Posted by tiopenster on August 4, 2010, at 23:33:36
In reply to Re: All my drugs work for 2-7 days then stop working, posted by ed_uk2010 on August 4, 2010, at 16:49:52
Hi Ed,
I assume you're from the homeland of Britain. We love you chaps out there across the pond. I was just photographing a political conference tonight (that's my day job) and I sat next to 3 Young Britons. There were 20 at the conference total. They were so nice and interesting. I love your kind.
Back to business.
A few follow up questions If you don't mind. I suggest taking this offline, but there has to be one poor soul that will benefit from the conversation in 10 years.I do seem to have a problem specifically with the 5ht1 receptor, hence all my problems with SSRIs. They's what they hone in on. My worst reaction was to Lexapro and that's because it's laser like focus on serotonin and nothing else. The was the devil for me. I've never been depressred or manic before I was put on that drug. It needs an exorcist.
I've had moderate success with Remeron, probably because it doesn't touch 5ht1 directly and this it "modulates" as opposed to doing RI. And Geodon focuses on 5ht2
Below is what wikipedia says about Geodon: If you can understand what it's says, I wondered if you could compare it to what wikipedia says about Surmontil: The fact that they both antagonize at the 5ht receptor indicates some sort of similarity. I wonder if I'm reading it all wrong.
"Trimipramine's mechanism of action differs from other TCAs. It is only a moderate reuptake inhibitor of norepinephrine, and a weak reuptake inhibitor of serotonin and dopamine. Its main effects are due to considerable receptor antagonism as follows:
Strong: 5-HT2, mACh, H1, H2, α1-adrenergic
Moderate: D2
Weak: 5-HT1, a2-adrenergic""
"Ziprasidone has a high affinity for dopamine, serotonin, and alpha-adrenergic receptors and a moderate affinity for histamine receptors, where it is believed to act as an antagonist.[2] Ziprasidone also displays some inhibition of synaptic reuptake of serotonin and norepinephrine[2][3], although the clinical significance of this is unknown. The mechanism of action of ziprasidone is unknown. However it has been theorized that its antipsychotic activity is mediated primarily by antagonism at dopamine receptors, specifically D2. Serotonin antagonism may also play a role in the effectiveness of ziprasidone, but the significance of 5-HT2A antagonism is debated among researchers.[4] Ziprasidone has perhaps the most selective affinity for 5-HT2A receptors relative to D2 and 5-HT2C receptors of any neuroleptic.[5][6] Antagonism at histaminic and alpha adrenergic receptors likely explains some of the side effects of ziprasidone, such as sedation and orthostasis.And furthermore, this is what it says about Remeron: Mirtazapine is an antagonist/inverse agonist at the following receptors:[71][72]
▪5-HT2A receptor (Ki = 69 nM)
▪5-HT2B receptor (Ki = ? (~20-fold lower than for 5-HT2A/2C))[73]
▪5-HT2C receptor (Ki = 39 nM)
▪5-HT3 receptor (Ki = ? (similar to 5-HT2A/2C))[74]
▪5-HT7 receptor (Ki = 265 nM)
▪a1-adrenergic receptor (Ki = 608 nM)
▪a2A-adrenergic receptor (Ki = 20 nM)
▪a2C-adrenergic receptor (Ki = 18 nM)
▪H1 receptor (Ki = 1.6 nM)
▪mACh receptors (Ki = 794 nM)
Covers every serotonin receptor except 5ht1. Maybe that's why I've done half way decent on it.My psch clued into the fact that it was the 5ht1 that I don't do well on.
I should note, that I had moderate success on Zyprexa. Not sure what that acts on. It made me eat like a horse, my blood surgar levels were increased and I was so fatigued all the time. That was a deal breaker for me. I had to be on 10mg for the anti-anxiety to kick it It gave me this 3 days good, 2 days bad. I could switch from normal to anxious on the flip of a switch.
So my final questions is whether I should talk to my doctor about Trimipramine or Nardil. I'm game for both. The former sounds easier than the latter.
poster:tiopenster
thread:956187
URL: http://www.dr-bob.org/babble/20100731/msgs/957254.html