Cari Loader treatment

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Cari Loader treatment

Postby mscaregiver » Tue Oct 12, 2004 8:30 am

I found this today and found several of the areas interesting, as I was reading a forum I saw this mentioned and it was stated it had helped the poster greatly , yet her friend with MS it did nothing for, seems like another treatment that works for some and for some it doesn't.

The post was from last week but this patent was from 95-96..

Interesting as to the anti-depressant part..

1. Tablets of 500 mg L-tryptophan, or L-phenylalanine or the two combined to be taken at a dose of 1-10/day in accordance with an appropriate daily dose of an antidepressant chosen from the classes of tricyclic or tetracyclic antidepressants, monoamine oxidase inhibitors or serotonin reuptake inhibitors. Examples of such drugs and some typical doses per day include lofepramine (70 mg), imipramine (100 mg), clomipramine (50 mg), amitriptyline (150 mg), nortriptyline (75 mg), mianserin, protriptyline (40 mg), venlafaxine, fluvoxamine (150 mg), fluoxetine (20 mg), maprotiline (75 mg), sertraline, pargyline, moclopemide, triazolopyridine, pheneIzine (45 mg), tranylcypromine (20 mg), desipramine, dothiepin (70 mg), doxepin (100 mg), paroxetine, trimipramine, oxazine or viloxazine (500 mg). However, any other member of these classes of drugs not listed here may be used in this way, in doses indicated in standard texts.
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Postby OddDuck » Tue Oct 12, 2004 9:54 am

Yea, that's what I've said all along, also. A treatment for at least "some" patterns or syndromes of MS. And I at least dissected the mechanisms of actions of desipramine down to minute detail and correlated it with many researchers' findings (i.e. they'd say "if we had a drug that would do THIS, then we could help MS.) Those are the correlations I found with desipramine and that I showed. Ok....McGill says if you can inhibit CPLA2, you can help MS. Desipramine inhibits CPLA2. Then you have those who found that if you can keep the immune system more predominantly TH2, then THAT helps MS, also. Well, there's proof that desipramine does that, also, and on and on (I refer people back to my original research narrative and subsequent posts). That's what my original research paper was all about. I didn't just claim that it works "just because"......I hypothesized that it SHOULD help and here's precisely why and how; whereas most other "claims" don't show an exact correlation of how the drug actually works on the disease.

You know what my old neuro said? (You gotta give him credit for his PhD in pharmacology/toxicology AND his lifelong research into MS). He said "'s just that nobody has EVER compiled all these findings into one!" I'm still watching and waiting to see what, if anything, he eventually does with it. He has my permission to do whatever he thinks best with the information. Remember, he also saw no flaws in it.

My thought was to do a clinical trial with this for the progressive MS patterns, at least at first. There is NOTHING for them to even really try. Remember, in progressive MS, there is little to no inflammation. The immunotherapy and steroid treatments for MS are aimed at reducing inflammation. Hence, why they don't work much for progressive MS.

My suggestion, also, is in using desipramine as a combination drug (or an adjunct). In combination with an AED, though. The most synergistic that I found was in combination with levetiracetam, partly because of levetiracetam's unique composition and efficacy, also. The composition of desipramine, though, is unlike any other TCA when you really break it down and research it in depth. (You would not believe the MOUNDS of substantive material I have at home. LOL)

Remember, the Auckland research group (that Arron posted on here not long ago) showed the same thing as I was claiming, also. But their article said it was a "breakthrough" "miraculous".....etc. ROFL At least I'm not claiming THAT much! Their results were similar to what my hypothesis was showing, though. So have the results of the Netherland folks, and now the Chinese are on the same wavelength. What's missing, though, in all of this is the fact that desipramine has shown efficacy in those very physiological areas that they are finding need "treatment".

You know what the sole problem is regarding doing reputable research studies on desipramine and its direct application for MS? It's money, Phil. Desipramine is an oral tablet....simple to take........and compared to injectables, CHEAP! Probably very little profit margin. The pharmas would lose their shirt if it even helped 25% of MSers. They aren't about to let THAT happen! (Not unless they can liquify it and put it in a hypodermic needle, rename it, and sell it for thousands.) Gee...did I just say that? HAH!

What I also found, too, though is that dosage is critical. If you go too high on a TCA, you get the opposite effect from what you are looking for. (Again, I previously posted my substantive material regarding dosage, too.)

As holds true for LDN, minocycline, etc., where's the harm in doing reputable studies on it? Note I say "reputable". Even if it helps just ONE patient, Phil.......ya know? (I know you feel the same as I do regarding that.) That one patient may be someone who had no other options otherwise, if not for this (if it works for some). (The same holds true for LDN, minocycline, etc. etc.)

Thanks in finding some additional substantive material for me!! The NMSS indicated that I wasn't alone in my thinking. And they have acknowledged desipramine's much broader spectrum of action than other pharmacological therapy proposals to date.

I still am of the opinion that if anybody really thinks that someone will come up with a "one drug fits all" approach to treating MS, I think they are sadly mistaken, and perhaps that's why they are getting basically nowhere. :?:

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