Posted by linkadge on January 20, 2007, at 8:06:13
In reply to Can you repost that link? » linkadge, posted by Jimmyboy on January 20, 2007, at 1:50:14
The link should work, (but you may need a registration to medscape - is free, might be worthwile)
I do think that the neurotrophin hypothesis holds more water than the monoamine hypothesis.
There is only one thing that concerns me (personally) about ingesting substances exclusively for their effects on brain neurotrophins. (The archives are probably full of my search for neurotrophic agents)
Sometimes neurotrophins are upregulated in reponse to a neuronal injury. For instance, epilepsy, after a seizure, levels of certain neurotrophins are very high. As well, some authors have shown that after traumatic brain injury, neurotrophin levels are very high - I suppose almost like a injury response system designed to further protect and aid in repair.
Indeed ECT has the ability to increase BDNF much more than antidepressant treatment. I remember reading that ECT increases BDNF by 120%, wherase antidepressants only by perhaps 20%http://biopsychiatry.com/bdnf-antidep.htm
Also in this study, the antidepressants did not increase BDNF in the hippocampus, an area supposedly responsable for the AD effect.
Anyhow, my point was that just because an agent increases BDNF doesn't mean that it is a good thing. It may be infact that the agent is causing brain dammage, and that BDNF is simply a response.
Now, I don't think that things like royal jelly or turmeric are by any means causing brain dammage, but when it comes to agents like ECT I wonder. Could this just be a response to brain injury, just like with other brain injury?
Linkadge
poster:linkadge
thread:724151
URL: http://www.dr-bob.org/babble/20070119/msgs/724347.html