Dec-04.19 Steve Branscom
How does a supplement slow or stop the demylenation of the nerves? Wouldn’t this be something that would show up in human trials for ALS? What does yours do that others that claim to do but don’t. I’m sure you can see that it might prey on desperate people looking for anything to help their dogs from suffering.
Thank you Steve for at least getting into a bit of polite conversation instead of just announcing that I AM an “unscrupulous scammer” preying on owners of pets with DM. I don’t mind discussions such as this (actually, really enjoy them) but what I find appalling is that these people adopt an attitude of “I do not believe what you say and I will make sure no one else is exposed to your thoughts”. I greatly value my integrity and to have people behave in this manner is upsetting.
I have no doubt that there is a neurotrophic “active” in operation based on several observations. First, the initial response reported by owners (and this applies to the vast majority of old dogs given the capsules – not necessarily because they have a presumptive diagnosis of DM) is that there is an improvement, quite marked, in intractiveness, playfulness and brightness. These are all features of some effect on the CNS. Second, I myself had the beginnings of Essential Tremor which virtually vanished within days of starting on the capsules. (Note here, I would not give anything to my canine patients that I did not consider safe to take myself.) Again, an indication of CNS activity. Third, there is also an indication that there maybe activity related to melanocytes, cells of nervous origin. Note that the last two factors are very inconsistent, person to person. And finally, there are the observations associated with DM.
There is another factor important to mention and that is that response appears to be much better the earlier the patient starts on the capsules, although this is also not consistent. My feeling is that those with DM that don’t improve certainly seem to have progression of the disease slowed or halted. As an aside I have also seen this with a few patients with Spino Cerebellar Ataxia. So, how do you marry all this up?
My view, at the moment, is that cells involved with progressive, neurodegenerative diseases will lose function progressively but at different rates in different patients (human or canine) but that in the very early phases these cells are simply effete; they are not functional but are a long way from dead. It is currently my view that these cells can respond to neurotrophic influences. I don’t think it is an untenable suggestion to say that there can exist a great variation, patient to patient, in the rate of progression from effete to “irretrievable” and, in the case of demyelination, what actually happens: is the cell demyelinated or does the cell lose the ability to produce/maintain its myelin sheath?
It is not an area I have investigated deeply and it appears there are various views re auto-immune “attacks” on the nervous system which then prompts the query as to why the demyelination only occurs in certain areas. I did a lot of work many years ago on a condition known as Juvenile Pancreatic Atrophy in German Shepherds and, histologically, it was beautiful (in a way) to see the manner that the immune system just targeted the enzyme producing cells and left the islets alone. But the important feature was that ALL enzyme cells were attacked. Probably the same with Hashimoto’s Disease of the thyroid. But, I digress (a bit). A great deal of money has been invested in research into SOD1 and SOD2 in relation to ALS. Frankly, my view is that one of the worst things that can happen with research into a given malady is that someone finds a mutated gene because most research efforts are then concentrated in that area. I think the figure is that only about 5% of ALS patients have mutated genes. I know that within my profession there is a view that if there are not mutations associated with SOD1 and/or SOD2 then that patient has not got DM. I am not a believer.