- Due to blogger's diarrhea of the keyboard, I thought it best to split this blog into two parts. A recap of Part 1 includes: a confession of my time warp regarding ALS treatments; the present day voluminous research and clinical trials going on for ALS; the knowledge that a viable treatment still does not exist, yet there is hope; and some amazing people with ALS who simply blow my mind.
At the end of Part 1, I wondered what I would do today if I or a member of my family was diagnosed with ALS. Given the present research available right now, and the knowledge that no dietary regime or nutrient supplementation program has yet been definitively declared to be effective, and no treatment (except for the useless drug Ritulek) has also not been definitively declared effective, I would:
- Keep up to date with the ALS TDI and the Scoop It - ALS Lou Gehrig's disease websites
- Enroll and contribute information about myself to the Patients Like Me: ALS website, and read what has helped and what has not helped others
- Enroll in a clinical trial only if: 1) I met the qualifications for it, 2) I was within reasonable traveling distance to the research center, and 3) I believed in the treatment being used, even if I received a placebo. (There are a few substances being used in clinical trials around the world that make sense to me. There are many others that I believe will end up being duds, along with the many other treatments that have already been laid to rest. I would not participate in a clinical trial that made no sense to me).
- Diet. As with any condition, I would ensure that any food I consumed did not add to the possible inflammatory body burden of my nervous system. I would have food intolerances and food allergies determined so that these foods were not part of my diet. I would eat a balanced diet high in MCTs (medium chain triglycerides) that consisted of whole grains (likely gluten-free), lots of fresh fruits and vegetables, wild game, fish, lamb (including the fat), and lots and lots of coconut oil. Dairy products often prove to be food intolerances or allergies in many people and may need to be avoided. I would completely avoid all food additives, preservatives and colourings, so too for refined sugar and artificial sweeteners. At the very least, even if this diet did not improve or slow the progression of my symptoms, my energy would be much better.
- Supplements. The ones I would be confident about taking are: Acetyl-L-Carnitine, Taurine, Magnesium Glycinate or Magnesium Taurate, DHA, and Vitamin B complex.
- Self-administer regular Methylcobalmin injections
- Rule out any possible infectious cause of the symptoms in the rare possibility that the ALS diagnosis is inaccurate
- Correct any hormone deficiencies with appropriate replacement therapy (unless contraindicated)
- Pro-actively foster an open mind
- Keep my eye on the NP001 clinic trials and the off-label WF10 treatments
I haven't listed dosages because any cocktail that I would try would be a crap-shoot. Self experimentation would always reign supreme when it would come to multiple supplementation regimes, because there are no guiding scientific trials to suggest otherwise and no strong evidence of any case reports to date showing long-term efficacy, that I am aware of. There is however, a scientific understanding of how various nutrients affect the body and how they affect various pathophysiological states.
Scientists have not yet pinpointed the cause of ALS, and that is why it has been so difficult to come up with a viable treatment plan. Most clinical trials are based on various hypotheses regarding the cause. Present hypotheses include: a genetic defect of superoxide dismutase (SOD1) in the few that have the familial version, glutamate excito-toxicity (impaired transporters), oxidative stress, neurofilament dysfunction, altered calcium homeostasis, impaired neurotrophic factors, mitochondrial dysfunction, impaired cellular energy production, increased motor neuron apoptosis, increased cytokine activity, and microglial (nervous system macrophage) inflammation.
In this disease, there seems to be a weird oxidation dance going on between the necessity for ROS (reactive oxygen species) and the damage that they cause . There is no question that oxidative damage is part and parcel of ALS. But is the oxidative damage the cause of the neurodegenerative cascade, or is it an adaptive response? Oxidative stress is not all "bad", because oxidants are not only vital for life, some activate proteins that protect cells. On the other hand, anti-oxidants are not all "good" because they have the potential for squelching the body's necessary adaptive response to oxidative damage. ALS seems to be a high-wire balancing act, where the body is desperately trying to adjust between too much and too little oxidation, and throwing either process off its adaptive response track seems to lead to further neurodegenerative consequences.
The use of high doses of multiple antioxidants in ALS does not make any sense to me. While I have listed a few supplements that are antioxidants (Taurine, ALCAR), my rationale for their use would not be because of their antioxidant properties, but because they function in other capacities that assist with neurological functioning.
How does one address this weird dance of oxidation, while waiting for the compassionate drug use of NP001 to become available, or waiting for scientists to figure out why zebrafish can regrow their motor neurons and we humans can't?
Doing nothing is one option. Doing something is another. In the end, the results may be the same regardless of what is chosen, but then again, maybe not.
There are a few brave souls who have been experimenting with a substance they believe to be similar to NP001. It is called Oral Sodium Chlorite (OSC) and is typically used as a bleach cleaning agent. OSC is a strong oxidant, and the theory behind its use is that this substance modulates macrophages (specialized white blood cells) and therefore decreases neuro-inflammation. The compilation of data regarding this on-line experiment at present is sporadic and anecdotal. However, in the world of ALS, even the most rigid-minded science-based neurologist would lack a heart, if he or she did not at the very least, keep an open mind regarding anecdotal evidence and treatments that could possibly be helping his patient.
Would I try OSC if I had ALS? I don't know. I suppose it would depend on what stage of the disease I was at. I would however, give other things that have well-known long-term safety track records a try first, before taking a substance in concentrations where there is little known data regarding its safety use.
Personally, I would try the following regime for myself: a diet high in MCTs (medium chain triglycerides) and DHA (docosahexaenoic acid); Reduced Glutathione; the few supplements I have listed above; and Ozone therapy (taken 4 h away from dietary fats and DHA).
The reason I was so fascinated with the OSC on-line experiment, is because there appeared to be interesting similarities between it and ozone. Both are oxidants, both are used as disinfectants for pools, both OSC and ozone increase VEGF (vascular endothelial growth factor), both WF10 (which is similar to OSC) and ozone are extremely effective for healing wounds, and the anecdotes of those who were taking OSC were very similar to what my mom experienced while she was receiving ozone treatments. She had initial improvement in her tongue movement and in her general strength after the first treatment of major autohemotherapy (intravenous reperfused ozone). I just chalked it up to placebo because I didn't believe neurovascular inflammation could improve that quickly, even if it was a small improvement. And like some OSCers, she plateaued out (in her case for 1 1/2 years) with no further improvement and minimal deterioration. When she decided to finally stop because she experienced no further reversal in her symptoms (other than during the initial "honeymoon" period), she deteriorated toward death within 6 months. Was it the ozone that helped my mom to stabilize? Who knows? Is it the OSC that is helping some of those who have improved a little and who have stabilized on it? Who knows? It may or may not be the natural individual progression of the disease state. That is why clinical trials are so important; to definitively determine whether improvement and plateau are related to the therapy in question, or just to natural disease progression.
The mild oxidative effect of ozone is hypothesized to be neuroprotective by the activation of Nrf2 (a protein that encodes for antioxidant enzymes). For those that entertain the possibility that ALS may be due to microvascular ischemic hypoxia, ozone is known to improve cerebral ischemia and is known to be beneficial for those who have had strokes.
The most effective route of ozone administration is via major autohemotherapy, where a specific volume of blood is taken from the patient, mixed with ozone gas, and then re-infused back into the patient. However, major autohemotherapy is a treatment that is quite cumbersome, expensive, and could not be done at home. As well, ozone cannot be delivered via the inhalation route because it is a potent respiratory toxicant. The only appropriate route for DIY self-administration is through rectal insufflation, where ozone gas diffuses into the vasculature of the rectum for about 10 minutes, and eventually crosses the blood brain barrier. The half life of ozone is fairly short at about 40 minutes, so the medicinal effect would only last for just over 3 hours. An ozone generator with medical oxygen and rectal catheters would be necessary for this type of therapy. It's a pretty simple procedure, but a unit unfortunately runs around $2000. It is also my belief that companies that sell these units should loan them out free of charge for compassionate use for people with ALS, should they choose to experiment with this very safe therapy. Side effects are practically non-existent when self-administered correctly.
Glutathione has a very short half-life of about 10 minutes, so the medication would be cleared out of the body in less than 1 hour. The oral form of glutathione is useless. The intravenous form has shown some efficacy in other degenerative neurological conditions. The nebulized form is helpful for those with lung conditions like COPD. However, there is a new mode of administration being tried out with Parkinson's patients that is self-administered via nasal inhalation. In theory, this is exciting because of the proximity of the brain to the nasal cavity and its potential to quickly cross the blood brain barrier in about 10 seconds.
Glutathione is a potent detoxifier of neurotoxins, it improves endothelial dysfunction by improving nitric oxide, and it helps with DNA repair and protein synthesis. There is much data regarding its safety, and side effects are rare. There is very little information as to whether or not glutathione could be helpful in ALS, and its use as a potential neuroprotective agent is based only on theory at present.
Intravenous reduced glutathione is cost-prohibitive running approximately $600-900/month for 3 treatments per week. On the other hand, intranasal reduced glutathione would cost about $40-$55/month. I have no experience with the use of intranasal glutathione, but I would imagine it to be a very simple procedure using a nasal atomizer.
However, reduced glutathione is a potent antioxidant and reducing agent, so mixture with an oxidant would be unwise. I would never recommend that someone try glutathione while experimenting with OSC. The half life of OSC is presumed to be a few days, which would mean that the oxidant would still be in the body just over a week after having stopped it. I can't imagine anything good coming from the combination of those two therapies. One of 3 possibilities would occur: the glutathione would immediately be oxidized and not provide any possible benefit (which would be a waste of money), or the beneficial action of the OSC would be negated, or an adverse reaction could ensue.
On the other hand, ozone has a short half-life as does glutathione. One could very easily spread those two therapies apart in a given day so that they did not interfere with each other, and both of those therapies are known to be safe. When I think about it, it seems almost comical what I would do for myself if I had this disease. A shot of gas up the butt and multiple squirts of liquid up the nose everyday.
If I were in the very, very early stages of ALS, I would probably forgo any oxidant therapy and just do intranasal glutathione 3 - 4 times daily. (However, because I have easy access, I'd more likely self-administer intravenous glutathione).
There are no clinical trials whatsoever to support my ideas. There are however, smatterings of plausible science that may support my rationale for these alternative therapies and my opinions regarding them.
Until men and women in white lab coats with their mice, monkeys and zebrafish come up with something sustainable, all anybody can ever do is guess at what could be most helpful. Even those pharmaceuticals that are now being fast-tracked for compassionate use prior to the completion of Phase III clinical trials, are only best guesses. The proof in the pudding will be found in the years following the Phase III clinical trials.
Every general CAM (complementary alternative medicine) practice contains patients with other diseases who have received every conventional medical treatment possible, and are then told: "there is nothing more we can do for you, it's time to get your things in order". While not every patient given a death sentence by his or her doctor defies that prediction, many, many do. I've seen complete reversals in diseases like wide spread metastatic renal carcinoma, primary lung cancer, severe PVD, etc., etc. These patients are not writing books. They are not on the internet sharing their success stories. They are living their lives quietly, healthfully and gratefully.
I would wonder if there are any PALS living their lives quietly, healthfully, and gratefully who have also defied the odds? That's a question that I would be interested in knowing. If so, is there anything that they would attribute their progression toward good health to?
Here are other questions I also have. Do neurologists report spontaneous remissions in ALS? Are those who have gone into remission or who have experienced long-term plateaus, involved in any studies that compare these people to those whose disease has progressed rapidly? I would think that that kind of data would be invaluable.
And thus, the march goes on. A march toward a future vision of a world where ALS is easily and successfully treatable; a vision of a world where there is less heartbreak and much, much more hope.
It starts with more money to fund research, which starts with much, much more awareness about this disease in the first place.
The dream continues.
Disclaimer: The above information contains my own personal and medical views regarding what I would hypothetically do for myself or a family member if faced with this life threatening disease. In no way is it a recommendation for anyone with ALS to follow. It is always best to seek the advice of your medical care practitioner when undertaking any type of therapy.