Rank: Advanced Member Groups: Member
Joined: 8/14/2007
Posts: 1,540
Location: El Paso, TX USA
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Just bumping Aketri's thread, sure miss that guy!
The recent excitement over chlorite therapy has made it difficult for any other subject to be gotten onto the table and kept there for a while. Same thing happened during the lithium excitement. At least this time it's different from lithium-- patients we know by name, providing anecdotal data that passes even the Ron Test (if Ron says it works, that one data point has a higher level of confidence than Packard Center will ever have, no matter how creative their statisticians get).
The nature of ALS is that there aren't many old-timers, it's mostly newbies. So for the benefit of the newbies I'd like to put a bit of perspective on the state of the art of theories of ALS and the therapeutic options that those theories imply.
1. Chlorite therapy is where the action is at right now because of the advent of do-it-yourself oral sodium chlorite therapy (OSC)together with credible reports of benefit. The prevailing theory as to why it works (to the extent that it does) has to do with inhibiting reactive gliosis. There is debate over how it does that, or even if that's how it actually works.
2. Prior to the excitement over OSC there were (and are) credible reports of self-treatment achieving varying degrees of success. There was, however, nothing like the present situation with OSC-- multiple patients doing more or less the same thing "in public" and some of them reporting rather quick benefits. So there was not much to get excited about.
3. ALS is not one disease: nobody knows how many diseases it really is, but just in the 10% familial group several have been identified. We don't know where this OSC thing is going to lead, but it is safe to say that many patients will receive no benefit from it, and among those who do benefit the degree of benefit will be variable. Therefore, we can't let interest in other therapeutics fall off the table. We still need alternatives.
4. Among credible reports of successful self-treaters, that of JoelC stands out as unique in that he wasn't doing a "c0cktail", he was doing IV glutathione. Some others have tried IV glutathione without any apparent benefit, but it's my understanding that JoelC based his decision to go that route based on some reports of success in Germany so he evidently wasn't alone. The conventional thinking is that glutathione support protects against excitotoxicity by mopping up reactive oxygen inside the neuron, but it's entirely possible that glutathione could be beneficial for reasons entirely unrelated to antioxidant activity in the neuron. Glutamine is a well known immune modulator: glutathione is probably an immune modulator as well. Maybe it helps to inhibit reactive gliosis.
5. One of the facts that's emerged from PLM data, is that antioxidant therapy to protect the neuron, as a standalone strategy, is probably almost but not quite useless. Adding vitamins to the mix, same story. Those few patients who report success with c0cktail therapies almost always include curcumin (an anti-inflammatory), glutathione support (NAC especially), calcium channel inhibition (magnesium, taurine, betaine/TMG), and mitochondrial support (carnitine,lipoic acid). The degree of success reported varies, and many patients who have done similar things have reported no obvious benefit. The bottom line I read from conventional "natural medicine" c0cktail therapies is that there is a "make sure you hit all the bases" approach that has shown merit. The difference between that and OSC is probably not in efficacy, but in the nature of the evidence of the efficacy. Back in the bad old days, it was dogma that nothing works, and any patient who reported success learned in a hurry how thick their skin was or wasn't. It mostly wasn't: the worst attackers were other patients who didn't know crap. Because I hung in there despite the attacks, other patients who had experienced some degree of self-treatment success but who had no stomach for the abuse they'd get on forums, contacted me through PM. That's how I can say with confidence that my own success was not an anomaly, it was part of a pattern. The pattern was kicked out of public view, therefore I can't prove it to anyone, you can either take my word for it, or dismiss it.
6. If you have access to prescription drugs either through access to a sympathetic medical doctor or through other means, you've got some interesting options for c0cktail formulation available, for example memantine for calcium channel inhibition and valproate for inhibition of apoptosis. Just remember that unless you think you've got a one-drug wonder, take a c0cktail approach, dealing with as much as possible of what goes wrong in ALS.
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BACK TO THE "REACTIVE GLIOSIS" THEORY OF ALS, my take on it (most of this is for newbies)
1. It's been well established that it's processes that go on outside the motor neuron drive a neurodegenerative cascade that leads to death of motor neurons. One of the most common stories in ALS is "a year ago I was running marathons", which indicates a before and an after. Before, no neurodegenerative cascade: after, relentless progression with occasional symptomatic plateaus which probably don't represent temporary remission of degenerative processes.
2. There is widespread belief (which I subscribe to) that the basic nature of the neurodegenerative cascade is that glial cells are trying to get rid of neurons that the glial cells think are diseased and need to be eliminated. The neurons of course then become more diseased, releasing molecular signals that further aggravate the attack. It's a self-sustaining vicious cycle.
3. ALS is actually many diseases, but as a generality we can say that it's a disease that tends to hit people in their 50's and 60's, even in the case of most familial ALS where the molecular defect that destined the patient to ALS was present from the moment of conception. So clearly, the molecular defect itself does not cause ALS: it sets the stage for a condition of imbalance in "something" to happen. The body exhibits the property of "homeostasis"-- that is, the tendency to stability about a satisfactory operating point of temperature, fluid balance, oxygen saturation, etc. With aging, the body changes and with it its ability to compensate changes. If you've got a substantial risk factor for ALS, the data suggest that somewhere between the ages of 45 and 70 your body will lose the ability to compensate it, and the neurodegenerative cascade is no longer inhibited from happening.
4. Notice that the foregoing interpretation of the "age factor" suggests that there is something shared in common between most sporadic and familial forms of ALS. Either something about the degenerative cascade that's normally inhibited that in ALS patients-to-be is missing an essential inhibition factor; or, a factor conducive to the degenerative cascade which is increased in ALS patients-to-be leading to failure of compensation.
5. From the perspective of someone who has already been diagnosed with ALS (and therefore no preventative measures can be taken), this looks pretty grim. Therapy has to consist of more than simply restoring a previously achieved imbalance, it also has to stop a new self-sustaining process that wasn't happening before. The first order of business is to attack the degenerative cascade at its weakest point, which is what chlorite therapy seems to do when it works. The "natural c0cktail" approach presupposes no knowledge of the weakest link, but simply attacks the whole chain with whatever it can, and hopes for the best. NOTE: of the stuff that's presently in clinical trial, virtually none of it even pretends that it may have the capacity to stop the neurodegenerative cascade even though the people who have the designed the trials understand this stuff and could be targeting a lot of the neurodegenerative cascade. I'll save the rant about wholesale medical malpractice against ALS patients for some other post.
6. What arguably makes it not so grim, is that enough is known nowadays that a rational treatment plan can be formulated. The problem is not that nothing can be done, the problem is that there are so many choices and you ain't got much time to make those choices and then do them.
7. There is a difference between stopping the neurodegenerative cascade process, and curing ALS. According to the theory of ALS I've presented above, if you stop the neurodegenerative cascade and then halt treatment, the imbalance that was there in the first place will re-initiate the cascade. So an optimum therapeutic regime should first attack as thoroughly as possible the cascade, and also fix the imbalance that led to the cascade in the first place. This latter part of therapy is equivalent to preventive therapy, the sort of thing that might be done in a fALS patient prior to onset hoping to delay onset for say another 50 years.
--Dave J.
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