsening my progression. My 5-hydroxyl vitamin D level was quite low. It is well known that low vitamin D levels causes all kinds of inflammatory and degenerative conditions. I boosted my Vitamin D levels by taking 15000IU D3 supplementation per day, with vitamin K to be safe. Now my 25-hydroxyl Vitamin D levels are near the maximum end. I also take methyl B12 10000mcg per day as it was shown to significantly speed-up axonal generation on rats. As you all know, a recent study shows that all PALS have high free copper levels, which is extremely toxic to motor neurons. Mine even came 10 times the average of other PALS. Mine lowered by 30% in a week using the protocol explained there, by mainly taking zinc supplement. An ALS patient should also get his PVO2 levels monitored regularly. PVO2 (venous blood oxygen pressure) PVO2 is usually measured in a hospital environment. This is very veryImportant and you will have a hard time getting it done. The test is very cheap, your insurance covers it, but it is only done for a specific type of hypoxia called “Histotoxic hypoxia”, which you have as an ALS patient, which is totally ignored by neurologists. The higher, the worse for this measurement. A healthy person should have a value like 30. Mine came 64. High PVO2 simply means your cells cannot utilize oxygen, which is vital for ATP production. You can lower this value by taking hyperbaric oxygen therapy daily, 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 motoneurons 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 motoneurons are slowly being attacked and killed. I also used an anti-fungal medicine called Voriconazole, as it was reported to work on the ALS patients in the patent, which you should read from start to end.:http://www.google.com/patents/WO2008021970A2?cl=en. 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. Before starting corticosteroids, I have been following a strict Paleo diet for the last month, which I am well enough and no longer following now. Compared to my previous corticosteroids attempt between July-September, this time things were much better. All my upper-motor-neuron signs disappeared more rapidly, and twitching is almost totally gone (maybe %1 of what it was before). Currently I am on 3.75 Dexamethasone and 15 mg Prednisolone.

I have also been taking some additional supplements, which are proven to boost the numbers of mitochondria inside cells. Please consider adding them to your daily regimen. These are PQQ 20mg, Niagen 250mg, nicotinamide 2000mg. It currently feels like waking up from a two years old ALS nightmare for me. 4 weeks ago my ALSFR-S score was 32, yesterday when I computed it again, it came 36, which was unbelievable for me. I can hold a pen and write again after almost 9 months. I can move all my limbs faster and have more overall strength.  As we all know, corticosteroids cause muscle atrophy.  As was suggested to me by my friend Paul Aiken, which was also tested on mice on corticosteroids, boosting testosterone levels stops atrophy. I started getting testosterone injections in Turkey, Primobolan Depot (weekly), Sustanon (once in two weeks). I am doing quite well at the moment. Getting stronger every day. I am definitely sure that I stopped my progression with the combination of corticosteroids, testosterone and correcting whatever was going wrong in my body in the last months. My latest Creatine Kinase bloodwork came 69 U/L. 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. Personally, i never heard anyone whose fasciculations didn’t reduce with corticosteroids, which is your worst enemy. What I mean is, the percentage can be huge, much bigger than the sum of mutant ALS cases. My wife used 40 mg prednisone for her nickel allergy last week. I have used it for tinnitus 7 years ago. Why do they so afraid to try it on a death sentence named ALS at the symptom onset? Ii believe that some big pharma already knows corticosteroids stop ALS progression for a majority of cases, but they somehow couldn’t invent a billion dollar single target drug for ALS, which will never gonna happen when I look at the problem as an engineer, since a person with ALS has many things going wrong in his/her body simultaneously. While they are waiting, people are dying or loosing their loved ones because of this treatable condition, which I find impossible to forgive.

My recommendation to any newly diagnosed ALS patient is:

1- Stop neuroinflammation whatever the cost is. I waited 1 year for that and unfortunately lost so much functionality just because of waiting.

2- Then start correcting whatever is wrong in your body.

3- Supplement yourself with correct stuff to speed up your recovery.

4- Slowly taper your corticosteroids, be very slow, you don’t want your ALS symptoms to return while tapering. If you ALS symptoms return, restart corticosteroids.

My hypothesis about how ALS happens

Like other stubborn but more simpler and less fatal inflammatory conditions, I personally believe that ALS is a more complex inflammatory condition of motoneurons, where the inflammation starts at the neuromuscular junction, travels through axons to lower motor neurons of your spine and again through axons to your motor cortex upper motor neurons. When it reaches upper motor neurons, the inflammation naturally travels from motor neuron to the neighboring motor neuron, and then again follows downwards to lower motor neurons and neuromuscular junction. The inflammation itself is triggered by your T-cells. This is why corticosteroids help, as they suppress your T-cell production. The complexity of T-cells unfortunately make them weak, make them easy to confuse your own cells with pathogens. From my perspective, my hypothesis also explains why people into sports get ALS more frequently than other people. as people into sports stress their neuromuscular junctions more frequently, and the resultant oxidative stess causes neuromuscular inflammation at some unlucky instant.

Please feel free to leave a comment if the described protocol also works for you.