Posted 19 December 2009 - 11:41 AM
I took Amitriptyline in 1996 for my depression and anxiety, as I couldn't tolerate with SSRI's/SNRI's.
It is a Tertiary Amine, metabolised via cytochrome P450 2D6 into Nortriptyline.
Amitriptyline is categorised as a "dirty-mood-brightener" ( as stated in Biopsychiatry.com), because it affects many neurotransmitters, such as cholinergic-antagonist causing dry mouth, histamine-1 antagonist causing sedation.
Apart from that, it is a Tertiary Amine of Tricyclic antidepressnt, which also blocks the re-uptake of Serotonin/Noradrenaline/Dopamine into the pre-synaptic clefts, making those neurotransmitters more available in the brain.( It blocks the re-uptake of Serotonin more than Noradrenaline.)
Nortriptyline, a secondary Amine, an active metabolite from Amitriptyline, has less anti-cholinergic and antihistaminic side-effects. ( It blocks the re-uptake of Noradrenaline more than Serotonin.)
In my experience with these 2, Nortriptyline is more activating, after taking it for 3 weeks or more.
But as for Panic disorder, Imipramine, which is a "gold standard" TCA antidepressant, also a Tertiary Amine is more effective.
The active metabolite, Desipramine, a Secondary Amine, has less anticholinergic and antihistaminic effect, so it is more activating.
But according to many researches, Desipramine in high dose can cause a sudden death incident, compared to other TCA's.
Depending on the use off-label, for depression/Panic disorder/anxiety, Imipramine I find it very useful.
But for neuropathic pain/depression accompanied with insomnia/migraine/tension headache, I find that Amitriptyline is more useful.
All TCA's have tendency to cause constipation, hand-tremors, dry mouth and arrhythmias.
Nowadays, there are better atypical antidepressants, Mirtazapine which I've been taking, which has a wide margin of safety, as it is not cardiotoxic nor does it cause anticholinergic effect. But the problem is, it causes weight gain as it has a strong anticholinergic effect. It is a NaSSA, an analogue of Mianserin which is a Tetracyclic Antidepressant.
NaSSA works oppositely to SSRI's/SNRI's like Fluoxetine, Paroxetine, Sertraline, Fluvoxamine or Venlafaxine and Duloxetine. So NaSSA does not cause insomnia, akathisia, nausea; but it is very sedating in low dose, in higher dose it is more stimulating.
I tried almost all antidepressants to cure my depression, anxiety/panic attack, tension headache. I've been suffering from insomnia for years, also hypersomnia->making me hard to wake up early in the morning.... and always feeling fatigue, loss of interest in activities.....tired all the time during the day.
The wonder drug Piracetam helps me a lot .....along with caffeinated drinks such as NO-XPLODE (BSN company), which has a combination of Nootropic stimulants such as caffeine,vinpocetine,L-Tyrosine..... , RedBull drink also helps me a lot.....all in combination with Piracetam.
I used to try Aurorix ( Moclobemide), a RIMA ( Reversible Inhibitor of Monoamines-type A), in a dose higher than 600mg/day, it inhibits the deaminations of Serotonin, Noradrenaline......also Dopamine and PEA. But the dose lower than 600mg, it only inhibits the deaminations of mainly Serotonin and Noradrenaline. Aurorix and Deprenyl are MAO Inhibitors, but reversible, unlike Parnate and Nardil.
I'm not too sure about TCA's, whether they are neurotoxic or neuroprotective, but I read some research in Medline that Moclobemide and Selegiline are Neuroprotective.
Selegiline has an active metabolite which is an amphetamine, but it only works peripherally not centrally, and when I tried it daily I got restlesness, so I cut down to 3 times/week.
With Aurorix, I crushed the tablets before swallowing it, and it really gives me a feeling of wellbeing/euphoric kind of feeling. But, according to MIMS Annual, it is best to take it after food, not before, as some tyramine in the food needs to be broken down/oxidised by the Monoamines, so taking Aurorix before food blocks the Monoamines that is required to oxidise the tyramine. Moclobemide has a half-life of 2 hours, but the inhibition effect is reversed within 24 hours.
Piracetam, or Racetams do not affect liver enzymes Cytochrome P450, so they do not interact with other medications. ( however, it is best not to combine any MAOI with any medications or even tyramine rich food, as it will cause hypertensive crisis and Serotonin syndrome/toxicity with meds that work via Serotonin pathways.)
LongeCity
