Hi Ben, 'steroids' is a very broad term, which steroids exactly? Ananbolic or cortisol?
I am currently trialling anabolics with positive effect.

Merc

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If it is done in secret, it is done in vain.

New information... Perhaps, it will not amount to anything useful, but it is worth considering nevertheless.
After the first infusion cylce, my brother felt better.He thought he was experiencing some movement in the fingers and better gripping strength.
Something happened right after the second cycle. He had very harsh side effects, and then, within a few days, his progression rate increased significantly. By the end of the 4th cycle, he lost both arms and both legs, some speech and breathing ability... In contrast, during the first several months since the onset, he had only lost partial function of the right hand.
He is now experiencing kidney related complications.Some recent studies show that anabolic steroids can cause kidney damage ("kidney disease, marked by excessive loss of protein in the urine, along with severe reduction in kidney function"). He revealed to us, just now, that he was on anabolic steroids. I remember after the 2nd cycle, when the problems started, he was happy about the muscle gain on his chest.Hence, steroid use and the second cycle coincide.
I suspect steroid use is responsible for his negative experience. It might be that chlorite reaction with steroids leads to adverse effects. Or, steroids damage certain organs and fuctions thus preventing chlorite from doing its repair work. Another possibility: ababolic steroids increase the sodium retention in the body...
I will continue to look into this, though I think there are others on this forum who are much better qualified to think about the relationship between steroids (anabolic or not) and chlorite.

Thanks for this Ben

Very difficult to comment constructively without knowing exactly what steroids he was taking and at what dose? All anabolic steroids have an androgenic component, some more than others and there are ways to mitigate the androgenic component in, for example, in a typical bodybuilding stack. A stack comprises a number of different anabolics being combined over a set time period. Anti estrogens are typically used to mitigate potentially unwanted androgenic effects such as gynecomastia or ‘’bitch tits’ as it is more commonly called.

Anabolics without resistance training will do nothing. You can’t just stuff yourself with anabolics and expect muscle gain; it’s not going to happen. The fact that this PALS mentioned muscle gain on his chest? I can only assume that this perceived muscle gain was in fact gynecomastia as the PALS was obviously unable to exercise. One would not normally record the side affect of gynecomastia with low or infrequent steroid use, so I would speculate here that significant steroid use had occurred.

Would this have caused death thought? Sure, abuse of anabolics has caused death in the past even in healthy individuals but there may have been other underlying problems exacerbating the situation in these individuals and often doses in excess of 30 times the recommended therapeutic doses are being taken.

Again, it is really difficult for me to comment objectively unless I know what was administered in this case. Liver toxicity is far more prevalent and of greater concern than kidney damage particularly with oral compounds as anabolics are metabolized by the liver. This is one of the reasons why I prefer injectables.

I would very much doubt that there would be any drug interaction between NP001 and anabolics if as we are led to believe that active ingredient of the drug is sodium chlorite. All anabolics are really just synthetic derivatives of testosterone at the end of the day.

I currently take 100mg testosterone injectable a week, down for 200 mg per week. At 200mg I was gaining about 1kg of bodyweight a week, muscle mass plus water, don’t know in what ratio exactly.
Tried testosterone for 5 weeks then took a two week break and switched to nandrolone decaonoate. Nandrolone has a similar profile to Anavar (oxandrolone) which is often indicated in ALS as a treatment but this drug did nothing for me and I discontinued it after 3 weeks and went back on the testosterone at 100mg per week dosage. Nandrolone was taken at 250mg per week injectable.
In the two week break I lost 2kgs of body weight and on nandrolone I maintained weight. Anavar is not available in my country.

I take both anabolics and sodium chlorite although I am becoming somewhat sceptical abouth the sodium chlorite protocol.

Cheers

Merc

Pers - do you have any further information concerning results? When, or maybe new graphs?

Thanks for update, P.

This whole lawsuit reminds me of a family that has a toy that has been gathering dust on a shelf in the garage for years. Finally one day one of the kids starts playing with it, and sure enough, another decides all of a sudden to fuss over it.

Of course this case, we have lives at stake and no mother to settle a childish spat quickly and sensibly.

I am hopeful about this ruling. Even though the Court accepted the timing under Swiss law and noted the indeterminant time for assignment purposes, McGrath brought up a point under Swiss law that the indeterminant length is illegal as damaging to economic freedom. Although the Court refused to consider that argument for this particular ruling it did give leave to consider it in future pleadings which sets the stage for dismissal of the 2nd claim.

The 3rd and 4th claims were dismissed with prejudice. Although Nuvo has leave to amend the 3rd, that claim was pretty well gutted.

I haven't looked but does anyone know what happened to the 1st claim?

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= Le meilleur vin, avec les meilleurs amis. =

Nope. Nuvo dropped the suit last week.

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= Le meilleur vin, avec les meilleurs amis. =

Someone involved in the litigation.

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Hi OG,

My wife died in March 2012 after 2 years of als. Symptoms appeared in January 2010. In October 2009 she woke with an inflamed right hand which had curled into a claw and which she could not use. She felt that maybe she had slept on it and it would sort itself out. By early evening she had no change but the inflamation was starting to show in her arm. This was Saturday and uk GPs don't do weekends so we went to a local out of hours service. The doctor on duty had worked in Australia and reckoned the problem came from an infected bug bite. The bite had been one sustained the previous July on a sailing holiday in Greece. He prescribed an antibiotic and the inflamation subsided and normal function came back within a week. We thought no more about it. I don't know if this is a parallel for your daughter. Irene presumably had als before symptoms showed so could well have been there in October. She had complained of difficulty opening car doors when seated and also her handwriting deteriorated somewhat in 2009.
We did explore Lymes disease with her GP who assured us she had been tested and showed no signs. I did offer to pay for ceftriaxone which I think is the standard treatment for lymes disease but he was unwilling to prescribed something for which there was no evidential need. Reading about lymes disease on specialist sites they say antibodies may not necessarily show up in testing. It could well have been that all Irene's problems stemmed from the bite in July. It could be that what evolves is simply als with a different cause. The lyme disease sites say that if the disease is allowed to advance too far it becomes extremely difficult to treat.
In answer to your question I would say 1. I think it unlikely that pals have any special attraction for bugs unless you think there state is akin to rotting meat. 2. I see nothing to lose apart from the cost of the extra testing. However as the symptoms seem to have preceeded the bite in your daughters case I cannot see that it can be the source of her illness but if lymes disease is there then it won't be doing anything good for her health and would be best treated.

John

The body contains several barriers, for example the skin, the mucus mebranes and the blood brain barrier (BBB). Although they are different they still have basic similarities and that is why a problem in one of the more visible ones, say the skin, may indicate a problem in another more invisible barrier, for example the BBB.

This may for example be illustrated by dissiminated late stages of (Lyme) borreliosis caused by Borrelia afzelii, where a discoloration and atrophy of the skin of a limb, called acrodermatitis chronica atrophicans (ACA), is indicative of an ongoing peripheral neuropathy (i.e. a compromized barrier in the peripheral nervous system (PNS) caused by chronic spirochetosis). Similar reflections of synchronized barrier breaches may also be seen in tertiary stages of syphilis with gummas and neurosyphilitic dementia. The molecular similarities and patological links between these different barriers may also be illustrated by an autoimmune disorder like coeliac disease, where the immunological reaction that is causing the gastointestinal problems also may be manifested as a (facial) rash (called dermatitis herpetiformis) and also may cause various neurological symptoms. In the context of this forum it may be noted that the scientific literature minimally contains three cases where coeliac disease mimics ALS, sometimes quite credibly so.

With regards to gastric ulcers it may be noted that this particular ailment is significantly linked to the development of Parkinson's disease. Plus for example that the ulcer causing Helicobacter pylori (and borrelia sp.) are a bit special since they have steryl-glucosides in their membranes. In the context of this forum it may of course be noted that steryl-glycosides like BSSG have been implicated as possible etiologic agents behind the Guamanian ALS Parkinsons Dementia Complex of diseases..

However, In the context of this particular post and to illustrate the complexity of the problem we are dealing with, it may also be noted that steryl-glycosides (including BSSG) also are reported to be effective for treating/preventing peptic ulcers.

It furthermore deserves to be noted that there is a more recent alternative hypotesis for the development of Parkinson's which (also) is focussing on the gut and the enteric nervous system (ENS), with a prion twist to it, see e.g. this paper (but there are many more).

Those who are so inclined may even be interested to have a look at one of Judith Miklossy's latest attempts to provide convincing arguments for that a subset of Alzheimer's cases may be a spirochetosis.

I am still not convinced that bacteria or viruses are the direct causes, but I know from familial ALS experiences that gastrointestinal health minimally is linked to the relative succeptibility for percipitating with FALS. I.e. family members with frank peptic ulcers are the ones who percipitate with disease at a young age, while those with more benign GI problems get it later and the relative difference may be up to 20 years - for siblings.

That is why I am inclined to recommend that everyone that is dignosed with SALS (and perhaps especially those with other barrier breaches possibly caused by bacterial pathogens) should be empirically treated with ceftriaxone, say 14 days, just in case.

I don't think that it is a cure, but some may hopfully respond and deteriorate more slowly.

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Don't just ask what scientists can do to speed up the solution for ALS or when they will do it, instead ask yourself what you can do right now to solve ALS asap.