Abstract – Amyotrophic Lateral Sclerosis Protocol according to Dr. Retzek

Dr. Retzek’s ALS protocol is based on the experiences of Dr. Herman Schmid and Dr. Nadir Akinci, who achieved remarkable stabilization effects in Amyotrophic Lateral Sclerosis (ALS) through the use of corticosteroids. The aim of the protocol is to slow the progression of the disease and improve the quality of life of those affected by the targeted suppression of neuroinflammatory processes.

The core component of the approach is the controlled administration of low-dose dexamethasone, accompanied by supportive measures such as testosterone injections, immune modulation through Imurek and the intake of orthomolecular nutritional supplements (e.g. magnesium, vitamin D, Q10 and CBD).

The combination of these therapies aims to inhibit inflammatory processes, stabilize muscle strength and slow neurological deterioration.

the reason I publish now my protocol freely is the increasing number of affected patients  worldwide and my in about 2 years upcoming retirement.

Protocol for Amyotrophic Lateral Sclerosis

translated and compiled by Dr. Retzek – as of March 2021-03-21

Contents

• ALS disease by Dr. Herman Schmid 1-3
• ALS disease by Dr. Nadir Akinci 4-7
• Treatment protocol by Dr. Retzek according to Schmid and Akinci 8-14

ALS course by the doctor Dr. Herman E. Schmid

http://myalsremissionstory.blogspot.com/

Ernie, the son of Dr. Herman E. Schmid gives the following introduction

The following article was found in drafts in my father’s files and unpublished on September 21, 2013. It should have been published many months ago when we submitted Dad’s story to ALSUnTangled

Dr. Herman Schmid’s report is introduced with the following cover letter

Because I know my story is unique, I am sending all the details to ALSUntangled. Since the story spans a 50-year period, there is no recorded evidence.

I am a physician who has had a very active practice since 1972, and 12 years prior to that I was an associate professor of physiology at Wake Forest University School of Medicine.

In fact, I diagnosed myself, but only after careful consideration. My treatment described below is consistent and fact-based and has kept all symptoms of my disease at bay.

In reviewing the research studies on ALS, I found no study using fluorinated steroids in high doses as I found, used and described.

It would be very important to use these steroids especially in the early stages of ALS, because I am convinced that it helped me. I had previously sent letters with my detailed story to over 40 medical centers and received no response[1].

I believe it is responsible to tell my story and to consider this steroid option for everyone.

Respectfully,

Dr. Herman E. Schmid

Published on September 21, 2013 by Ernie Schmid

Dr. Herman E. Schmid: My Story

I have been self-medicating for many years with large doses of anti-inflammatory drugs that are prescription drugs but usually come from Neuneurologists, in remission from Amyotrophic Lateral Sclerosis.

Although the muscle fibrillation (fasciculations) has remained at a reduced intensity, the muscle weakness and other symptoms have not progressed.

In brief, at age 32, my left index finger began to twitch repeatedly and over the next month, the twitching spread to my left shoulder and left leg and then to my right side.

The coarse contractions of my left finger stopped, but the rapid twitching continued every few seconds throughout all parts of my body.

I consulted a neurologist, but during a brief examination, I could not detect any of the fine twitching movements.

He did not spend any time observing the fine twitching and explained that if it was Amyotrophic Lateral Sclerosis, there was no cure available and my life expectancy was 3 to 5 years.

I had then searched the medical literature and found that glucosteroids had been tried for ALS with some improvement in some patients.

The neurologist, however, told me that steroids were of limited value in ALS and that the side effects of the drug could worsen the condition and advised against the use of these drugs.

Over the next 8 months, the muscle twitches increased in both frequency and intensity, and increasingly affected larger muscles.

In addition, my speech became impaired and some words were difficult to pronounce, along with increased salivation. It was difficult to sleep because everything was constantly twitching.

I had just started my scientific career in teaching and research at the local medical college and felt that my research would end if these symptoms became known to my coworkers. So I did not return to the neurologist but decided to function as normally as possible for as long as possible without making my condition public. My research became more difficult as the muscle weakness progressed and fine hand movements became unstable.

In desperation, and having a large supply of a new fluorinated corticosteroid available in my research lab, I decided to self-medicate with maximum doses of this more powerful steroid (Aristocort) in the hope of improvement.

To my surprise, the general twitching was suppressed to about 50% within the first week. I felt that I may have slowed the progression of the disease and thereby increased my life expectancy. I continued to take the drug and similar drugs for the next ten years.

At this point I left research and stopped taking the steroid. During the entire time I was taking cortisone, the muscle weakness and speech slowly improved despite the continued fine twitching.

Because I had been in research, I knew that my self-treatment with high doses of corticosteroids was meaningless to the medical community unless a research study was conducted on a large group of ALS patients.

I have therefore contacted local neurologists and about forty ALS research centers by mail in the hope that they might be interested in developing a scientific study.

Unfortunately, I have received no responses and, to my knowledge, no report of a scientific study has been produced.

Therefore, with the help of my son, I am writing this blog (ALSuntangled) in the hope that patients with ALS will be willing to request a trial period of steroid treatment from their doctor.

Unfortunately, the fluorinated corticosteroid that I treated myself with is no longer available in tablet form, but another similar agent (dexamethasone) is available and is used by neurologists in high doses for many conditions such as multiple sclerosis, brain tumors, temporal arteritis and other inflammatory conditions.

Published on January 19, 2013 by Ernie Schmid

 [1] Ignorance and indifference towards the fate of those affected can now be seen in light of the corona crisis and the political wrangling over hydroxychloroquine. It is not the doctors – but the system in the background – that has no interest in the patients!

Nadir Akinci “My ALS story”

translated by Dr. Retzek

Dr. Nadir Akinci, BSci, MSci, PhD – Scientist at the Massachusetts Institute of Technology (MIT / Boston) for Computer Graphics / Simulation / Animation

Dr. Akinci conducted research at the Albert Ludwig University of Freiburg im Breisgau from 2010 to 2014sgau

• https://nadirakinci.com/
• https://nadirakinci.com/my-als-story/

Nadir: My Story

I was diagnosed with Amyotrophic Lateral Sclerosis in August 2013 while living in Germany.

My symptoms started with weakness of the left foot in February 2013. Because of the terribly slow health care system in Germany, my diagnosis was made quite late. I was initially diagnosed as “probable ALS”.

Interested readers can download my German medical report at the bottom of this page[1]

This diagnosis changed my life, just as it will change the life of every person, as a person with ALS usually dies within 2-3 years of being diagnosed.

When I was diagnosed, I was 28 years old, had a 6 month old daughter, and so much to leave behind. At that point, I stopped doing everything I had been doing and devoted all my attention to figuring out how to treat this normally untreatable condition.

Shortly after learning about the Deanne Protocol[2], I stuck with it for two years. Unfortunately, the disease just continued to progress under that protocol, even though I followed it to the letter. In addition to the Deanne Protocol, I have tried all sorts of other protocols, chelates, supplements, and vitamins, none of which have helped either[3].

My MGH ALS Clinic medical report at the bottom of this page has a good summary of the treatments I have tried so far[4].

After reading the posts on myalsremissionstory.blogspot.com (attached below) and reading many publications showing the major role of inflammation in ALS progression, I used dexamethasone for two months in the summer of 2014.

It significantly reduced my spasticity[5], which had been my main symptom. I could now move my muscles much more easily and climb up/down stairs faster. Life was much easier compared to previous months. I could also speak without difficulty, which I noticed in the first few days of my dexamethasone use.

I was given 4 mg of dexamethasone. After I started reducing the dosage to find a safer therapeutic dose, I felt like my ALS symptoms were returning.

In particular, spasticity, hyperreflexia, fasiculations and hypertension returned shortly.

After returning to the starting dose of Dexa (4mg) my symptoms were significantly reduced again.

I find it very strange that although inflammation plays such a large role in ALS, supported by many scientific publications, there is still no current study testing corticosteroids in Amyotrophic Lateral Sclerosis (at least none that I could find)[6].

The only study I could find was from the 1960s that tested corticosteroids in a very small group for other neurodegenerative diseases including ALS, and the study had mixed results.

If you try corticosteroids, you should see the improvements in the first week[7]. If you don’t, the protocol probably won’t work for you.

Actually, and surprisingly, it worked for most people who have tried it so far. My neurologist followed my request and prescribed me the medication, but then suddenly he wanted me to stop using the cortisone because he was worried about the side effects.

When I stopped the medication, I had another deterioration, then I started it again and felt much better.

My advice: if you try corticosteroids for your condition, you should do so under the medical supervision of your regular doctor and not your neurologist, as they are mostly biased against giving corticosteroids as a trial for ALS.

An ALS patient should also have their PVO2 levels monitored regularly. PVO2 (venous blood oxygen pressure) is usually measured in a hospital setting as a blood gas analysis.

A healthy person should have a reading around 30. Mine was 64. High PVO2 simply means your cells are not able to use enough oxygen, which is critical for ATP production.ution.

You can lower this level by taking daily oxygen therapy or some medications that push oxygen into the cells[8].

Another thing that is usually ignored by neurologists is the blood level ANA (anti-nuclear antibody), which is usually positive in ALS patients when autoimmunity is present[9].

What confuses neurologists is that these antibodies are significantly lower compared to rheumatoid arthritis or systemic lupus, which is to be expected since the number of motor neurons is significantly lower compared to the other inflamed cells in the other autoimmune diseases.

But this is again, unfortunately, beyond the understanding or comprehension of neurologists[10]. However, the positive ANA proves that an autoimmune disease is present. It is a clear biomarker that your motor neurons are slowly being attacked and killed.

Like many of you, I have used all kinds of supplements. None, however, had a positive effect on me until I started using corticosteroids again.

Side effects

Unfortunately, long-term use of corticosteroids can lead to cortisone-induced muscle atrophy, which is not caused by nerve destruction. This is because your liver is unable to synthesize enough protein under cortisone.

As suggested to me by my friend Paul Aiken, who also tested this on mice with corticosteroids, by increasing testosterone levels, such atrophies are significantly attenuated.

In Turkey, I then received testosterone injections[11].

My last creatine kinase blood count was 69 U/L, which is even lower than most healthy people.

In the past, it was between 250-800. This now finally means: no more muscle loss due to ALS[12].

So there is the obvious fact. Corticosteroids definitely work in a currently unknown percentage of ALS patients. Unknown because the ignorant neurologists have ignored this since the invention of corticosteroids (year 1944)[13].

I expect that in the unknown future these cases will be called autoimmune or inflammatory ALS.

Given this ignorance, I expect it will be several more decades before this is recognized.

My wife used 40 mg of prednisone for her nickel allergy. I used it for tinnitus many years ago. Why are people so afraid to try it at the onset of the symptom with a death sentence called ALS? While waiting for an FDA approved treatment, people are dying or losing loved ones to this treatable disease that I cannot accept. My recommendation to any newly diagnosed ALS patient is to stop the neuroinflammation with either my protocol or another appropriate immunosuppression protocol, regardless of the cost.

I waited 1 year for this and unfortunately lost so much functionality just because I waited.

[1] Dr. Retzek: I didn’t find the German KH report

[2] https://pubmed.ncbi.nlm.nih.gov/25061944/

[3] Dr. Retzek: I can confirm that we have only experienced improvements with NICO dental focus operations and biophoton realignment according to Renzo Celani. Neither detox nor infection treatments, parasite cures or homeopathy or blood washing (inupheresis) have brought about significant changes in this disease – in around 30 patients that I was also able to treat as a holistic doctor.

[4] not found

[5] is also often reduced by CBD

[6] like Dr. Hermann E Schmid, his successful treatment did not interest anyone, he wrote to 40 neurological institutions and pointed it out and urged a study. In fact, nobody is interested in simple or inexpensive solutions, since only through the development of new, high-priced drugs can the correspondingly expensive studies and investigations be financed by companies, since the state is unfortunately completely absent as a sponsor of such studies

[7] Dr. Retzek: I can confirm that, I experienced that with the first patients too.[8] Dr. Retzek: I don’t know of any such medication or laboratory where we could carry out this test

[9] Dr. Retzek: ACE can also be elevated (according to Dr. Elke Schäfer) and a new marker is the phosphorylated neurofilament NFH – in > 90% of ALS patients it is already significantly elevated in the serum (also in the cerebrospinal fluid) in the early phase.

[10] Dr. Retzek: Nadir seems to have had bad experiences with his neurologists, I would not generalize that in any way

[11] we inject NEBIDO as a long-term testosterone booster

[12] Dr. Retzek: I can confirm that for all ALS patients so far, the CK value becomes low-normal even with cortisone, not just with testosterone. Testosterone, on the other hand, gives a further boost in the direction of “reducing CK”

[13] Dr.Retzek: Nadir seems to be very angry with his neurologists, this intense form of criticism is not justified, since our “model” of ALS is a prion disease of SOD-1 with intracellular peroxide accumulation – it makes no sense to use cortisone here and you do NOT want to weaken such a fragile patient further with a therapy that potentially has side effects!