anciendaze
Senior Member
- Messages
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@adreno and @heapsreal
While there are always problems with anecdotal evidence, I'll contribute my own -- from way back. I had read research papers about fluoxetine before it was approved, and was eager to try it. The first go-around was sheer horror: anxiety, anorexia, insomnia. I completely stopped eating, and nearly stopped sleeping. This was discontinued after a few days, simply to keep me alive.
A second trial started lower and slowly titrated up to "a minimum therapeutic level". I ground my teeth for three months before the doctor became convinced it was never going to benefit me. From this point on, I dropped the serotonin hypothesis. It took longer before I dropped the idea that depression => fatigue rather than fatigue => depression.
Your comments about norepinephrine puzzle me, because the only psychotropic medication I have been able to tolerate long-term is Pristiq (desvenlafaxine), an SNRI. The main point we seem to have in common is the idea of damaged feedback paths and increased sensitivity to medication.
I'm convinced that arguments based on levels of neurotransmitters are missing the point. I can't think of a way an infant nervous system could be calibrated to respond to changes in levels by themselves. Normal variations are surprisingly large, for example after a meal. (If you have had any experience with the problem of calibrating laboratory assays I think you will see the difficulty.) If I were designing a signalling system for such an environment it would be based on differential signalling, which depends on ratios of rates. You can actually find awareness of this in some advanced research publications, including old ones, but the bulk of medical researchers still plod along the familiar, if unproductive, path. They are herd animals who fear being singled out as different.
(Chemical engineers tend to be much more concerned about reaction kinetics, which can lead to explosions. These are very bad for careers, and may be personally dangerous. Doctors generally took only enough mathematics to collect the required merit badges, like boyscouts, and seldom have any awareness of nonlinear differential equations. If pressed on this issue, they will fall back on "long clinical experience", ignoring the possibility doctors have had experience making the same mistakes for quite a long time. I have a collection of stories from the history of medicine to indicate the profession is capable of making the same mistakes for centuries before they get around to such radical ideas as washing their hands.)
One lesson I learned from this experience, and a long list of previous uncontrolled experiments based on the idea I had "treatment-resistant depression", is that doctors really don't know what is going on inside patients, either in terms of psychological states or biochemical responses.
While there are always problems with anecdotal evidence, I'll contribute my own -- from way back. I had read research papers about fluoxetine before it was approved, and was eager to try it. The first go-around was sheer horror: anxiety, anorexia, insomnia. I completely stopped eating, and nearly stopped sleeping. This was discontinued after a few days, simply to keep me alive.
A second trial started lower and slowly titrated up to "a minimum therapeutic level". I ground my teeth for three months before the doctor became convinced it was never going to benefit me. From this point on, I dropped the serotonin hypothesis. It took longer before I dropped the idea that depression => fatigue rather than fatigue => depression.
Your comments about norepinephrine puzzle me, because the only psychotropic medication I have been able to tolerate long-term is Pristiq (desvenlafaxine), an SNRI. The main point we seem to have in common is the idea of damaged feedback paths and increased sensitivity to medication.
I'm convinced that arguments based on levels of neurotransmitters are missing the point. I can't think of a way an infant nervous system could be calibrated to respond to changes in levels by themselves. Normal variations are surprisingly large, for example after a meal. (If you have had any experience with the problem of calibrating laboratory assays I think you will see the difficulty.) If I were designing a signalling system for such an environment it would be based on differential signalling, which depends on ratios of rates. You can actually find awareness of this in some advanced research publications, including old ones, but the bulk of medical researchers still plod along the familiar, if unproductive, path. They are herd animals who fear being singled out as different.
(Chemical engineers tend to be much more concerned about reaction kinetics, which can lead to explosions. These are very bad for careers, and may be personally dangerous. Doctors generally took only enough mathematics to collect the required merit badges, like boyscouts, and seldom have any awareness of nonlinear differential equations. If pressed on this issue, they will fall back on "long clinical experience", ignoring the possibility doctors have had experience making the same mistakes for quite a long time. I have a collection of stories from the history of medicine to indicate the profession is capable of making the same mistakes for centuries before they get around to such radical ideas as washing their hands.)
One lesson I learned from this experience, and a long list of previous uncontrolled experiments based on the idea I had "treatment-resistant depression", is that doctors really don't know what is going on inside patients, either in terms of psychological states or biochemical responses.
