Re: What caused SLS remission + » zonked

In my opinion, and in the opinions of a great many cliinicians and clinical researcheres, Nardil is currently the most effective sold antidepressant in the world. I certainly don't know every substance capable of exerting an antidepressant response, but the NIH had used clorgyline, a specific irreversible inhibitor of the MAO-A enzyme. This is a subjective interpretation of how Nardil affects me versus how Parnate effects me. I get the feeling that Nardil manages to inhibit MAO-A to a greater degree than Parnate.

Both drugs inhibit MAO-B, and thus increase levels of dopamine and epinephrine. I do not know numbers to compare relative magnitudes of these effects. However, in that only the MAO-A enzyme subtype inhibits the metabolism of serotonin metabolism, this might account for its statistical superiority over Parnate as an antidepressant, although many people respond to Parnate who didn't respond to Nardil.

Many people attribute the ability of Nardil to bring depressives into remission to its inhibitio1n of the GABA transaminase enzyme, which leads to more GABA within the synapse. Personally, I think this confers additional anxiolytic activity but not additional antidepressant activity.

Apparantly, clorgyline, which does not inhibit MAO-B at all, is an extremely potent antidepressant. As I mentione earlier, clorgyline will get more people well than any marketed antidepressant in the world. It was made available to me by the National Institutes of Health (NIH) when I was a research patient there in 1992-1993. In the United States, the NIH was the only source of a preparation for human consumption. It no longer is. There was some concern about cardiac side effects. I had to give clorgyline up. William Z. Potter, the department director, refused to allow me to add desipramine to it. My response to clorgyline monotherapy was significant, but unacceptible.

I believe that inhititing MAO-A is sufficient for producing a robust clinical improvements . Moclobemide is another selective MAO-A inhibitor that exerts an unequivocal antidepressant effect. However, it is reversible. Moclobemide attaches itself to and blocks the MAO-A enzyme. However, it dissociates from binding site, allowing that enzyme molecule to become available again. Moclobemind usually loses its therapeutic antidepressant effects at each dosage, forcing dosage escalation. The maximum dosage is generally accepted to be 1200 mg/day. Once relapse occurs at this dosage, there is nowhere to go. Moclobemid is most often a dead-end. I tried moclobemide and experienced this for myself. Clorgyline, which is a specific irreversible inhibitor of MAOI, clearly demonstrates that the inhibition of MAO-A is suffient to produce an antidepressant response.

I suppose some people need MAO-B inhibition in addition to MAO-A inhibition. However there is *no* selective inhibitor of MAO-B that gets people well. This most especially applies to selegiline / EMSAM / L-deprenyl. Selegiline does *not* produce and antidepressant response until one reaches a dosage high enough to begin inhibiting MAO-A. This is made clear on the drug's package label.

Phenelzine (Nardil): 90 mg/day
Nortriptyline (Pamelor): 100 mg/day
Lamotriginge (Lamicta: 300 mg/day(
Lithium (lithium ion): 450 mg/day - Recently increased from 300 mg/day.

I had been taking 300 mg/day of lithium for years. Lithium is absolutely essential for my robust therapeutic response. However, I recently had a manic break-through. Increasing the lithium dosage seems to have put the fire out.

Some see things as they are and ask why.
I dream of things that never were and ask why not.

The only thing necessary for the triumph of evil is that good men do nothing.

Re: What caused SLS remission + » zonked

Thread

Post a new follow-up

Notify the administrators

Start a new thread