Posted by SLS on April 18, 2001, at 9:53:09
In reply to Depression, Antidepressants, Life (ramble) » SLS, posted by Cam W. on April 18, 2001, at 0:37:10
Hi Cam.
> Scott - I've been doing a lot of thinking lately
Stop that! :-)
> (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 am surprised by this 1/3 get worse figure. You are in a great position to see how closely this reflects real-life, but it seems way to big to me. I never heard of this. Ouch. That 1/3 hurts. I know that I certainly fit into that category. I have dutifully contributed my share with great fidelity.
Has the rule of 1/3 become the generally accepted tenet among clinicians or researchers, or both? Where do these numbers come from?
I would want to know how much of that 1/3 represents a true exacerbation of depression as opposed to an intolerance to side effects. Not that I know any better, but perhaps this number is most reflective of difficult to treat cases with prior exposure to medications. This 1/3 figure sounds about right for the people posting on Psycho-Babble, where the preponderance fall into that class. What is the ratio of inpatients to outpatients that you service? Relative to the global population of depressives being treated, do you think your population is biased against de novo treatment so that it reflects more difficult to treat cases?
> Perhaps just actively doing something for the depression causes improvement in some.
Yes. This has become a consistent pattern among depressed patients entering NIMH clinical research programs, where they feel that they will finally be cured with the help of the "best of the best". This mild improvement seems to last between one and two weeks.
> 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).
I didn't know what were the targets or effects of NO. Thanks. I remember sneaking into a physician's lecture in 1992 when the notion of NO being a true transmitter was new and being presented to some for the first time. It seemed like a pretty bazaar finding. I guess I should pay a little more attention to it.
> 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.
Hmmm.
> Dr.Richelson doesn't believe that the genome is the place to look for correcting depression.Why not?
> I kind of agree with him here.
I definitely disagree with him here.
> The human genome is just too small to account for the number and variability of personalities in this world.
We are not talking about personalities. We are talking about the physiological dynamics of aberrant brain function, whether triggered by psychosocial stresses or not. I don't think such can be triggered in individuals who are without the biological vulnerabilities necessary to allows for it.
The genome comprises about 40,000 genes that encode for proteins. However, the proteome comprises hundreds of thousands of proteins. This is facilitated by the matrix of gene-transcribed proteins interacting with each other and with other materials present in the physiological environment, including those that are derived from the exogenous environment. The proteome is also responsible for the production of and incorporation of all of the non-proteinacious substances.
There are at least two ways to attack a search for the genes responsible for disease:
1. One can attempt to match genomic loci and identify the alleles responsible for a phenotype by testing for associations between the gene and the disease being studied.
2. One can work backwards. Once the detail of an aberrant physiological mechanism is identified and understood, the suspect protein polymorphisms can be reverse-decoded and its transcription nucleotide sequence derived. This sequence is then matched to its occurrence in the mapped genome. This is quite a bit more efficient to quickly identify pathology.
> 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 are looking for the source of biological vulnerability, not the myriad conditions that contribute to its expression.
I feel that studying and exploiting genomic information is a valid pursuit in the quest for understanding and treating some mental illnesses. Actually, it is through the elucidation of the genomic details of these mental illnesses that might actually produce a cure, rather than simply developing better ways to control and stabilize their expression. Gene therapy is no longer a fantasy. It is already here.
Studying the genetic has a critical place. Studying the epigenetic has a critical place. We are waiting for both to bear their fruits.
I think you already know my feelings regarding the unequivocal participation of psychosocial stressors and psychogenic evolutions expressed as clinical depression. I hope I am not viewed as having a "unipolar" mentality.
- Scott
poster:SLS
thread:60209
URL: http://www.dr-bob.org/babble/20010417/msgs/60299.html