Posted by Le Grande Fromage on December 19, 2004, at 12:34:01
In reply to Re: antidepressant afterglow » Le Grande Fromage, posted by francesco on December 18, 2004, at 20:33:33
> You said that the "more serotonin - less dopamine" theory is a fact and this seems to fit with my personal experience. I can 'feel' my dopamine drop when I take antidepressants, and, curious to say, I started smoking immediately after my first trial of an antidepressant.
> But how does this theory fit with the people who DON'T experience apathy on SSRI ? I find that antidepressants usually make me depressed so I have no problems in accepting your theory but what about people who find them useful ?
>Placebo response rate is 75% as high as medication response. This implies that some, if not most, of the benefit one gains from taking medication is itself placebo-related. Perhaps those who escape antidepressant apathy are not biologically affected by their dosage, but are enjoying a placebo response. An alternative explanation is that people have different responses to drugs depending on the efficiency or presence of various enzymes (not sure of the temrinology here). Some people cannot metabolize alcohol as efficiently as others (for instance, women, in general, cannot metabolize alcohol as quickly as men and get correspondingly more drunk on the same dose per mass). Similarly, some people feel more anxious on caffeine, and others simply feel more alert. Likewise, some people may not experience a dopamine-reduction apathy, because of their unique reactions to the drugs. Or else they may simply be enjoying a placebo effect. Or a combination of both.
> Second question. Do you think that TCA elevate dopamine ? I have not read many reports about TCA and apathy and I have read somewhere that TCA elevate also dopamine even if, more often, I read that they affect only NE and SE.Each drug has a unique profile for how much it effects each neurotransmitter. Each neurotransmitter has several sub-types, which the drugs also affect at differing amounts. As far as I know, tryciclics do not affect dopamine. However, it's possible that at different dosages, some of them may have an effect. Effexor, which in my opinion is more of a tryciclic than an SNRI (or, dare I say, a "rebranded" tricyclic vying for 21st century patent profits) also affects dopamine at higher doses. But for some people, an average dose is a high dose, so I'm certain that many people out there on "standard doses" of effexor are also having their dopamine tweaked. If effexor, which is similar to tricyclics can do it, then I'm sure the tricyclics can too.
It seems strangely anomylous that antidepressants are prescribed in standard doses, when each person has a unique physiology and will have an optimum response to a different dose. It would make more sense for the drugs to be sold as powders or liquids to be measured out according to, at the very least, the patients' mass. It's almost as if mere convenience of distribution has overcome the patients' best interest.
>
> Moreover I drink more often and more heavily when I'm on antidepressants, could it be maybe a way to boost dopamine ? If your statements are true it seem to me that the only genuine antidepressants are MAOIs. And this sucks considered how many people take other stuff.This could be caused by increased impulsiveness. When you take a drug which purports to reduce your inhibitions and make you worry less, then it stands to reason that you'll also take more risks.
Alternatively, you may enjoy alcohol more because it temporarily reduces the amounts of serotonin and perhaps NE (not sure about dopamine). In a brain flooded with these neurochemicals this may come as a welcome relief. I find alcohol sedating and stupefying whilst on SSRIs. I also like to drink when on pills simply because of the relief it brings to side-effects like nausea and restlessness.Your comment about MAOIs being the only true antidepressants may hold some truth. SSRIs did not rise to prominence because they are more effective, but because they have less, and less serious, side-effects. Their popularity is more a result of marketing and perception than neuroscience. Medical practitioners are more willing to prescribe them because they're avoiding the risk of fatal side-effects. Same as with benzos. If you spend months on an SSRI which doesn't work, your doc is less responsible because he's just current medical practice. If he prescribes you a MAOI and you suffer a hypertensive crisis, suddenly he's implicated.
Add to this predisposition to prescribe modern, safe medicines, the role of pharmaceutical companies and it becomes clear why most of us are on SSRIs. There are not many studies of, for instance, the effect of Nardil on Social Anxiety, because the patent has run out and no one stands to gain by increasing its salesm and no one is going to pay the vast sums required for a clinical trial. The only reason Paxil is so commonly prescribed for Social Anxiety is because GlaxoSmithKline saw the gap and knew that SSRIs were already prescribed off-label for the disorder. Millions of consumers on a less-than-suitable drug is the logical endpoint of the meeting between capitalism and medicine. So even if, as you suggest, MAOIs are better, they will remain underprescribed because of vested financial interests. The same cycle has already occured with benzos like Xanax, which used to be the most commonly prescribed medication, and it will undoubtedly be repeated with SSRIs (but not before the patent runs out).Sorry about the lenghth of this response.
poster:Le Grande Fromage
thread:429199
URL: http://www.dr-bob.org/babble/20041217/msgs/431644.html