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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 13 of 13. This is the beginning of the thread.
Posted by ihatedrugs on March 3, 2013, at 22:14:34
http://web.mit.edu/newsoffice/2012/better-antidepressants-by-targeting-dopamine-1212.html
Posted by SLS on March 4, 2013, at 0:34:10
In reply to http://web.mit.edu/newsoffice/2012/better-antidepr, posted by ihatedrugs on March 3, 2013, at 22:14:34
> http://web.mit.edu/newsoffice/2012/better-antidepressants-by-targeting-dopamine-1212.html
It has always been my feeling that dopaminergic neuronal circuit dysfunction represented the downstream consequences of pathologies appearing elsewhere in the brain. I actually presented this idea to my doctors at Columbia-Presbyterian in 1983. I was laughed at. If this theory is true, then dopaminergic drugs would be more palliative than curative. However, I would most gladly take a palliative drug were it to make me feel and function normally.
- Scott
Posted by B2chica on March 4, 2013, at 13:33:46
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr » ihatedrugs, posted by SLS on March 4, 2013, at 0:34:10
FINALLY someone is looking at this.
seriously the 2+ week wait for AD's, there's something they haven't figured out yet...If serotonin was directly underlying the antidepressant effects of Prozac, then the very first day you take Prozac you should feel the effects, because thats what its targeting immediately, she says. The fact that it takes so long for the drug to work makes me think that the immediate effect of the drug itself is not having an antidepressant effect. When you have the drug in your system for a long time, the brain adapts, and the adaptation might actually be what is underlying the antidepressant effects of these drugs.
Posted by poser938 on March 4, 2013, at 13:40:46
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr » ihatedrugs, posted by SLS on March 4, 2013, at 0:34:10
I like this article.
8 years ago when I first started seeing a psychiatrist I figuref there was some pretty strong science behind how the current meds help emotional problems. After a while I realized the science is very weak. I think 50 years from now everyone will look back and say WTF were they thinking!?
Posted by CamW on March 4, 2013, at 13:52:02
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr, posted by B2chica on March 4, 2013, at 13:33:46
B2chica
We've known for a long time that a lack of serotonin is a symptom of depression, not the cause. What SSRIs do is like a bandage, they seem to "put a floor" under your feet allowing you to function reasonably normally. They retrain the body to produce normal levels of serotonin, and it usually takes up to a year for this to occur. That is why you have to take SSRIs for at least a year.
As well as taking antidepressants, one should also have counselling.
The reason that the dopaminergic drugs we have aren't used as first line treatments for depression is because they are addictive. Opiates, amphetamines and the like do increase dopamine in the nucleus accumbens, but we cannot use them long term because of addiction potential, and they tend to cause tolerance, so one has to keep increasing the dose.
That said, researchers are looking for molecules that will immediately relieve depressive symptoms. There is a ketamine analog that is in development.
I hope that this is of some help. - Cam
Posted by joe schmoe on March 4, 2013, at 17:15:34
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr » B2chica, posted by CamW on March 4, 2013, at 13:52:02
I thought that the explanation for the delayed effect was that AD's cause neurogenesis, and it takes several weeks for the new neurons to grow?
Seem to recall some study in rats showing this, where they experimented with a particular brain region to allow or prevent it from growing new neurons.
Also I thought dopamine boosters tended to make anxious people even worse. And a lot of depressed people suffer from anxiety too.
Posted by SLS on March 4, 2013, at 18:32:48
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr, posted by joe schmoe on March 4, 2013, at 17:15:34
> I thought that the explanation for the delayed effect was that AD's cause neurogenesis, and it takes several weeks for the new neurons to grow?
>
> Seem to recall some study in rats showing this, where they experimented with a particular brain region to allow or prevent it from growing new neurons.
>
> Also I thought dopamine boosters tended to make anxious people even worse. And a lot of depressed people suffer from anxiety too.The thing that ketamine demonstrates so spectacularly is that it can encourage synaptogenesis and reinforce dendritic spines within hours of administration.
- Scott
Posted by CamW on March 4, 2013, at 18:47:40
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr, posted by joe schmoe on March 4, 2013, at 17:15:34
> I thought that the explanation for the delayed effect was that AD's cause neurogenesis, and it takes several weeks for the new neurons to grow?
joe - I don't think that the delay is in neurogenesis, but in down-regulation (getting rid of) post-synaptic serotonergic receptors (hence the increased anxiety & other start-up side effects) and forcing the body to make more serotonin, rather than reusing the serotonin it normally recycles.
I think that this is what is going on (partially) - Cam
Posted by ihatedrugs on March 5, 2013, at 1:32:34
In reply to http://web.mit.edu/newsoffice/2012/better-antidepr, posted by ihatedrugs on March 3, 2013, at 22:14:34
> http://web.mit.edu/newsoffice/2012/better-antidepressants-by-targeting-dopamine-1212.html
This must be why Adderall works so well for me. I'm just afraid of its addictive potential.
Posted by Phillipa on March 5, 2013, at 10:10:59
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr, posted by B2chica on March 4, 2013, at 13:33:46
This has always been my theory. But I honestly have to say that once when new a pdoc gave me prozac and first day had so much energy I wallpapered a foyer. Second day anxiety, third day panic. So dumped them and didn't take again. Now I wonder what would have happened had I done what the doc wanted and taken a 20mg capsule once every three days? But at the time wasn't depressed not even really anxious. Phillipa
Posted by CamW on March 5, 2013, at 11:10:21
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr, posted by ihatedrugs on March 5, 2013, at 1:32:34
> > http://web.mit.edu/newsoffice/2012/better-antidepressants-by-targeting-dopamine-1212.html
>
> This must be why Adderall works so well for me. I'm just afraid of its addictive potential.As long as you use the ADDeral as directed by the physician and don't increase the dose on your own there is little chance of addiction.
- Cam
Posted by jono_in_adelaide on March 5, 2013, at 20:26:32
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr, posted by poser938 on March 4, 2013, at 13:40:46
Well, drugs that influence monoamine levels have been in use for depression since 1957, and they are the most effective drugs found to date, so i think they have a reasonabkle knowelege base behind them
> I like this article.
> 8 years ago when I first started seeing a psychiatrist I figuref there was some pretty strong science behind how the current meds help emotional problems. After a while I realized the science is very weak. I think 50 years from now everyone will look back and say WTF were they thinking!?
Posted by rovers95 on March 6, 2013, at 19:29:26
In reply to Re: http://web.mit.edu/newsoffice/2012/better-antidepr, posted by jono_in_adelaide on March 5, 2013, at 20:26:32
> Well, drugs that influence monoamine levels have been in use for depression since 1957, and they are the most effective drugs found to date, so i think they have a reasonabkle knowelege base behind them
>
>
> > I like this article.
> > 8 years ago when I first started seeing a psychiatrist I figuref there was some pretty strong science behind how the current meds help emotional problems. After a while I realized the science is very weak. I think 50 years from now everyone will look back and say WTF were they thinking!?
>
>Playing devils advocate here, but wouldn't you agree they the best of a pretty bad bunch. And are there better drugs out there that haven't been licensed for depression e.g. riluzole, or we are scared of their addiction potential e.g. buprenorphine.
I would also propose that the scientific evidence for the many popular ADs are pretty weak when compared to placebo. One may also argue that opposed to the alteration in monoamines directly causing any improvement seen from many ADs, there could be something else going on e.g. increases in BDNF, that may lead to any antidepressant effect.
Cheers
Rover
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