Psycho-Babble Medication | about biological treatments | Framed
This thread | Show all | Post follow-up | Start new thread | List of forums | Search | FAQ

Depression, Antidepressants, Life (ramble) » SLS

Posted by Cam W. on April 18, 2001, at 0:37:10

In reply to Re: Globe and Mail Article From dj on ADs (long), posted by SLS on April 17, 2001, at 21:25:46

Scott - I've been doing a lot of thinking lately (hard to believe, huh). You know, it seems that no matter what you do for depression (or schizophrenia, for that matter) it's still the same old "1/3 theory". With treatment of without treatment, 1/3 get better, 1/3 stay the same and 1/3 get worse. I really haven't seen any change since the introduction of the SSRIs or other new ADs (the same with the atypical antipsychotics).

Perhaps just actively doing something for the depression causes improvement in some. It has been shown that there are links between placebo effect and relaxation techniques. The link is an increase in the activity of the diffusable neurotransmitter, nitric oxide (NO). Perhaps if we can harness the activity of this molecule we can sustain placebo effect into an actual long term therapeutic effect. This may be off the wall, but I have seen a few studies where there are hints that this may be possible.

Dr.Richelson doesn't believe that the genome is the place to look for correcting depression. I kind of agree with him here. The human genome is just too small to account for the number and variability of personalities in this world. Environmental experiences throughout our life through neuronal plasicity (changes in, and reinforcements of or losses of nerve connections in the brain) (eg efficiancy of synaptic pruning) decides what we will be like. Our particular genome is just the template upon which these changes are effected.

We all agree that it is both our genome and environmental stressors that set the stage for the development of depression (and other mental or physical disorders). It seems obvious to me that the faulty circuitry leading to disorders can be attributed to inadequate neuronal plasticity. There must be a reason for this. Perhaps it is that we have not evolved enough to overcome and accomadate the faster pace of life that began with the Industrial Revolution. Perhaps we have evolved to a genetic deadend because of our complexity and there is no easy way for our bodies to compensate for the increased stresses of the modern world.

Evidence for this can be seen in the dramatic rise in the incidence of depression and bipolar disorder since the second World War. This increase can not totally be shrugged off to better diagnosis or that bipolar disorder is being caused iatrogenically by the use of antidepressant acting as triggers.

I do think that we have to look beyond the reductionist view of neurotransmitter and the receptor site theories of mental illness. Perhaps it would be better to modify secondary receptors (eg G-protein-coupled responses) which effect changes in the production of proteins involved in neuronal plasiticity at the genomic level. In effect, rewiring aberrant signalling involved in disease process.

Whaddaya think Scott. Something different needs to be done because it just seems that all these new improvements turn out to be "same sh**, different day."

A pondering Cam


Share
Tweet  

Thread

 

Post a new follow-up

Your message only Include above post


Notify the administrators

They will then review this post with the posting guidelines in mind.

To contact them about something other than this post, please use this form instead.

 

Start a new thread

 
Google
dr-bob.org www
Search options and examples
[amazon] for
in

This thread | Show all | Post follow-up | Start new thread | FAQ
Psycho-Babble Medication | Framed

poster:Cam W. thread:60209
URL: http://www.dr-bob.org/babble/20010417/msgs/60274.html