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Re: Need Advice next Tricyclic Antedepressant to try » schleprock

Posted by SLS on January 7, 2013, at 21:19:54

In reply to Re: Need Advice next Tricyclic Antedepressant to try » SLS, posted by schleprock on January 7, 2013, at 20:30:47

> I was under the impression that nortriptyline dosage (for mdd/anxiety?) was to be determined through bloodwork and monitoring for the "therapeutic window".

The dosage can be worked with to some degree by using the statistical mode, which happens to be 75 mg/day. It is my observation that people seem to fall into one of two categories: slow metabolizers and extensive metabolizers. slow metabolizers tend to respond to 50 - 75 mg/day, while extensive metabolizers respond to 150 mg/day. I wouldn't bother with getting blood levels at 75 mg/day unless there is an inadequate clinical response or intolerable side effects. Nortriptyline is perhaps the only antidepressant for which it is possible to actually lose a response if the dosage is increased beyond its therapeutic window. A responder at 75 mg/day can be a non-responder at 100 mg/day.

> Also, there was just a report on the news stating that studies suggested taking beta-blockers help prevent the onset of dementia and Alzheimer's.

Yes. I saw that. I don't know what to make of it, though. Is it a neurochemical effect or a mechanical effect?

> By the way, my pdoc was skeptical when I mentioned the use of alpha-blockers for treating depression.

Well, prazosin has been shown to reduce both anxiety and depression in the PTSD patients that were studied. So far, I don't think non-PTSD patients have been studied methodically.

My personal theory regarding prazosin involves its ability to antagonize NE alpha-1b receptors in the frontal cortex, hippocampus, and amygdala. Tricyclics do not affect these receptors.

http://www.dr-bob.org/babble/20120202/msgs/1009565.html

Depression seems to be associated with hyperactivity, rather than hypoactivity, in several brain regions. That's why DBS works. DBS interferes with neurotransmission, thus reducing activity rather than stimulating it.

> Couldn't really get him to really explain the differences between alphas and betas.

You could really test him by asking him what are the three subtypes of NE alpha-1 receptors: NE alpha-1a/b/d. There is no "c" :-).

> He's pretty much a big supporter of buspirone.

At least someone is. There are people who report fantastic results for anxiety, but it may not begin working for two or three weeks. I haven't seen anyone report success when using buspirone as an augmentor of antidepressants for treating depression, but I'm sure it can. For me, it would probably be a bad drug because I react badly to NE alpha-2 antagonists. Although the buspirone parent molecule does not do this, its 1-PP metabolite does.

> Bringing up my buspirone dilemmas to the community will have to wait until another thread.

Now, you have me in suspense.

> He also immediately shot down Latuda as an option for treatment.

What exactly is your diagnosis or symptom?


- Scott


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

- George Bernard Shaw

 

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URL: http://www.dr-bob.org/babble/20121231/msgs/1034965.html