![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 32. This is the beginning of the thread.
Posted by AndrewB on April 30, 2000, at 19:33:32
Can fast trials be effective and, probably more to the point, can fast trials work for everybody or just a subpopulation. There are a couple studies which examine the predictive value of an early improvement in mood with an SSRI. Nothing earth shattering here. The studies just show some people respond faster than others to SSRIs. (Some people on this board respond incredibly fast!) In general an improvement or a lack of improvement within the first 2 or 4 weeks often indicates whether or not the SSRI will work for someone in the long run. But these studies also indicate the need for longer trials (6 weeks?) with SSRIs because of the large number of people who will show an initial improvement which fades away (placebo?) and the large number of people who will respond to an SSRI only after 6 or 8 weeks. Here are some excerpts from the abstracts:
*******Eighty-two subjects (57.3%) who started the trial responded by week 8. Of those subjects who showed no improvement at weeks 2, 4, and 6, the proportions of responders at week 8 were 36.4%, 18.9%, and 6.5%, respectively...... The proportion of patients with no response to antidepressant treatment by 4 or 6 weeks who responded by week 8 was substantially less than that for subjects who had at least a partial response. Nonresponse as early as week 2 predicted 8-week outcome.
From study entitled: Early nonresponse to fluoxetine as a predictor of poor 8-week outcome******Early responders at weeks 1, 2, and 3 were statistically significantly more likely to experience marked improvement or remission than those lacking early response. However, at week 3, this criterion correctly classified only about three-fourths of patients with regard to marked improvement and only about two-thirds with regard to remission. Moreover, about one-third of patients predicted to experience marked improvement and about three-fifths of those predicted to remit did not.
From a study entitled: Predicting response to fluoxetine in geriatric patients with major depressionThe next study is very interesting. It indicates that SSRI and buspirone trials may be shortened by the augmentation with propanol.
*****It has been reported that the 5-HT1A autoreceptor antagonist pindolol can accelerate the antidepressant response to the selective serotonin (5-HT) reuptake inhibitor (SSRI) paroxetine, presumably by preventing the initial decrease in firing activity of 5-HT neurons produced by the SSRI. The administration of the selective 5-HT1A agonist buspirone (20 mg/day for 1 week and 30 mg/day thereafter) with pindolol (2.5 mg TID) was used to activate selectively postsynaptic 5-HT1A receptors. This combination produced a greater than 50% reduction of depressive symptoms in the first week in 8 of 10 patients and the response was sustained for the remainder of the trial. The combination of the SSRI fluvoxamine (50 mg/day for 1 week and 100 mg/day thereafter) with pindolol produced a marked antidepressant effect but did not act as rapidly as the buspirone plus pindolol combination with none, four, and eight patients achieving a 50% amelioration after 7, 14, and 21 days of treatment, respectively
From a study entitled: Selective activation of postsynaptic 5-HT1A receptors induces rapid antidepressant response.Though SSRI trials may for many need to last 6 weeks or longer, many studies indicate that 2 week trials will suffice for MAOIs and tricyclics. Studies show a strong relationship between an improvement after 2 weeks and a long term response. Here are 2 study excerpts:
******The early onset of improvement (with moclemide, imipramine or amitriptyline) or was highly predictive of later outcome: on average, 70% of patients showing improvement within the first 14 days became responders. Differences between active treatments and placebo emerged within the first five days and reached a point of maximum distinction around day 14.
From, ‘Delayed onset of action of antidepressant drugs? Survey of results of Zurich meta-analyses’****** Onset of improvement occurred in the great majority of patients (79.1%) within the first 12 days of study, independently of the severity of depression at baseline. Early improvement was highly predictive of later outcome....
From, ‘The speech analysis approach to determining onset of improvement under antidepressants’If two week trials should be possible with MAOIs and tricyclics, even faster trials are possible with direct acting D2 and D3 meds. such as amisulpride, sulpiride, pramipexole, ropinirole and amineptine. Their fast antidepressant action is probably due to their direct action on the D2/D3 receptors within the nucleus accumbens. The neurotransmission of this area of the brain is improved by use of various antidepressants (SSRIs, MAOIs, etc.), but the direct acting D2/D3 drugs are able to act on this area more rapidly.
Posted by Scott L. Schofield - SLS on April 30, 2000, at 22:40:15
In reply to Shorter Trials with ADs, posted by AndrewB on April 30, 2000, at 19:33:32
> Though SSRI trials may for many need to last 6 weeks or longer,
They may.
> many studies indicate that 2 week trials will suffice for MAOIs and tricyclics.
Many studies may indicate this, but they are wrong. 2 week trials will not suffice. An absolute minimum of 3 weeks is required.
> If two week trials should be possible with MAOIs and tricyclics,
They are not.
> even faster trials are possible with direct acting D2 and D3 meds. such as amisulpride, sulpiride, pramipexole, ropinirole and amineptine.
Adam, I don't understand the logic behind this supposition. Anyway, it is not necessary to propose an association. If these other drugs work quicker, then they just work quicker.
As monotherapy, postsynaptic DA agonists may produce an improvement in depression more quickly than SSRIs, tricyclics, and MAOIs, but I don't think they work as well or last as long. Performing trials with these drugs as adjunctive agents is a different story.
Sulpiride and amisulpride (presynaptic DA antagonists) should not be placed in the same category as pramipexole and ropinirole (postsynaptic DA agonists), either pharmacologically or conceptually. This is not a meaningless technicality. Even if both groups of drugs initially potentiate dopaminergic neurotransmission, they would accomplish this through entirely different mechanisms. It would not be prudent nor justified to pretend that the phenomenology behind how these different drugs produce an antidepressant response is the same.
Do neurons adjust their receptor sensitivities similarly to both groups of drugs? Of course not. They respond in opposite ways.
Perhaps amisulpride monotherapy lasts longer than pramipexole monotherapy. Perhaps it takes less time for pramipexole to work than it does for amisulpride. Are there any differences? I would expect pramipexole to produce an improvement in one to three days. Does amisulpride take longer than three days to work? What has been your experience?Lumping agonists and antagonists together is no different than lumping together reuptake-inhibitors and releasers. We know that Prozac and Pondamin are not equipotent antidepressants.
Amineptine is not a direct acting DA med. It is a reuptake inhibitor. I know that this was just an oversight on your part.
> Their fast antidepressant action is probably due to their direct action on the D2/D3 receptors within the nucleus accumbens.
The neurotransmission of this area of the brain is improved by use of various antidepressants (SSRIs, MAOIs, etc.), but the direct acting D2/D3 drugs are able to act on this area more rapidly.This is probably true. But what if a reduction in activity within the nucleus accumbens is due to hippocampal malfunction? Where is the location of the first domino? How long can the last domino be held up superficially if the first domino keeps falling down? Is it even necessary to reset the first domino? These are rhetorical questions, but I am trying to present the complexity of the workings of the brain, and how an anomaly in one area can lead to a perfectly appropriate reaction in a healthy area and thus produce disease.
I lost my train of thought. What was my point?
Sorry. :-)
- Scott
Posted by Cam W. on April 30, 2000, at 22:58:23
In reply to Shorter Trials with ADs, posted by AndrewB on April 30, 2000, at 19:33:32
Andrew - Cool, thanks for the info.
I do not think that antidepressant drug trials should be allowed to be published unless the run at least six months.
The drug companies counter by saying that this would cost too much and require too many guinea pigs (..er, a large patient base). Then they send 100 psychiatrists to Victoria for a week, then to Spain for a week, just to tell them the merits of their drug (guess I won't be lecturing for that company any time soon, now).
As for pindolol augmentation, my experience has been that it is less than adequate. If someone needs to have an AD work faster than 4 to 8 weeks, they need taking a low dose atypical antipsychotic.
Sorry for the rant - Cam W.
Posted by AndrewB on May 1, 2000, at 8:44:50
In reply to Re: Shorter Trials with ADs, posted by Scott L. Schofield - SLS on April 30, 2000, at 22:40:15
Scott,
I can see that you didn't find much to agree with in my post. You didn't even agree with my name it seems!
Concerning 2 week vs. 3 week or longer trials with tricyclics and MAOs, I'm open to what you have to say. Studies and their conclusions can be wrong. But I tenatively agree with the idea itself behind 2 week trials; if after two weeks of taking an MAOI or a tricyclic a person should in good likelihood (70%-80%) have seen improvement, then it is time to move on to a new med. Let me know why you think the way you do.
Concerning the D2/D3 agonists pramipexole and ropinirole, I'm not ready to say they are as efficious or as long lasting as amisulpride or sulpiride. But neither am I as certain as you are that they aren’t. I understand why you feel the way you do, knowing what you do about bromocriptine and the other older agonists. But perhaps these are different. At least one small study has indicated that pramipexole is long lasting (6 months). As far how effective it is on its own I’ll wait to hear other people’s personal experiences with it.
Yes, D2 agonists act on the postsynaptic receptor and a drug like amisulpride acts on the presynaptic (at low doses). But I don’t see this as a big difference. In the end, amisulpride acts via stimulation of the postsynaptic receptor, just as pramipexole, the only difference being that the postsynaptic stimulation is done by the body’s dopamine instead of an agonist. Whether an agonist or the body’s dopamine is involved, the same issues of upregulation and downregulation and receptor sensitivities are involved and the effectiveness of amisulpride demonstrates that long term stimulation of the D2/D3 receptors does not need to lead to poop out. But I have to admit, I’m sure there is a lot I don’t understand here.
To answer your question, it has been my personal experience that both amisulpride and mirapex act in about 1 to 4 days.
And yes, amineptine has been described as a direct acting DA medicine in relation to SSRIs and other ADs. It is all relative you know!
Finally, we both may agree that some of the D2/D3 receptors are located in parts of the brain central to some aspects mood (the limbic system). Causes of D2/D3 hypofunction that I have read of include lesions in the area and stress induced downregulation. Regardless of the ultimate cause of the downregulation, some D2/D3 active medicines have been shown to be efficious in upregulating D2/D3 receptor function on an ongoing basis.
Thank you for your stimulating and well informed disagreements. Best wishes as always,
AndrewB
Posted by AndrewB on May 1, 2000, at 8:48:27
In reply to Re: Shorter Trials with ADs, posted by Cam W. on April 30, 2000, at 22:58:23
Cam,
So pindolol doesn't speed up SSRI effect in actual practice. Thanks. Are you saying low dose atypicals speed up SSRI effect?
Posted by SLS on May 1, 2000, at 12:43:37
In reply to Re: Shorter Trials with ADs, posted by AndrewB on May 1, 2000, at 8:44:50
> Scott,
>
> I can see that you didn't find much to agree with in my post. You didn't even agree with my name it seems!Sorry. Damned dementia.
> Concerning 2 week vs. 3 week or longer trials with tricyclics and MAOs, I'm open to what you have to say. Studies and their conclusions can be wrong.
These are.
Perhaps their observations are correct, but their conclusions are wrong. Dead wrong.
> But I tenatively agree with the idea itself behind 2 week trials; if after two weeks of taking an MAOI or a tricyclic a person should in good likelihood (70%-80%) have seen improvement, then it is time to move on to a new med. Let me know why you think the way you do.
What about the 20-30 percent? This is not acceptable. How can this 2 week protocol possibly be considered a logical way to treat a life-threatening illness, when 20-30 percent of cases will slip by? What is 7 more days to make sure that we catch them? No way does this make sense.
When treating outpatients, the clinician must rely upon the self-reporting of the patient. Such self-reporting is often very unreliable, and I doubt that most clinicians hand out HAMDs or facilitate daily observations by a professional. Even if they did hand out rating sheets, self-ratings are still unreliable. I am well aware that in a sizeable percentage of cases, a small improvement in mood can appear as early as one week into treatment. But this improvement is usually very small, and is often not recognized by the patient. This is especially true if there are associated psychological or emotional disturbances that mask any changes in biological function. In addition, there are often comorbid presentations with anxiety disorders, dysthymia, and other psychiatric conditions. How can it possibly be expected that 100 percent, or even the great majority of patients will be able to recognize the small improvement that MAY occur before their 14 day trial expires? No way does this make sense.
Oh yeah, remember that in quite a few cases, there is a tendency towards increased suicidal ideation early in treatment as they "improve". It appears BECAUSE their biology improves. I'm not sure a patient will report this suicidal ideation as an improvement.
> Concerning the D2/D3 agonists pramipexole and ropinirole, I'm not ready to say they are as efficious or as long lasting as amisulpride or sulpiride.
Neither am I. I really do hope to know, though.
> But neither am I as certain as you are that they aren’t.
I hope the questions I offered were not construed as certainty. My expression of certainty (believed certainty) is more similar to that which I have written above. I really did expect pramepexole to work in 1-3 days. However, I had no reason to believe that amisulpride wouldn't. That is why I asked you about your personal experience with it.
> I understand why you feel the way you do, knowing what you do about bromocriptine and the other older agonists. But perhaps these are different.
I was thinking the same thing, but I didn't want to substitute these older agonists for the ones you mentioned in my reply. It would have made for a forensic slight-of-hand.
> At least one small study has indicated that pramipexole is long lasting (6 months).
Was this pramepexole monotherapy? If not, what was it added to?
> As far how effective it is on its own I’ll wait to hear other people’s personal experiences with it.
That's why I am so interested to see someone create an inventory of what goes on here. You would make a good candidate to embark on this endeavour. From what I can surmise, you already have a hell of a head start.
"This mission, should you choose to accept it..."
This post will self-destruct in 5 seconds.
Oops, I guess not.
> Yes, D2 agonists act on the postsynaptic receptor and a drug like amisulpride acts on the presynaptic (at low doses). But I don’t see this as a big difference.
There are fundamental difference between them. They do very different things inside the synaptic-cleft. How "big" (important) is this difference, beyond the pharmacological activity, remains the judgement of the person contemplating it.
> In the end, amisulpride acts via stimulation of the postsynaptic receptor, just as pramipexole, the only difference being that the postsynaptic stimulation is done by the body’s dopamine instead of an agonist.
Different is different. The clinical end result cannot be deduced by the initial net effect at the synapse.
Prozac versus Pondamin. Provigil versus reboxetine. Amineptine versus Pemoline. Valium versus Depakote. Dexedrine versus Ritalin. Desipramine versus yohimbine. Celexa versus tianeptine? Paxil versus pindolol? Wellbutrin versus who the hell knows.
> Whether an agonist or the body’s dopamine is involved, the same issues of upregulation and downregulation and receptor sensitivities are involved and the effectiveness of amisulpride demonstrates that long term stimulation of the D2/D3 receptors does not need to lead to poop out.
Then what does? I have read posts from people inquiring what they should do next, as their amisulpride has pooped-out. I think you can find them archived over the last few months. Didn't you report diminishing returns, or was it simply that it did not address anhedonia? I don't remember exactly.
> But I have to admit, I’m sure there is a lot I don’t understand here.
Seeing as how this is such a common complaint among our most brilliant neuroscientists, you shouldn't be too hard on yourself.
:-)
> To answer your question, it has been my personal experience that both amisulpride and mirapex act in about 1 to 4 days.
But you were taking reboxetine at the time, weren't you?
> And yes, amineptine has been described as a direct acting DA medicine in relation to SSRIs and other ADs. It is all relative you know!
It is not relative. It either is or is not a ligand for those synaptic receptors being referred to. I have seen this same statement made before about other drugs. They are made out of ignorance.
> Finally, we both may agree that some of the D2/D3 receptors are located in parts of the brain central to some aspects mood (the limbic system).
I like the concept of primary versus secondary sites (or mechanisms) of dysfunction (or states of activity). I tend to lean in the direction of using at least one drug that targets the primary site to ensure continued response. Targeting the secondary site may provide a boost to compensate for any residual deficit (or excess) of activity there. Perhaps doing so can also help "kick-start" a response when a chronically hypostimulated or hyperstimulated area has become dysregulated. I thought it was an interesting concept, anyway.
> Causes of D2/D3 hypofunction that I have read of include lesions in the area and stress induced downregulation.
How would you compare the characteristics of D2 and D3 receptor sites and their associated pathways? Do you think the incorporation of D3 activity in a medication is particularly important in treating mood-disorders?
> Regardless of the ultimate cause of the downregulation, some D2/D3 active medicines have been shown to be efficious in upregulating D2/D3 receptor function on an ongoing basis.
Are these agonists of antagonists?
If the answer is not "both", then one must recognize the validity of discriminating between them. This would be a big difference.
I don't know the answer, so it wasn't a loaded question.
> Thank you for your stimulating and well informed disagreements.
Ditto.
Best wishes as always,
>
> AndrewB
Right back at ya',- Scott
Posted by Cam W. on May 1, 2000, at 16:23:14
In reply to Re: Shorter Trials, Cam W, posted by AndrewB on May 1, 2000, at 8:48:27
Andrew - Pindolol does speed up the effect of SSRIs, but it is not worth the money for the amount of effect that it does have. The low dose atypical can be used for people who are suicidal or extremely depressed (ie should be in hospital). Atypical antipsychotics do not speed up the effect of SSRIs, but they are a stop-gap until the SSRI takes effect.
Hope this helps - Cam W.
Posted by AndrewB on May 2, 2000, at 0:40:11
In reply to Re: Shorter Trials, Cam W, posted by Cam W. on May 1, 2000, at 16:23:14
> Cam,
Atypical antipsychotics as stop gaps until the ADs kick in? Since the antipsychotics are being used at low doses, do they act differently than they do at their normal doses. If so, could you describe how they act at the low doses.
By the way, Amisulpride is an atypical antipsychotic that is used at large doses for schizophrenia but at low doses it acts very differently and is used for depression and other things. There is post in Dr Bob's tips from a psychiatrist who uses antipsychotics in small doses to treat the fatigue of chronic fatigue syndrome!
Best wishes,
AndrewB
Posted by AndrewB on May 2, 2000, at 2:36:57
In reply to Re: Shorter Trials, Cam W, posted by Cam W. on May 1, 2000, at 16:23:14
Scott,
I'll be kind of brief since my bedtime is creeping up.
Your comments supporting the use of 3 week trials make perfect sense to me. Thanks for explaining it to me.
The information I have on studies done with pramipexole is sketchy. One unpublished study concluded that pramipexole was as effective as fluoxetine for major depression. A new study came out this month that examines the use of pramipexole as an adjunct with an SSRI. The abstract is not available yet though. In another study pramipexole was used as an augmentor to various ADs with 6 patients after they failed to respond to an 8 week course with those antidepressants. Five of six of the patients had a greater than forty percent reduction in their depressive symptoms after 4 weeks. Most of their improvement had occurred during week 1.
In a separate case study they gave pramipexole to a bipolar man who was in a vegetative state. He was severely depressed and on a variety of mood stabilizers. He was taking no antidepressants though had tried a great variety of them, all without success. After six weeks on pramipexole a marked antidepressant response occurred. His functional improvement, with only low grade depression and no cycling, continued through his six month follow up. It was speculated by the author of this case study that pramipexole’s D3 activity may be responsible for pramipexole’s efficacy with psychomotor retarded conditions. It was also speculated that pramipexole may have a preferential response in atypical depression versus melancholic.
As far as differences between presynaptic D2 antagonists versus D2 postsynaptic antagonists I’m still not convinced there has be to much of a difference between the two. I don’t see why you would use the examples you do to make your point (reboxetine versus provigil?). Anyway, in my mind the major difference between the amisulpride and pramipexole may be the receptor sites they are selective for. Both are D2/D3 selective. But pramipexole has a preference for D3 over D2 receptors and has a preference for the D2/D3 receptors in the striatum over those in the limbic system. Contrast this with amisulpride which has limbic system selectivity and probably a preference for D2 over D3 receptors. By the way, pramipexole is a full agonist and bromocriptine and peroglide are partial agonists.
Yes keeping track of people’s responses to meds is a good idea. I have been soliciting and tracking peoples’ responses to amisulpride, pramipexole, amineptine and sulpiride. I also have tracked reboxetine responses, though less completely.
I’m the only one who has mentioned poop out on amisulpride on this board. I am sure of this. I had a partial poop out, where it lost its fatigue prevention properties. After about a month of this partial poop out I quit it for 4 days, and when I restarted, it was working fully again. I started reboxetine after this. I stopped amisulpride again for 4 days recently and I got quite depressed in the interim. I’ve been on it now for nearly 10 months. It takes 1 to 4 days to kick in whether I am on reboxetine or not.
You talk about targeting a secondary site to kick start a response at the primary site. I’m doing something like that, at least I think I am. The D2/D3 is the primary site for me but the D1 is a secondary site since D1 stimulation potentiates (or creates a supersensitivty) at the D2 (and D3?) receptors. I use amineptine to stimulate the D1 receptors.
The D3 receptor seems to be very much involved with mood. I don’t think its function has been clearly defined yet, as D3 specific agonists and antagonists have only recently been developed. To describe all that the D2/D3 are involved in and where would take a bit of space but relating to depression these receptors are involved with mood, anxiety and one’s sense of energy or fatigue.
Well, this post is a lot longer than I intended and I have stayed up longer than I should. So I shall say goodnight and again I thank you for this wonderful dialogue.
AndrewB
Posted by Peter S. on May 2, 2000, at 13:52:58
In reply to Re: Pramipexole, Scott, posted by AndrewB on May 2, 2000, at 2:36:57
I'm not sure where you get your information on shorter trials, but I can speak from direct experience: I started Nardil 7 weeks ago and have only really noticed a major effect in the last week. To advocate shorter trials without some very serious research seems to be giving people who might really benefit from a med the wrong information. Just my two cents. Peter
Posted by AndrewB on May 2, 2000, at 14:55:29
In reply to Shorter trials: don't believe it! , posted by Peter S. on May 2, 2000, at 13:52:58
> I'm not sure where you get your information on shorter trials, but I can speak from direct experience: I started Nardil 7 weeks ago and have only really noticed a major effect in the last week. To advocate shorter trials without some very serious research seems to be giving people who might really benefit from a med the wrong information. Just my two cents. PeterThank you Peter for your input. It seems that some people, myself included along with various professionals have made false conclusions concerning the advisability of shorter trials. Î think it is very tempting to say shorter trials are appropriate in our impatience to arrive sooner at a remission of depression. Perhaps some people, with special metabolisms, benefit with short trials but I wonder how such people would be singled out from those that may take longer to respond.
Posted by AndrewB on May 2, 2000, at 15:00:27
In reply to Re: Pramipexole, Scott, posted by AndrewB on May 2, 2000, at 2:36:57
Amiuslpride has an equal affinity for the D2 receptor and the D3 receptor rather than having a greater affinity for the D2.
The D2 receptor MAY NOT be involved with mood. The D3 receptor seems to be involved in mood, anxiety, motivation and general sense of well being.
Posted by JohnL on May 3, 2000, at 5:05:30
In reply to Shorter trials: don't believe it! , posted by Peter S. on May 2, 2000, at 13:52:58
I think to assume that either long trials or short trials are appropriate is too narrow-sighted. That's because it assumes some common underlying cause of the depression. I just don't believe that. One person's chemistry may be such that a downregulation of receptors is needed, and thus a long trial is needed to accomplish that. In other people, it may have nothing at all to do with downregulation of anything, but simply a matter of raising serotonin, or calming down overly excited neurons, or stimulating sluggish ones, or whatever.
I don't think it's an either/or proposition. It's not like only one way is correct and the other isn't. It all comes down to basics...chemistry. To assume either approach is always correct and the other is always wrong assumes that we know more about psychiatry than we actually do.
I am an advocate of short trials in most cases (not all) simply because I've seen it over and over and over in real life. It is a very real phenomenon that occurs. I can't understand why more people haven't stopped to ask themselves, "Why does this phenomenon occur? Is there some way we can better grasp it and take advantage of it?" Rather than ignoring it as if it didn't exist.
But in NO case do I advocate short trials in place of long ones for longterm therapy. Instead I advocate short trials for identifying superior drug matches, and weeding out inferior ones. Once that is done, then the longer trials focus only on the superior matches. Those were the ones, or one, that showed remarkably fast results with few side effects. If everybody could sample every drug for one week each, I guarantee you everybody would discover one that fits that description. Everyone would discover they have a favorite, and that favorite is different than someone else's. Again, chemistry. Then once the weeding process has provided the needed clues to know what the heck is going on with this patient, we can then focus on getting them completely well with longer trials on the identified superior meds. I think too often patients submit to a drug for months or years that is working OK, not being aware that a much better drug was ignored. Without short trials--or as I prefer to look at it, short 'comparisons'--we would never know.
So I think there are two important points for consideration:
1. They aren't short trials, but rather comparisons. Purpose is to find a favorite for a longer trial.
2. Neither short comparisons or long trials are correct in all cases. Each patient is different. But the more time and the more drugs a patient has failed, the more crucial it becomes to do some quick 'probing'. The first-time patient with no drug experience is probably better off with standard long trial psychiatry. But after multiple failures, I feel standard psychiatry should step aside in embarrassment and let a different strategy take priority.But the bottom line is, regardless of the many different opinions, we all know for a fact that some people do indeed respond fast to the right drug. We've seen it. We've heard of it. Search this board for a few hours going back months and you'll see the proof. And some doctor's office's see more of it than not. Why is that? Why should we not try to better understand this phenomenon? Are we intersted in getting the patient as quickly as possible or not? Are we open to discovery, or are we too set in our ways to think there isn't something else out there we don't know?
JohnL
Posted by AndrewB on May 3, 2000, at 10:54:29
In reply to Re: Shorter trials: believe it! , posted by JohnL on May 3, 2000, at 5:05:30
John,
You are an excellent spokesperson for Dr. Jensen’s methods. If you are not a PR professional already, you should consider such work!
I did a Medline search. I could find no evidence to support Dr. Jensen’s claim of a correlation between an initial improvement (or non response) and a long term AD response. This idea of one’s first reaction being the true reaction is so simple it seems naive to think that it wouldn’t have been confirmed by now. After all, it seems diagnostic criteria that would allow for faster trials has been something of a holy grail of the psychiatric community. Dr. Jensen’s ideas still need to undergo rigorous testing before they can be separated from the long parade of various fallacious claims made by the ambitious and self promoting. But there is some truth in most everything and I wonder if there is a subpopulation of treatment resistant depressives who, because they respond quickly to antidepressants, would be well served by Jensen’s protocol.
Best wishes, as always,
AndrewB
Posted by KarenB on May 3, 2000, at 12:07:21
In reply to Re: Shorter trials: believe it! , posted by AndrewB on May 3, 2000, at 10:54:54
Hi.
Just me with my $.02 again...from a strictly emotional point of view:
If nothing else, it seems to me that when in the pit of despair, one unsuccessful 6-8 week trial after another is enough to send one straight to the bottom of the pit.
Why not try to find an AD (QUICKLY!) that opens the suffering patient's eyes at least for a moment, to see that there is hope and that feeling well IS POSSIBLE. Even if there is no solid proof as of yet that it continues in the long term, it would give me the will to go on - to try other meds within the same class at least.
When I have been at my lowest, the one thought that conjures the strongest suicide ideology is the one that says, "I'm never going to get better - I'm always going to feel like this."
If I had put my trust in a doc who was bent on SSRIs and insisted on the long term trials suggested, I may be dead today.
Karen
Posted by SLS on May 3, 2000, at 16:02:15
In reply to Re: Shorter trials: believe it! , posted by AndrewB on May 3, 2000, at 10:54:29
> > I'm not sure where you get your information on shorter trials, but I can speak from direct experience: I started Nardil 7 weeks ago and have only really noticed a major effect in the last week. To advocate shorter trials without some very serious research seems to be giving people who might really benefit from a med the wrong information. Just my two cents. Peter
>
> Thank you Peter for your input. It seems that some people, myself included along with various professionals have made false conclusions concerning the advisability of shorter trials. Î think it is very tempting to say shorter trials are appropriate in our impatience to arrive sooner at a remission of depression. Perhaps some people, with special metabolisms, benefit with short trials but I wonder how such people would be singled out from those that may take longer to respond.
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Thank you, Andrew. I am continually admiring of your temperament.There have been some pretty passionate subject headers here.
How we Babblers approach this issue, and the posture we take as we discuss it, will influence and affect many people here, possibly the majority. This bears a great deal of responsibility. In my opinion, it is incumbent upon us to realize that there will be some people here, lurkers included, who are on the cusp of making critical treatment decisions.
My mind has been open regarding the validity and applicability of the method proposed by Dr. Jensen of using short trials of antidepressants to treat depression. I consider it to be a reasonable approach when testing certain drugs in certain situations, but not for most others. I have posted an opinion detailing a dichotomy of these drugs in another thread. There are many reasons why I cannot at this time support short trial periods, some of which have not yet been mentioned.
Do some doctors let their patients linger too long on drugs that are ineffective, have intolerable side effects, and actually worsen the condition being treated? Of course. Should these doctors modify their treatment algorithms? Probably.
Let us not allow ourselves to fall into the trap of bipolar thinking.
My doctor, a clinical investigator who spends more time attending psychiatric conferences worldwide than he does in his office, has never heard of Martin Jensen, MD. This may or may not be important. Yesterday, I spoke to a clinical researcher at Columbia Presbyterian in NYC. His name is littered throughout the medical literature. He has never heard of Martin Jensen, MD. I described to him the premise (as described here by others) of his treatment method of performing short trials to screen for the *best* antidepressant. In short, he said that this idea is not consistent with everything he believes or has experienced. He offered some characterizations of these sorts of claims and the types of people who usually make them. This may or may not be important.
This doctor at Columbia did make one very salient point that I think is relevant and possibly revealing. To his knowledge, Dr. Jensen has never presented any of his ideas or research material at a psychiatric conference or symposium. The idea of using short trial periods would not withstand critical review by the psychiatric community. This is not because the members of this community are fixed to some dark-ages narrow-minded bias, but because such claims do not hold up to the scrutiny of simple questions. Regarding the explanations offered by Dr. Jensen as to how different drugs work, this researcher reacted by saying "we are not there yet". I found this to be an interesting choice of words. He then described to me in some detail why it is obvious that we are not.
If the proposals of Dr. Jensen would greatly improve the lives of the millions of people suffering from depression, why would he not offer them for peer review, rather than be content only to write a book? Perhaps he feels that he can reach more sufferers more quickly that way. He may passionately believe everything he claims. I remain dubious of his accuracy.
I have not read Dr. Jensen's book. There may be a great many valid and applicable perspectives that it has to offer. However, the use of short trial periods is the issue being discussed here.
I am playing with some ideas to further pursue the evaluation of the short-trial strategy using our Babble-board as a source of information.
In the mean time, I would not recommend to anyone that they terminate a trial of a "traditional" antidepressant (one for which depression is its primary indication) before allowing it at least three weeks to work. It may well take longer if dosage adjustments are required.
This post could have been much longer. There is quite a bit more that I could have added, and many aspects of this issue I haven't addressed here. I am sure this is true of the other participants in this discussion. It is of such great importance.
- Scott
Posted by JohnL on May 4, 2000, at 1:29:07
In reply to Re: Shorter trials: believe it! , posted by AndrewB on May 3, 2000, at 10:54:29
> John,
>
> You are an excellent spokesperson for Dr. Jensen’s methods. If you are not a PR professional already, you should consider such work!
>
> I did a Medline search. I could find no evidence to support Dr. Jensen’s claim of a correlation between an initial improvement (or non response) and a long term AD response. This idea of one’s first reaction being the true reaction is so simple it seems naive to think that it wouldn’t have been confirmed by now. After all, it seems diagnostic criteria that would allow for faster trials has been something of a holy grail of the psychiatric community. Dr. Jensen’s ideas still need to undergo rigorous testing before they can be separated from the long parade of various fallacious claims made by the ambitious and self promoting. But there is some truth in most everything and I wonder if there is a subpopulation of treatment resistant depressives who, because they respond quickly to antidepressants, would be well served by Jensen’s protocol.
>
> Best wishes, as always,
>
> AndrewBToo funny Andrew. lol. I didn't realize I was sounding like a spokesperson until you pointed it out. I'm embarassed. That wasn't at all what I was attempting to do. Jensen isn't even my own physician. He isn't the one that got me well. Personal application of his methods did though.
It's true we need empirical evidence to backup any new theory. Theory...that's an important issue here. After all, everything we know about psychiatry is theory. There aren't any facts. Even the best empirical evidence we have of any one theory suggests about a 70% success ratio in reducing symptoms by 50%. That's not exactly something to be embracing or doing handstands over. But it is the best we have, and the tendency over time is to accept longstanding theories as facts, even though they aren't.
Just a few centuries ago everybody knew the earth was flat. Then some innovative quack named Columbus came along and challenged the theory. What was accepted as fact for so long soon became a point of humor. Don't get me wrong, I'm not likening Columbus to Jensen at all. Not even close. But it kind of makes the point that other less known and less accepted theories sometimes do prove to have merit. And just a decade ago it was fact that ulcers were caused by stress and/or the wrong foods. All kinds of behavioral programs and diets changes were the treatments. And they worked. But today, a mere decade or so later, we know ulcers are caused by a specific bacteria. They are aggravated by stress and food. But the root cause is bacteria. And the treatment is an antibiotic, with or without behavioral or diet changes. Just another example of a longstanding theory challenged--one assumed to be fact by empirical evidence.
I think I'm trying to make the point that I am not a spokesperson for Jensen, but rather a spokesperson for any new theory that works. Jensen's or anyone else's. Doesn't matter. If it's new and it works, I'm all ears. In Jensen's case, it's not as if he has built some theory around a few isolated cases. Not even. His theories are based on hundreds of patients who achieved excellent results in his office by way of his approach...after being failed by multiple doctors and drugs. These were the kind of patients we see here a lot. Nearly 100% get excellent results in 8 visits or less. Usually 2 or 3. Any theory with those kinds of results is welcome in my book. Even if it is limited at this time to one doctor's office. But the fact that it is now being studied in some medical schools is promising. Hopefully the generations of doctors 5 and 10 years from now will have a different approach and better results than the ones today.
Geeezz, I sound like a spokesperson again, don't I? lol. Hey, I just love to see people get well. And I really don't care how that is achieved. Whatever works. For the time being, there is one little ole doctor's office in California where a lot of longtime sufferers are getting well, by the hundreds every year. I wish I knew a local doctor with that kind of performance.
JohnL
Posted by JohnL on May 4, 2000, at 1:57:09
In reply to Re: Shorter comparisons breed hope , posted by KarenB on May 3, 2000, at 12:07:21
> Hi.
>
> Just me with my $.02 again...from a strictly emotional point of view:
>
> If nothing else, it seems to me that when in the pit of despair, one unsuccessful 6-8 week trial after another is enough to send one straight to the bottom of the pit.
>
> Why not try to find an AD (QUICKLY!) that opens the suffering patient's eyes at least for a moment, to see that there is hope and that feeling well IS POSSIBLE. Even if there is no solid proof as of yet that it continues in the long term, it would give me the will to go on - to try other meds within the same class at least.
>
> When I have been at my lowest, the one thought that conjures the strongest suicide ideology is the one that says, "I'm never going to get better - I'm always going to feel like this."
>
> If I had put my trust in a doc who was bent on SSRIs and insisted on the long term trials suggested, I may be dead today.
>
> KarenKaren,
You make a very good point. In reading a book called The Successful Treatment of Brain Chemical Imbalance, by Dr Jensen, he discusses your point also. He stresses it is very important to give the patient hope, to keep them busy, and to offer them a sense of ownership in their own treatment. When leaving the doctor's office with three trial-size prescriptions of three different meds to be compared seperately in three short trials, in addition to one or two antidote pill samples for adverse reactions, and training/instructions on exactly how to dose them, how much time, washout time, what to do if an adverse reaction, etc...this all gives the patient a sense of ownership and keeps hope alive. The patient is no longer a suffering guinnea pig of some doctor, but rather a recovering sufferer engaged in the aggressive active mode of their own recovery. Worth mentioning though, I think, is that this method is not appropriate for someone who is in a suicidal state or a psychotic state.But for the patient who has a history of multiple failures with multiple drugs and/or doctors, this method does indeed provide hope. And as you mention, there are times when nothing is more important than mere hope. That is number one before anything else. Being involved in a quick trial regimen accomplishes that.
As a personal example, my doctor already knew I had tried Paxil, Zoloft, and Prozac. All were somewhat effective after 2 to 3 month trials, but there were still considerable residual symptoms. By then more than a year has passed, and I was still suffering. My hope was very very low, actually nonexistent. So it became obvious I should try drugs of other classes, but he wanted to be sure I was on the best match SSRI before doing that. So he prescribed two weeks each of Effexor, Celexa, and Luvox, with a one day washout inbetween. I was of course skeptical of any more SSRIs, BUT I suddenly had HOPE. He said I could then choose my favorite. I liked that idea. Personal ownership. Hope. Unfortunately none of the SSRIs turned out to be the best match for me. But it didn't take long doing the same procedure in other drug classes to stumble onto something that did work. And the whole time the one most important thing I had lost was revived....HOPE.
JohnL
Posted by JohnL on May 4, 2000, at 2:25:28
In reply to Re: Shorter trials: believe it! , posted by SLS on May 3, 2000, at 16:02:15
Scott,
You are correct, in my opinion, of everything you so eloquently stated in your post. (Have you ever considered being a writer?)Jensen hasn't to my knowledge presented his ideas at conferences and such. Maybe he has, I don't know. That's because he's too busy getting patients well instead. As I've mentioned, that's his passion. He's not your typical political or academically involved psychiatrist, but rather one who spends all his time doing what he was trained to do...get people well. Hard to do that when spending time on the road doing conferences. He is absolutely thrilled at getting people well, and that's what he spends his time doing. But he has presented his ideas to medical schools, where it can make a real difference in longterm psychiatry, and it is actually being taught at this moment as we speak. So though yours and my doctors won't likely be aware, the upcoming generation will.
And on the subject of conferences, there are so many. How could anyone keep up. I drove to Boston (1 1/2 hours away) to see Dr Bob when he was there at a conference. The place was flooded with hundreds upon hundreds of people with MD, psychologist, or psychiatrist on their name badges. But you know what, neither of my two psychiatrists had even heard of that conference.
And of course quick trial methods wouldn't stand critical review by the psychiatric community. Neither would Columbus's theory of a round world, or a bacterial theory of ulcers. Additions or modifications to longstanding theories don't happen overnight. And there is usually a lot more resistance and critique than acceptance early on.
And it's true when researchers say "We aren't there yet". But that doesn't mean nobody is there yet. Some few people are already there. Just because the masses aren't doesn't really mean one thing or the other. Just that while some people might already be there, we as a whole are not.
All I know for sure is the facts...the best psychiatry as whole can offer us in empirical evidence is 70% success in reducing symptoms by 50%. And which drug choice accomplishes that is not much better than flipping a coin. I personally cannot do acrobatics over that. I actually do not embrace one theory or another, but I do relish exploring new ideas. I try to find fault. When I can't, I begin to accept. Every fault and critique you have offered so far, I've already been there. I was at first a stronger critic than you. But the more I read, studied, and pondered the issue, the more sense it all made. But it didn't happen overnight. It will take even longer for psychiatry as a whole.
Posted by Cam W. on May 4, 2000, at 7:04:44
In reply to Re: Shorter trials: Scott , posted by JohnL on May 4, 2000, at 2:25:28
John - I've tried to stop myself from writing this about 3 times. I, like Scott, have began asking around about Dr.Jensen and also respect your opinion. I asked some of the pdocs at work and a couple of antidepressant researchers (and their "Doogies") from the University. A total of about ten docs in all and all said, "Who?".I got the lecture on "extraordinary proof of extraordinary claims" and "doesn't this fly in the face of all we know about physiology" and "where has he published, outside of Chapters?" (one of the Doogies - residents - thinks he could get published at Chapters, too).
I'm not saying that Jensen's theories may not work, it is that an explicit mechanism of action is missing. Jensen needs to get in the face of the major researchers and prove his claims to be accepted or he will be shrugged off as another "New Age Nutcase".
Sorry to post before reading the book (not at our University medical library), but I just thought you might like to know what they think out here in the sticks. Sincerely - Cam W.
Posted by DC on May 4, 2000, at 15:33:22
In reply to Shorter Trials with ADs, posted by AndrewB on April 30, 2000, at 19:33:32
I agree with Peter. I took Nardil for three years and it was very effective, but it didn't start to work until about 6wks, and I didn't get maximum improvement until maybe three months later. (At first I didn't notice much of anything). IT DEPENDS ON WHAT MEDICINE YOU ARE TAKING! Be careful about the advice you are giving here. --Dwight
Posted by Peter S. on May 5, 2000, at 1:46:54
In reply to Re: Shorter Trials with ADs, posted by DC on May 4, 2000, at 15:33:22
> I agree with Peter. I took Nardil for three years and it was very effective, but it didn't start to work until about 6wks, and I didn't get maximum improvement until maybe three months later. (At first I didn't notice much of anything). IT DEPENDS ON WHAT MEDICINE YOU ARE TAKING! Be careful about the advice you are giving here. --Dwight
I would just like to add that I truly understand the frustration that people feel about spending months and sometimes years trying to identify the appropriate anti-depressant and in the meantime dealing with incredible feelings of desperation and hopelessness. I myself have spent the last four years in a desperate quest for the right med and failed many trials of practically all the meds on the market.
It would have been wonderful to have some way to identify the right drug within a week or so by some simple comparison test. Looking back on it it is very difficult to say whether I could tell within a week what felt like the "right" medication. I know the side effects for some of the meds were really nasty; but the traditional advice is to "start low and go slow" and sometimes the side effects would ease after time. I would stop a drug because of the side effects or because it had no clinical effect or even would make me feel worse. The side effects of Nardil were bearable and that is the only reason I stuck with it this long.
If Dr. Jensen has success with his technique, more power to him, however my main objections would be:
a) It seems that there is a huge amount of individual variation in response to meds, including time of onset. If you respond immediately to a med then great, but how do you know you are not one of those who respond after 3 weeks?b)From everything I've read noone really knows how or why these drugs work, or especially why there is a lag time between first taking the drug and it's therapeutic effect. From what I gather, all the theories about down regulation of receptors is purely speculative. It is possible that the good Doctor Jensen knows something that nobody else does, but where and how did he come up with this information?
Anyway JohnL: if it works for you that's great and I appreciate your sharing your experience with us. However, I believe that people need to be aware that Dr. Jensen's ideas are very controversial and that they do not agree with most current, accepted psychiatric knowledge.
Peter S
Posted by JohnB on May 5, 2000, at 2:33:32
In reply to Re: Shorter trials: believe it! AndrewB , posted by JohnL on May 4, 2000, at 1:29:07
>Jensen isn't even my own physician. He isn't the one that got me well. Personal application of his methods did though. -JohnL
John; I for one would like to hear in more detail the story of how you used those methods to claw your way out. How you moved from meds that didn't work that well to where you are now. I'm curious, for instance, how you found out about Adrafinil, why you thought it would help, etc.
I mean, only if you want to tell it . . . . I know you've covered some things in various posts . . . . . would love to hear it all in one post -JohnB
Posted by JohnL on May 5, 2000, at 4:35:40
In reply to Re: Shorter trials: John L , posted by Cam W. on May 4, 2000, at 7:04:44
Cam,
I know. I'm aware of Jensen's skeptics. After all, there was no bigger skeptic than me. My skepticisms were the same as everyone has been mentioning in these threads. Believe me, I understand.
When I was calling Jensen a new age nutcase, a quack, crap, etc....one of his patients calmly and humbly suggested I read his book or talk to him first. I humbly pass on the same suggestion. When all one knows is the general concepts as summarized by some nobody (me)--in the absence of greater detail--it is very easy and tempting to be skeptical.
Though I could spend pages and pages blowing holes in every skeptical stance encountered, I will merely repeat the most important thing. That is,...Jensen's methods do NOT fly in the face of what we know about physiology. It appears to at first on the surface, but it doesn't. There isn't an explicit mechanism of action missing in his practice, but rather one missing in mainstream practice.
Jensen--as Head of Psychiatry--is no stranger to mainstream psychiatry. He's been in there for decades. He is merely attempting to answer questions that mainstream psychiatry has not 'adequately' anwered for him.
Why do some patients respond quickly? Why some slowly? Why some not at all? Why do many get worse instead? Why residual symptoms? Is there something else besides receptor downregulation going on? Why 70% success rates? Why settle for 50% reduction of symptoms as measurement criteria? Why do different patients with identical symptoms respond 100% to drugs of totally different classes? He was not satisfied with the answers mainstream psychiatry provided. He was not interested in finding answers to gain praise or scientific acknowledgement. Rather he wanted to get patients well. That's all.
That's his passion--not merely his career--that's what he does. I doubt seriously he is about to compromise his office time with patients to go out and 'prove' his ways to the world. I think he could care less what others do in THEIR hospitals, he just wants extraordinary results in his own. And the fact is, he is getting them. Regardless of what me or you or anyone else thinks, we can't argue with results. His patients are happy. Nearly all of them were failed by traditional psychiatry and conventional physicians. The proof's in the pudding, so to speak.
The one most important concept to grasp is that his methods do NOT fly in the face of what we know. They instead add on and enhance. It's not an either/or proposition. His methods and traditional psychiatry are married, not divorced. They go together, not in opposition. Without reading the book, it would be way to lengthy here (already is) to explain why.
I think I do not do a good job of communicating on this topic. I would probably best stop trying. All I can say is, read the book. Then be skeptical or not.
JohnL
Posted by SLS on May 5, 2000, at 10:22:26
In reply to Re: Shorter trials: Scott , posted by JohnL on May 4, 2000, at 2:25:28
Hi John.
Consider me the Devil's advocate.
I have not excluded the idea of using short trials of antidepressants to screen for effective treatments, but...
> Jensen hasn't to my knowledge presented his ideas at conferences and such. Maybe he has, I don't know.> That's because he's too busy getting patients well instead.
How do you know that this is the reason?
> As I've mentioned, that's his passion. He's not your typical political or academically involved psychiatrist, but rather one who spends all his time doing what he was trained to do...get people well.
He is not any different from the hoards of local practitioners and internationally renowned researchers, most of whom do not seem to give any credence to the idea that an antidepressant can be evaluated within a week.
> Hard to do that when spending time on the road doing conferences.
He seems to have plenty of time to lecture at small conferences outside the milieu of mainstream psychiatric review, consult with the staffs of yet unnamed medical schools, tour, give interviews, and promote his book.
> He is absolutely thrilled at getting people well, and that's what he spends his time doing.
My doctor does too.
> But he has presented his ideas to medical schools,
How many? Which ones? Are these ideas presented as proposed alternatives to ponder or as putatively effective treatments to be endorsed and deployed?
> Jensen hasn't to my knowledge presented his ideas at conferences and such. Maybe he has, I don't know. That's because he's too busy getting patients well instead.
He would succeed in getting more people well if he were to demonstrate to the international psychiatric community that his methods work and that his ideas are valid with regard to the mechanisms by which drugs exert their therapeutic actions in the brain. He has not. He must feel absolutely sure that these ideas would be rejected. Why else would he not have tried? Where is the altruism here?
> And on the subject of conferences, there are so many.
There are not so many important well-recognized conferences that his presentations would have gone unnoticed by so many people in the field who are so dedicated to figuring things out. There are grapevines within the psychiatric community, just as there are in other fields of scientific endeavor. After all, this is how the echo of the "Big Bang" was first recognized in 1965.
> How could anyone keep up. I drove to Boston (1 1/2 hours away) to see Dr Bob when he was there at a conference. The place was flooded with hundreds upon hundreds of people with MD, psychologist, or psychiatrist on their name badges. But you know what, neither of my two psychiatrists had even heard of that conference.
I guess it must have been a pretty small one, and not well recognized as being important. Either this, or your two psychiatrists are ignorant to important psychiatric conferences. I hope that it is not the latter. Are your two psychiatrists limited to private practice, or are they published researchers on the staff of a university or other institutional program? The doctors that I have spoken to over the last three weeks belong to the latter category.
> And of course quick trial methods wouldn't stand critical review by the psychiatric community. Neither would Columbus's theory of a round world, or a bacterial theory of ulcers.
This is probably the easiest trick in the book of forensic strategy. For every valid idea for which it applies, there must be millions for which it does not.
> Additions or modifications to longstanding theories don't happen overnight. And there is usually a lot more resistance and critique than acceptance early on.
Yes, there seem to be many examples of this. Initial skepticism is often part of a healthy process of affirmation. It helps prevent the embracement of invalid, ineffective, or dangerous ideas.
> And it's true when researchers say "We aren't there yet". But that doesn't mean nobody is there yet.
Is Dr. Jensen? Regarding what, specifically?
> Some few people are already there.
Are you sure? Who? Where is it that they have arrived?
I don't believe it. When one reads through the medical literature, it quickly becomes apparent that *we* do not have the information nor the understanding to arrive at the conclusions reached by Dr. Jensen. As to what causes depression, what somatic anomalies exist during depression, and how antidepressants work cannot possibly be anything more than speculation. Of course, there may be a covert conspiracy to keep corroborative information away from the rest of the world.
> Just because the masses aren't doesn't really mean one thing or the other. Just that while some people might already be there, we as a whole are not.
Might, maybe, possibilities. Just because none of the samples of lunar rock brought back during the Apollo program did not include Swiss cheese, does not mean that there isn't some up there.
> All I know for sure is the facts...the best psychiatry as whole can offer us in empirical evidence is 70% success in reducing symptoms by 50%.
Facts continued... These numbers represent the results of clinical trials that use ONE drug for ONLY 4-6 weeks. It is becoming increasingly apparent that many people require more than one drug, all of which may take more than one week to work. These facts are not at all relevant to the justification of short trials, anyway.
> And which drug choice accomplishes that is not much better than flipping a coin.
This statement contradicts the those made by Dr. Jensen, who claims to be able to choose drugs based upon symptom profiles. Right?
> I personally cannot do acrobatics over that. I actually do not embrace one theory or another, but I do relish exploring new ideas.
So do I. I've even come up with a few of my own. This sort of thing is obviously a critical necessity when the current state of psychiatry is inadequate to treat people effectively. I would need to explore further the validity and applicability of Dr. Jensen's ideas and methods by reading his book. However, from those words of his that I have read on the internet, I cannot at this point agree with them.
> I try to find fault. When I can't, I begin to accept. Every fault and critique you have offered so far,
Any one in particular?
> I've already been there. I was at first a stronger critic than you. But the more I read, studied, and pondered the issue, the more sense it all made. But it didn't happen overnight.
> It will take even longer for psychiatry as a whole.
If at all. This will depend upon whether or not these notions are consistent with the workings of God's universe. If the notion that one-week drug trials can be used to screen for an individual the best of those antidepressants currently available is not, this would be a dangerous one.
- Scott
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