Posted by SLS on June 4, 2005, at 8:27:38
In reply to Re: How is it..., posted by blueberry on June 4, 2005, at 5:38:05
Hi Blueberry.
Thanks for your concern and such a well thought-out post.
> That is one of the most powerful drug combinations I've ever seen here. Why only 15% improvement is a painful puzzle. I have thought about your situation and came up with a few theories. Just opinions, and just theories.
It's a good a place as any to start. I'm betting that someone other than me will come up with the answer. My track-record isn't too good. :-)
> Contrary to what most people believe, I believe that the closer a med is to targeting whatever is wrong, the lower the dose is required to do that.
The further away a med is from targeting the real problem, the higher the dose needed.
There have been very few people whom have acted under this premise. There is (or was) a doctor Martin Jensen who thought exactly the way you do.
> If that theory was true, then it would indicate to me that increasing serotonin and NE levels a lot is not targeting the actual underlying problem in your case.
> You clearly have the bases covered in terms of increased serotonin, NE, and DA. But that doesn't seem to be helping much. What has been left out? The GABA system is left out.
Interesting. Both Neurontin and Depakote can produce perceptible transient improvements that I can trigger by abruptly changing dosages either up or down. I have tried Depakote at a steady dosage for several months at dosages between 1500-3000mg. I don't remember what other drugs I was on at the time. Unfortunately, both of these drugs can worsen my depression at therapeutic dosages. Although Neurontin has lost the favor of most psychiatrists, I believe it still has therapeutic potential in mood disorders that should not be abandoned.
> The opioid system is left out.
Yes, it is. I once took some Vicadin that a friend had hanging around to see what it would do. Since I didn't feel the immediate improvement that many people report, I sort of shelved the idea. If I had had more of the stuff to work with, I think I would have persisted beyond two days. I haven't ruled out opioids. I guess I'll run it by my doctor at some point.
> I've known people in your situation who experienced quick and almost miraculous recovery with either a benzo or an opioid after failing everything else. If there is a malfunction in one of those circuits, the meds you are currently taking will only affect them slightly and indirectly.
Exactly.
> Your current meds are creating a huge buildup of serotonin, NE, and dopamine. But that isn't helping much. Think of a dam blocking a river...it results in a huge buildup of water. But what if that river is only a trickle? It won't matter how large the dam is, there won't be enough buildup in water at the dam because there is hardly any water coming in. With that in mind, maybe some meds that will stimulate neurotransmitter production and release. Like stimulants. Maybe the huge buildup of neuros from your current meds has shut down production, or maybe production has been the actual problem all along.
This is what I took at one time:
Parnate 120mg + desipramine 200mg + Dexedrine 40mg + thyroxine (T4)
Parnate 120mg + desipramine 200mg + bromocriptine
Parnate 120mg + desipramine 200mg + Lamictal
I really should have pushed the desipramine to 300mg, but I doubt it would have helped.
> Basically, no matter how I look at it, I tend to feel that your symptoms are not directly or even indirectly related to low serotonin, NE, or DA levels. It's something else. In your shoes, I would be very suspect of any neurotransmitter circuit that has not already been addressed, like GABA or opioid.
There's nothing like pure logic...
What circuits would you focus on if you were in my situation? What drugs would you suggest?
> Going forward, I would toss out all theories you have been going on for years, because they are clearly off base.
I have always suspected dopamine as having a role in all of this, but I grew from believing it the primary site of dysregulation to believing it is just a secondary site; a downstream consequence of a primary problem located elsewhere - much as you have suggested so eloquently.
> The clues and the evidence are striking. At least, to me anyway.
I wish there were more clues to what the problem is than what it is not. Right now, I plan to play with antiglucocorticoids to manipulate the HPA. I wish those CRH antagonists were closer to making it to market.
> Just my thoughts. Psychiatry is so hard. Symptoms can be caused by any malfunction in any one of the brain's circuits.I even looked at Lyme disease and took a course of doxycyline for a few months.
> Trying to figure out which one of those circuits is primarily at fault is difficult, because only trial and error of different meds will give the needed clues. In your case, and it is just my opinion, all the clues seem to point to something else besides serotonin, NE, or DA. My top theories for your situation would be the GABA circuits, opioid circuits, or neuro stimulation and production. I could be way off base, but those are my thoughts.
Thanks. You gave me some more food for my own.
:-)
- Scott
poster:SLS
thread:507285
URL: http://www.dr-bob.org/babble/20050601/msgs/507562.html