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Re: Dr. Tracy on SSRIs.. » linkadge

Posted by Larry Hoover on December 10, 2005, at 17:32:08

In reply to Re: Dr. Tracy on SSRIs.., posted by linkadge on December 10, 2005, at 14:36:35

> "Elevated serotonin is not the problem, because there is no such condition."
>
> Elevated serotonin is implicated in a number of conditions. If you visited the Buspar website a year ago, it would have told you that anxiety is related to elevated serotonin.

Excepting serotonin syndrome, no demonstrated condition of excess serotonin is known.

Your brain just doesn't work that way, like there is a reservoir with serotonin in it, that can get over full. Or that there is too much on the loose. It is a simplistic concept, with no physiological correlate.

> There is a lot of research that shows that anxiety may actually be related to high serotonin levels.

Not high serotonin levels. High activity at specific serotonin receptors.

> Serotonin can be anxiogenic.

And anxiolytic. Depends on the receptor.

> Hence the SSRI start up anxiety,

or somnolence.

> and GI effects that don't go away for many people.

5-HT7 receptor subtype, not due to serotonin per se. Serotonin agonism by drug.


> Hinting that high serotonin leads to agression is not unfounded. Many doctors have noted that artificially increasing serotonin can lead to emotional indifference. Studies on animals sometimes show similar results, ie. MAO-A knockout mice are unusally agressive.

MAO-A is not specific to serotonin. Flooding the brain with free serotonin does not mimic any known physiological process.

> "Serotonin is a precursor to melatonin, so how could it suppress melatonin? What is premature aging? She cannot bring these ideas into a coherent whole. "
>
> I don't know, you tell me.

It's her theory.

> Most of the SSRI's decrease melatonin concentrations. Infact, melatonin administration reduces the antidepressant effect of fluoxetine. In the night time melatonin levels are at their highest, and serotonin levels drop. SSRI's supress melatonin production via agonism at the 5-ht2a receptors.

Then that is not a serotonin effect. It's a drug toxic effect.

> The 2a blocking antidepressants tend to increase melatonin production.

Again, conflating drug effect with endogenous agent effect.

> Lowering melatonin levels will lead to premature aging.

?? What is premature aging?

> The connection to LSD is also not unfounded. I experienced visual halucinations on SSRI's.

I'm sorry that happened, but LSD is quite a different drug.

> A number of other people on this board have too.

I'm sorry that's happened.

> Prozac seems to have the highest propensity to do this, since it seems to more strongly agonize the 5-ht2a receptor, via 5-h2c blockade.

I try to stay away from these mechanistic arguments, because they require that you believe the premise to believe the conclusion. Petitio principii.

> She is attempting to make these connections, so that we have a basis for understaning the kind of behavior that they can produce.

She doesn't make those arguments. You did.

Here's an example I just heard her say, in that interview:

SSRIs are likely to produce a "gummy gooey glossy substance on heart valves". That sure sounds scientific. She goes on to declare that Alzheimer's is a hyperserotonergic state, and that "the same gummy gooey glossy deposits are found at autopsy". In the very next breath, she argues that SSRIs are prophecied in the Bible, and I just stopped listening at that point.

> I have what I call APPD, "antidepressant induced perceptual disorder"
>

> Linkadge

I'm sorry it's been such a hard road, link.

Please try to separate from the emotional appeals, with seemingly plausible arguments, based on zero evidence. The woman scares me.

Lar

 

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Psycho-Babble Medication | Framed

poster:Larry Hoover thread:587690
URL: http://www.dr-bob.org/babble/20051203/msgs/587856.html