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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 4 of 4. This is the beginning of the thread.
Posted by zonked on June 5, 2023, at 16:38:10
I guess I'm not doing a very good job at using the search function... I have followed Scott for years and was delighted to hear he's in remission. What caused it? What was the magic bullet? If there's a post here describing it, could someone link to it?
So curious. So happy for him.
Posted by SLS on June 6, 2023, at 10:13:40
In reply to What caused SLS remission +, posted by zonked on June 5, 2023, at 16:38:10
Hi, Zonked.
It's great that you have found relief.
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.
I think:
Nardil = more serotonin.
Parnate = more norepinephrine.
Both = Dopamine.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.
This is my current treatment regime: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.
* How long did it take for Nardil to begin working once you started it? Thanks.
Good luck, Zonked.
- Scott
Posted by zonked on June 9, 2023, at 16:44:05
In reply to Re: What caused SLS remission + » zonked, posted by SLS on June 6, 2023, at 10:13:40
Scott, Nardil stopped having any significant effect for me years ago, nevertheless I still take it because every time I try to taper it, I get worse.
Nardil 90mg
Lithium 900mg
Prazosin 15mg (night terrors, only partially effective)Because of this, I started TMS (theta burst) on Thursday. I already feel better, and it seems too different to be placebo effect. Interesting, we are both on similar drug regimens.
I'm so glad you're doing well. Consider sticking around babble. I'd give you my personal contact info, as I don't have access to babblemail anymore, but this forum is so easily indexed. I think I might change my posting name so I can use babblemail again.
Would you like to hear updates about tms? I'm really excited about it..
-z
Posted by SLS on June 9, 2023, at 20:58:46
In reply to Re: What caused SLS remission +, posted by zonked on June 9, 2023, at 16:44:05
Hi, Zonked.
I'm sorry for writing so much. It can be irksome to the reader. My refractoryh weakness is that "once I start writing, I'm too lazy to stop." That's my favorite line from the movie "Lincoln".
Still...
> Scott, Nardil stopped having any significant effect for me years ago, nevertheless I still take it because every time I try to taper it, I get worse.
>
> Nardil 90mg
> Lithium 900mg
> Prazosin 15mg (night terrors, only partially effective)
>
> Because of this, I started TMS (theta burst) on Thursday. I already feel better, and it seems too different to be placebo effect. Interesting, we are both on similar drug regimens.
>
> I'm so glad you're doing well. Consider sticking around babble. I'd give you my personal contact info, as I don't have access to babblemail anymore, but this forum is so easily indexed. I think I might change my posting name so I can use babblemail again.
>
> Would you like to hear updates about tms? I'm really excited about it.The ONLY magnetic brain-tissue treatment I would bother with is Stanford's SAINT device. I can't remember all of the differences, but location of the stimulators cycling of
.
>
> -zI would leave the Nardil in place and design a combination regime around it. Of course, I am partial to adding a tricyclic to a MAOI because there is nothing that has ever worded for me as well. As I mentioned, I cannot achieve remission without lamotrigine 300mg/day and lithium 300 mg/day. I have tried to lower the dosages of, or remove entirely both drugs. If the state of the art in 1996 was to be able to choose drugs based upon biomarkers, I could have achieved remission that year. With the approval of lamotriginge (Lamictal), all four drugs that I am currently responding to were available. I am 63 now. I began responding to treatment over two years ago. I was 60.
I could have been well at age 36. That's 25 years of guessing wrong.
Because of Hugh and Jay's excellent information, I decided that should I relapse, I would remain on my current regime and add psilocybin microdosing if I can figure out how to get my hands on some. It might take only a few treatments to increase neuroplasticity enough to recapture the antidepressant response. Nardil has a reputation for losing efficacy at some point. I guess I should be more specific here. Nardil will produce more remissions than any other (traditional) antidepressant. However, its liability for relapse doesn't necessarily make it the best antidepressant. Some SSRIs often allow for relapse. Paxil is the worst. In the past, I received a huge improvement from Nardil that lasted for 2-3 days. My first time, remission lasted for about 3 weeks.
Now, this is a crucial observation: After 2 1/2 years, I remain in remission. The difference? Nortriptyline, lamotrigine, and lithium. So, it is not inevitable that Nardil will fail to maintain a remission. Then again, it is disappointing that some people whose remission was maintained by Nardil monotherapy for over a decade will go on to relapse.
Of course, one suggestion that I would make is combining a MAOI with a TCA. I have *never* experienced a robust improvement without both of these drugs on board. There are other valid alternatives, of course. However, if you do opt for a MAOI-TCA combo, your choices of TCA are limited to amitriptyline, nortriptyline and desipramine (and possibly trimipramine). Most of the rest are too strong as serotonin reuptake inhibitors. This and can elicit serotonin syndrome. It is not as rare as some people assert. I experienced SS while I was taking 60 mg/day of Parnate. So, one day in the 1990s, out of in the desperation, I didn't want to exclude the possibility that Parnate + SRI would work, despite my doctor's refusal to use such a combination. So, I nibbled off a very small piece of an Effexor tablet. I figured that if I experienced anything untoward, its relatively short half would limit an SS episode. Well, within a 1/2 hour, I was completely delirious. I told my parents not to worry about me, and that I just needed to reboot my brain. It's kind of funny that I still had the wits about me to ask my mother to take my temperature. I don't remember the number, but it was normal enough. As SS grows in severity, one's body temperature can become dangerously high - hyperpyrexia. After 1-2 hours, the SS dissipated.
Again, I'm sorry for writing so much. I won't proofread it. It's late.
- Scott
This is the end of the thread.
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