![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 25 to 49 of 86. Go back in thread:
Posted by SLS on January 5, 2008, at 6:43:29
In reply to Re: STAR*D confirmed what patients already knew, posted by Cecilia on January 5, 2008, at 6:04:46
> The other thing I don't understand about the study is where they found these depressed people who hadn't already tried these very common drugs already. They certainly didn't include anybody with chronic depression or they would have already tried them. So they probably got much better results than in the "real world". Cecilia
"Entry criteria were broad and inclusive
Patients had to:
• Be between 18 and 75 years of age
• Have a nonpsychotic major depressive
disorder, identified by a clinician and confirmed
with a symptom checklist based on
the Diagnostic and Statistical Manual,
fourth edition revised,20 and for which
antidepressant treatment is recommended
• Score at least 14 on the 17-item Hamilton
Rating Scale for Depression (HAMD17)
21
• Not have a primary diagnosis of bipolar
disorder, obsessive-compulsive disorder, or
an eating disorder, which would require a
different treatment strategy, or a seizure
disorder (which would preclude bupropion
as a second-step treatment)."
The investigators made no other exclusions. Unless I missed it, and with my reading skills so impaired, this is entirely possible, there is no mention of excluding subjects whom were previously treated with psychotropic drugs. The subjects studied seems to be representative of the general population - the objective of the study.
"FEW DIFFERENCES BETWEEN
PSYCHIATRIC, PRIMARY CARE PATIENTS
The patients seen in primary care clinics were
surprisingly similar to those seen in psychiatric
clinics.27,28 The two groups did not differ in
severity of depression, distribution of severity
scores, the likelihood of presenting with any of
the nine core criteria of a major depressive
episode, or the likelihood of having a concomitant
axis I psychiatric disorder in addition
to depression (about half of participants
in each setting had an anxiety disorder).
Recurrent major depressive disorders were
common in both groups, though more so in
psychiatric patients (78% vs 69%, P < .001),
while chronic depression was more common
in primary care than in psychiatric patients
(30% vs 21%, P < .001). Having either a
chronic index episode (ie, lasting > 2 years) or
a recurrent major depressive disorder was common
in both groups (86% vs 83%, P = .0067).
That said, primary care patients were
older (44 years vs 39 years, P < .001), more of
them were Hispanic (18% vs 9%, P < .001),
and more of them had public insurance (23%
vs 9%, P < .001). Fewer of the primary care
patients had completed college (20% vs 28%,
P < .001), and the primary care patients tended
to have greater medical comorbidity.
Psychiatric patients were more likely to have
attempted suicide in the past and to have had
their first depressive illness before age 18"
From: "The STAR*D study: Treating depression in the real world"- Scott
Posted by bulldog2 on January 5, 2008, at 9:54:58
In reply to What have we learned from the STAR*D study?, posted by SLS on January 4, 2008, at 5:42:45
> What have we learned from the STAR*D study?
>
> What are its strengths and weaknesses?
>
>
> "The STAR*D study: Treating depression in the real world"
>
> http://sl.schofield3.home.att.net/medicine/the_star_d_study_real_world.pdf
>
>
> - ScottDid this study include the number of people who drop out of treatment because of side effects? That seems to be a big problem especially on this board. For instance how many people will not try an maoi because of all the restrictions even though they may be very effective.
Posted by linkadge on January 5, 2008, at 11:00:50
In reply to Re: STAR*D confirmed what patients already knew, posted by Cecilia on January 5, 2008, at 6:04:46
They probably had tried many of these drugs before which begs the question as to why they got better this time. The possible reason being the quality of care they got from this study, which is another reason a placebo seems crucial IMO.
Linkadge
Posted by linkadge on January 5, 2008, at 11:06:29
In reply to Re: STAR*D confirmed what patients already knew » Cecilia, posted by SLS on January 5, 2008, at 6:32:26
>Using comparator drugs with established efficacy >saves a lot of time.
Yes, placebos are good comparitor drugs with well established efficacy.
>Is it ethical at this point in the evolution of >psychiatric drugs to treat suffering with >nothing but sugar pills?
We havn't evolved with psychiatric drugs much in the past 15 years. One would have likely got the same responce to treatments available in the early 90's, that is, at a rate highly comparible to placebo. So is it ethical to use a highly efficactious treatment (ie placebo)? The answer is yes IMHO.
Linkadge
Posted by Larry Hoover on January 5, 2008, at 13:08:41
In reply to Re: STAR*D confirmed what patients already knew, posted by Cecilia on January 5, 2008, at 6:04:46
> The other thing I don't understand about the study is where they found these depressed people who hadn't already tried these very common drugs already. They certainly didn't include anybody with chronic depression or they would have already tried them. So they probably got much better results than in the "real world". Cecilia
The only exclusion factor with respect to the medications in levels 1 and 2 of this study was: "a clear history of nonresponse or intolerance (in the current major depressive episode) to any protocol antidepressant in the first two treatment steps ." Not never used, only not failed use in this actual depressive event. If you read the study demographics, you'll see that the majority of subjects were chronic recurrent depressives.
The design of this study was absolutely "real world". Subjects were simply individuals who presented to their doctor, seeking treatment for depression. Comorbid medical conditions, past history of drug failure, yadda yadda, did not prevent enrollment. The exclusion factors were really quite limited. Again, reading the study methodology would answer these questions.
Here's one such link:
http://ajp.psychiatryonline.org/cgi/content/full/ajp;163/1/28
Lar
Posted by Larry Hoover on January 5, 2008, at 13:31:01
In reply to Re: STAR*D confirmed what patients already knew » Cecilia, posted by linkadge on January 5, 2008, at 11:00:50
> They probably had tried many of these drugs before which begs the question as to why they got better this time. The possible reason being the quality of care they got from this study, which is another reason a placebo seems crucial IMO.
>
> LinkadgeThe methodology could not include placebo. It is an ecological study. Has your doctor ever offered you a placebo? Do you consider placebo treatment to be a common clinical practise?
The study rationale and design is fully discussed in this paper: "Sequenced treatment alternatives to relieve depression (STAR*D): rationale and design." Unfortunately, full text is only available to subscribers. I'd love to read it, if anyone could send me a copy.
The methodology was not designed to show what works. It was designed to deal with non-responders. How do you treat people who fail with the most popular treatment option (i.e. citalopram)? Subjects were allowed to choose e.g. augmentation, but they didn't know which augment they'd receive. If that failed, they could choose a complete change in meds, but again not knowing which they might receive. I don't think placebo would have told us anything about how to treat the non-responders to Level 1 treatment. (Particularly, if one holds the view that antidepressant response *is* placebo response.)
The real meat of the study, IMHO, was the collection of all the patient histories, which can then be correlated to treatment options. Some of the variables considered are: "1) demographic features (e.g., age, race, ethnicity, and gender), 2) social features (e.g., education, employment status, income, insurance, and marital status), and 3) clinical features (e.g., age at onset of major depressive disorder, length of the current major depressive episode, number of major depressive episodes, length of illness, course of illness [single or recurrent], major depressive disorder subtype [anxious, melancholic, and atypical features], family history of depression, concurrent general medical and axis I psychiatric disorders, symptom severity, and functional status at baseline)." These variables may go some way to predicting responsivity, something that the artificial construct of a placebo-controlled efficacy trial can never show.
There are more than eighty papers on Pubmed referencing STAR*D, many of which take a look at one or more of these demographic, social, or clinical features.
Lar
Posted by linkadge on January 5, 2008, at 15:24:47
In reply to Re: STAR*D confirmed what patients already knew » linkadge, posted by Larry Hoover on January 5, 2008, at 13:31:01
>The methodology could not include placebo. It is >an ecological study. Has your doctor ever >offered you a placebo? Do you consider placebo >treatment to be a common clinical practise?
Well, then change the methodology. Its not so much that doctors can offer placebos, but if they knew that medications were essentially no better than placebos, they might decide against riskier treatments in favor of other treatments. For instance, they might choose lower (safer) doses, or choose drugs with a more benign side effect profile. Ie, you might be taking 25mg of trazodone as opposed to developing heart disease on 375mg of effexor etc.
>The methodology was not designed to show what >works. It was designed to deal with non->responders. How do you treat people who fail >with the most popular treatment option (i.e. >citalopram)? Subjects were allowed to choose >e.g. augmentation, but they didn't know which >augment they'd receive. If that failed, they >could choose a complete change in meds, but >again not knowing which they might receive. I >don't think placebo would have told us anything >about how to treat the non-responders to Level 1 >treatment.
Well, strong response to a placebo might have helped support the finding that pretty much all choices are essentially equivilant. That most treatment algorigthms essentially led to the same rate of response seems suggestive in itself of a potentially high response to placebo.
I do think it really matters that doctors know the true incidence of placebo response. Many of these treatments are not benign treatments and so, loading sombody up with neurotoxic doses of certain AD's may not be justified. That is important to know.
>These variables may go some way to predicting >responsivity, something that the artificial >construct of a placebo-controlled efficacy trial >can never show.
You could include these same types of analysis in a study that includes a placebo. It might even help to uncover exactly what factors predict placebo response.
I personally think that the study purposly did not include a placebo. This was an important study which was not funded by drug companies. It was intened in some ways to (re)establish the efficacy of treatments in general. The last thing they wanted in this study was to have a pesky little placebo response disclaimer tagged to the end.
Consider the fist round, %30 of people responded to citalopram. That is slightly less than what previous studies for citalopram have stated. However, in many of such studies, the placebo response comes in about the same rate. On to round two...Eventually, you're going to get a final result saying yeah sure %70 of patients can improve, with one drug or another, yet %60-80 can improve with placebo. Wow, all of a sudden that %70 is meaningless.
Its one of those things where sometimes the most basic assumptions are wrong IMHO.
Linkadge
Posted by Dinah on January 5, 2008, at 15:50:49
In reply to Re: STAR*D confirmed what patients already knew, posted by linkadge on January 5, 2008, at 15:24:47
SSRI's clearly have an effect on emotions.
I'm not saying I am immune to the placebo effect. Often just going to a doctor and hearing what's wrong with me cures me with physical ailments. I have funny shaped external ear canals, and was trying to use earbuds and got an awful ear-ache. All the doctor had to to was peer in, tell me it was only an exterior irritation, not an infection, and I barely needed the drops he gave me.
But I was on Luvox long enough to catalog the effects, good and bad, it had on me with reasonable assurance of accuracy. Why can't it be true that those effects ease depression in some or many people? Not that Luvox necessarily targets the illness "depression", but that the effects it produces are helpful in ameliorating the symptoms of depression or possibly mitigating the contributing factors?
And I have to say that the SSRI effect was helpful for me at the time I was taking it. The emotional numbing was a relief after the overstimulation of postpartum depression and a normally stimulating baby. If overstimulation is a large part of someone's depression or contributes to depression, why wouldn't SSRI's help?
Not for everyone maybe, but that doesn't negate the value for those for whom it works.
Most people would probably agree on a set of objective tangible results of being on an SSRI, wouldn't they?
I was put on mood stabilizers to counteract the Luvox originally, and kept on them and had the mood stabilizers adjusted by my neurologist for migraine prophylaxis. Yet I still see that they have an effect on my emotional regulation system. My guess is that they do exactly what they were meant to do as anticonvulsants. And that some people find the result helpful to them for mental health.
I occasionally take Risperdal as a major tranquilizer, as an alternative to being on long term medication for anxiety. I like it better because I'm not consistently anxious. I like to use as needed medications because I can control them to a greater extent. I know what Risperdal does, and I've known what antipsychotics do in terms of tranquilizing since I was a teen and my parents and pdoc lied to me about what medication they were giving me, for sleep terrors it says in my chart. They definitely have an effect, and it's an effect I find helpful at times.
Isn't it possible to say that none of these things is a cure for depression, particularly since depression is likely not a monolithic entity, and still say that different people will find different medications helpful for different aspects of their well being?
And isn't it just as possible for any given person to say that they don't find this or that medication helpful to them, given the underlying needs of their specific condition?
I'm not a genius in medications. I don't even particularly like taking them. But I do know what suits me, and I'd be happy for others to find a medication or group of medications that addresses their specific needs.
Can't that be phenomenon that the study is witnessing?
Posted by Jamal Spelling on January 5, 2008, at 16:37:43
In reply to Re: STAR*D confirmed what patients already knew, posted by linkadge on January 5, 2008, at 15:24:47
It may be true that 67% of patients who follow the STAR*D algorithm can be brought into remission, but it is not necessarily as a result of following this algorithm. If each treatment phase lasted 14 weeks, that means this 67% figure was attained only after 56 weeks - more than a year! Since major depressive episodes often only last a few months, the observed remission may be little more than regression to the mean.
Posted by bleauberry on January 5, 2008, at 17:34:10
In reply to What have we learned from the STAR*D study?, posted by SLS on January 4, 2008, at 5:42:45
Thank you Scott for your presence. Everyone I know of misses you a lot here. Thanks too for the powerful topic of discussion.
What these studies tell me is...
1) Whatever med is chosen, a patient needs to be able to tolerate to get to a decent dose. If intolerable, or if depression worsens, the deal is off. But the program is still on. Move on to another that can be tolerated.
2) If a med is working partially, don't discard it. Add to it.
3) No matter what the med is, it needs 8 weeks.My only comment on the study is that they maybe could have subgrouped patients into categories depending on their symptom clusters. For example, anorexic insomniac depression would start with Drug A. Withdrawn fatigued anhedonic depression would start with Drug B. Crying sobbing worthless guilty depression would start with Drug C. Sure, most of the symptoms of the entire depression cluster are probably evident, but there are certain clusters much stronger than others that pinpoint a different type of depression and hint toward which neurochemistries might be more likely involved.
For me the biggest problem is just finding something tolerable. I can't do 8 weeks if I can't get to a reasonable dose, which can't happen if I have side effects that incapacitate my ability to be my family's wage earner or make me feel considerably worse than I started. If I get past those hurdles, I'm following the STAR protocol. My one advantage is that I am not afraid to access all available meds, FDA or not.
Posted by bleauberry on January 5, 2008, at 17:39:55
In reply to What have we learned from the STAR*D study?, posted by SLS on January 4, 2008, at 5:42:45
Scott I am interested and was hoping you could answer a few questions for me?
First, what meds are you taking and what doses? Do you take any specific supplements, vitamins, or minerals with them?
The one med that really made the difference for you (I'm guessing it was Nardil?)...how many weeks did you wait for major improvements?
Your doctor will use non-FDA meds. Cool. How the heck did you find such a doctor? Where do you live? I'm jealous. I didn't know a doctor could even legally consider using adrafinil, milnacipran or some others.
Nice to see you Scott. I know you're enjoying a better life, but please keep your absences from here a little shorter, eh? :-)
Posted by Racer on January 5, 2008, at 18:27:25
In reply to Re: STAR*D confirmed what patients already knew, posted by linkadge on January 5, 2008, at 15:24:47
> >The methodology could not include placebo. It is >an ecological study. Has your doctor ever >offered you a placebo? Do you consider placebo >treatment to be a common clinical practise?
>
> Well, then change the methodology. Its not so much that doctors can offer placebos, but if they knew that medications were essentially no better than placebos, they might decide against riskier treatments in favor of other treatments. For instance, they might choose lower (safer) doses, or choose drugs with a more benign side effect profile.>
> >The methodology was not designed to show what >works. It was designed to deal with non->responders.
>
> Well, strong response to a placebo might have helped support the finding that pretty much all choices are essentially equivilant.
>
> I do think it really matters that doctors know the true incidence of placebo response.
>
> >These variables may go some way to predicting >responsivity, something that the artificial >construct of a placebo-controlled efficacy trial >can never show.
>
> You could include these same types of analysis in a study that includes a placebo. It might even help to uncover exactly what factors predict placebo response.
>First of all, what you say in that last short paragraph is right: it might be useful to know what factors predict a placebo response, and how strong that response might be. That's a good start for another study some day, once someone decides how to do it.
As for your very first sentence, though -- that the methodology should have been changed in this study -- I disagree strongly. This study was done to explore treatment algorithms for those who fail to respond to a trial of a single first line anti-depressant. That is the purpose of this study, and the methodology used seems appropriate to me for that purpose. This was not a study of the placebo response in depression treatment.
Your suggestion regarding lower doses directly contradicts what the study found: that in many cases, increased doses of tolerable medications increased response. That non-response may be a question of inadequate dosing in some (or even many) cases. As far as I'm concerned, that's something good to know.
As for the basic premise that response to antidepressants is no better than response to placebo, I'm going to argue that.
First, as Dinah said, most of us can point to effects of these medications. Many of those effects do mitigate our symptoms, even if they do not "cure" the disorder or even result in complete remission. Still, if the effects of the medication affect our symptoms, isn't that response to the medication? Or do you still consider that to be a placebo response because it may not have resulted in complete remission?
It is your stated opinion that anti-depressants are no more effective than placebo. Regardless of what studies you can cite to support this opinion, it is a valid opinion, and it is your right to hold this opinion -- regardless of whether it is right or wrong in fact. In the opinions of others, however, antidepressant medications are more effective than placebo. Some of the others who hold that opinion are researchers, doctors, other patients who take those medications, etc. It is the right of those who hold the opinion that antidepressants are more effective than placebo to hold that opinion. It is also a valid opinion. Perhaps their opinion is wrong.
Perhaps your opinion is wrong.
I'd also like to point out that the whole "placebo response rate" question involves statistics. In a large, double blind, placebo controlled study, the placebo effect may be higher than some pharmaceutical companies might like. In the real world, though, most of us don't care if 30% or 70% of the participants in a research study responded to a particular drug: we're looking for a 100% response rate with an n of 1. Do *I* respond to a particular medication? That's quite a different question, don't you agree?
I know that I have experienced placebo responses, good and bad, to medication. When I felt that a doctor was not hearing me, not listening, not treating me with respect -- and I've had some bad experiences with doctors in my life -- I have not responded well to certain medications. I've tried some of those medications again with similar results, although not as thoroughly negative as the first time around. I know that tolerability, for me, is strongly influenced by my relationship with my doctor. That is a placebo response. The outcome is the same, though, either way: either I feel better or I don't. That's what matters to me. And that hasn't been influenced, as far as I can tell, by how well I get along with my doctor.
Frankly, I'd be inclined to cheer that anyone has done a real world style study of the way depression is treated, if only because it's a nice relief from the usual sort of short term study one usually sees. Is this particular study perfect? I don't think so, because I don't think it's possible to create a perfect study when you're dealing with the diversity of the population being studied. For that matter, I'm not sure what sort of study could be done perfectly in anything involving any living creature, just because of the diversity involved.
What say that it would be nice to have a study into the value of the placebo effect in treatment of depression, with especial interest in the factors which predict response to a placebo, and that we all fervently hope that someone designs and carries out such a study at some point?
And then maybe we can look at STAR*D and say, "wow, someone finally did a study into treatment algorithms for depression that more accurately reflected real world treatment." Regardless of one's opinion regarding the efficacy of placebos in the treatment of depression, or one's opinion regarding the uselessness of antidepressant medication for the treatment of depression, isn't it nice that someone did study the outcomes in a longer term design, with emphasis on what to do next if the first choice didn't work?
I think I've had my say for now.
Posted by SLS on January 5, 2008, at 19:20:14
In reply to Re: STAR*D confirmed what patients already knew » linkadge, posted by Racer on January 5, 2008, at 18:27:25
Hi Racer.
> I think I've had my say for now.
I would say that you have indeed - and with such eloquence.
How you have grown so smart, I still can't figure out.
:-)
- Scott
Posted by SLS on January 5, 2008, at 19:40:16
In reply to Re: correlation does not imply causality, posted by Jamal Spelling on January 5, 2008, at 16:37:43
> It may be true that 67%...
I thought the STAR*D claimed a success rate of 70%. Where can I find a reference stating that it was 67%? Just curious. Thanks.
> Whereof patients who follow the STAR*D algorithm can be brought into remission, but it is not necessarily as a result of following this algorithm.
Thank God it was the result of something.
> If each treatment phase lasted 14 weeks, that means this 67% figure was attained only after 56 weeks - more than a year!
If you happen to be stricken with depression, how long have you been trying unsuccessfully to treat it? More than 56 weeks? If so, you might want to try following a protocol similar to that used in the STAR*D study.
> Since major depressive episodes often only last a few months, the observed remission may be little more than regression to the mean.
So, you see how the STAR*D investigation thus indicates that there were quite a few members of the study population who were chronic and difficult to treat, otherwise their depressions would have remitted spontaneously during what you acknowledge is an extended period of time. Where is the selection bias here?
I'll tell you what. For as much as this treatment population remained unremitted at each step, I would conclude that there had not been terribly much conspiracy to be perpetrated. Maybe just a little? There would be no drama if there weren't just a little. Damned NIH liars.
:-(
- Scott
Posted by linkadge on January 5, 2008, at 19:53:31
In reply to Re: STAR*D confirmed what patients already knew » linkadge, posted by Racer on January 5, 2008, at 18:27:25
>That is the purpose of this study, and the >methodology used seems appropriate to me for >that purpose. This was not a study of the >placebo response in depression treatment.
It doesn't matter how it was designed. In the end, people need to ask themselves if they want the results to have meaning, or to be meaningless. Even if you are designing a study to determine what is the optimal choice for treatment, without a placebo arm one doesn't really know if that 'optimal' strategy is infact optimal or just the product of chance. Only when results outperform those of the placebo do they have meaning.
If, for instanse, a drug algorithm fails to outperform placebo, then if could simply be that the chosen algorighm was the one that produced the fewest side effects.
>That non-response may be a question of >inadequate dosing in some (or even many) cases. >As far as I'm concerned, that's something good >to know.
I personally didn't get that as a strong impression from the results I read.
>As for the basic premise that response to >antidepressants is no better than response to >placebo, I'm going to argue that.
I don't care.
>First, as Dinah said, most of us can point to >effects of these medications.
Placebos with a buzz.
>Many of those effects do mitigate our symptoms, >even if they do not "cure" the disorder or even >result in complete remission.
Placebos mitigate too. That is the premise of the placebo effect, that one part of the brain can override another.
>Still, if the effects of the medication affect >our symptoms, isn't that response to the >medication? Or do you still consider that to be >a placebo response because it may not have >resulted in complete remission?
A placebo response is one that would have occured if the same patient was given a placebo.
>It is your stated opinion that anti-depressants >are no more effective than placebo.
My stated opinion is based on fact. That more than half of all published clinical trials on SSRI and newer antidepressants fail to show superiority of the active drug over the placebo. Take that fact as you will.
>In the opinions of others, however, >antidepressant medications are more effective >than placebo.
For some, thats the only way they will work.
>In the real world, though, most of us don't care >if 30% or 70% of the participants in a research >study responded to a particular drug: we're >looking for a 100% response rate with an n of 1. >Do *I* respond to a particular medication? >That's quite a different question, don't you >agree?I agree that in the end a response is a response. However, in understanding the way that depression works, it is critical to have a good idea of what gets people better. You can't just believe in anything, you need to believe in something that is established, something that you believe will work. People enter the system with the wrong assumptions IMHO.
>Frankly, I'd be inclined to cheer that anyone >has done a real world style study of the way >depression is treated, if only because it's a >nice relief from the usual sort of short term >study one usually sees. Is this particular study >perfect? I don't think so, because I don't think >it's possible to create a perfect study when >you're dealing with the diversity of the >population being studied. For that matter, I'm >not sure what sort of study could be done >perfectly in anything involving any living >creature, just because of the diversity involved.
The more studies the better. I am not against studies, I just believe that its important to get a good idea of what a result means and what it doesn't mean. In the end, it is good that people can recover, I just hate to see people become institutionalized by psychiatry (not in the literal sense).
>And then maybe we can look at STAR*D and >say, "wow, someone finally did a study into >treatment algorithms for depression that more >accurately reflected real world treatment." >Regardless of one's opinion regarding the >efficacy of placebos in the treatment of >depression, or one's opinion regarding the >uselessness of antidepressant medication for the >treatment of depression, isn't it nice that >someone did study the outcomes in a longer term >design, with emphasis on what to do next if the >first choice didn't work?
I think it is necessary to continually challenge the fundimental assumptions psychiatry makes. You have to get past level a. before you can go on to level b. If we can't statistically beat the placebo, then all else is meaningless. Such studies don't answer real world questions because they are not starting with real world assumptions.
Don't you see, it doesn't matter if effexor/remeron beats parnate if both are worse than placebo.
Linkadge
Posted by linkadge on January 5, 2008, at 19:55:03
In reply to Re: STAR*D confirmed what patients already knew » linkadge, posted by Racer on January 5, 2008, at 18:27:25
Antidepressnats will never die, because there are many people who base their lives on the notion of their efficacy. Its like a religion.
Linkadge
Posted by linkadge on January 5, 2008, at 20:07:24
In reply to Re: correlation does not imply causality, posted by SLS on January 5, 2008, at 19:40:16
>If you happen to be stricken with depression, >how long have you been trying unsuccessfully to >treat it? More than 56 weeks? If so, you might >want to try following a protocol similar to that >used in the STAR*D study.
That doesn't make sense since we have no idea of the length of time the average STAR*D patient has been depressed. Even so, to make such an assumption one would need to perform a subgroup analysis to determine that such a proposed efficacy extends to those who have been treating depression for such a lenght of time.
>So, you see how the STAR*D investigation thus >indicates that there were quite a few members of >the study population who were chronic and >difficult to treat, otherwise their depressions >would have remitted spontaneously during what >you acknowledge is an extended period of time. >Where is the selection bias here?
Where has the study indicated the percentage of participants who have been depressed for more than a year or so? Depression can be diagnosed after two weeks. What Jamal said is very important. If a good portion of the participants had the type of depression that generally remits within a year, then the length of the study is a major factor to consider. In my opinion, extended trials are only good in so much as they can work to show continued efficacy of treatments that initially work. That a patient gets better in the remaining minuates of a trial doesn't say much.
Linkadge
Posted by SLS on January 5, 2008, at 20:17:09
In reply to Re: SLS Tell Me More » SLS, posted by bleauberry on January 5, 2008, at 17:39:55
> Scott I am interested and was hoping you could answer a few questions for me?
Your hopes will be actualized, but let's discuss this along another thread.
http://www.dr-bob.org/babble/20080105/msgs/804533.html
-Scott
Posted by seldomseen on January 5, 2008, at 20:33:38
In reply to Re: STAR*D confirmed what patients already knew, posted by linkadge on January 5, 2008, at 19:55:03
I agree with you that a major concern of the STAR*D study is that the subject might have simply gotten better on their own without intervention. It's true in any study really.
However, there is a difference between an effictive drug and an efficacious one.
Placebos can be quite effective.
Perhaps one problem with the STAR*D design is that it was not an efficacy trial. It was an effectiveness trial. It showed that these drugs and this protocol can be effective in treatment resistant depression. Now whether it is an efficacious protocol? Now that's a different story.
There is plenty of evidence out there that drugs are efficacious against depression, and there is plenty of evidence out there suggesting that they aren't efficacious at all.
Does it matter? Yes and no.No study no matter how well designed can predict what a drug will do in an individual person. No drug is perfectly efficacious and no drug is 100% effective.
I had my response to the SSRI's, someone else might not and that's what it comes down to IMO.
I think what matters is how the docs present these drugs to us. I think it is irresponsible for a physician to say - hey take this pill it's going to cure you and there's going to be no side effects.
If we chose to, we consent to take these drugs and throw our ball on the roullete wheel and see if we are lucky enough to get a winner. I think that's the take home message.
It's the same whether it is a blood pressure med, or an anti-psychotic.
I don't think it is a religion, or some conspiracy to keep these drugs in play.
Posted by SLS on January 5, 2008, at 21:05:34
In reply to Re: correlation does not imply causality, posted by SLS on January 5, 2008, at 19:40:16
Hi.
Please thank Larry Hoover for providing us with the citation I used later in this post.
> > It may be true that 67%...
>
> I thought the STAR*D claimed a success rate of 70%. Where can I find a reference stating that it was 67%? Just curious. Thanks.
>
> > Whereof patients who follow the STAR*D algorithm can be brought into remission, but it is not necessarily as a result of following this algorithm.
>
> Thank God it was the result of something.
>
> > If each treatment phase lasted 14 weeks, that means this 67% figure was attained only after 56 weeks - more than a year!
>
> If you happen to be stricken with depression, how long have you been trying unsuccessfully to treat it? More than 56 weeks? If so, you might want to try following a protocol similar to that used in the STAR*D study.
>
> > Since major depressive episodes often only last a few months, the observed remission may be little more than regression to the mean.
>
> So, you see how the STAR*D investigation thus indicates that there were quite a few members of the study population who were chronic and difficult to treat, otherwise their depressions would have remitted spontaneously during what you acknowledge is an extended period of time. Where is the selection bias here?
>
> I'll tell you what. For as much as this treatment population remained unremitted at each step, I would conclude that there had not been terribly much conspiracy to be perpetrated. Maybe just a little? There would be no drama if there weren't just a little. Damned NIH liars.
>
> :-(
>
>
> - Scott-------------------------------------
http://ajp.psychiatryonline.org/cgi/content/full/ajp;163/1/28Evaluation of Outcomes With Citalopram for Depression Using Measurement-Based Care in STAR*D: Implications for Clinical Practice
Am J Psychiatry 163:28-40, January 2006
doi: 10.1176/appi.ajp.163.1.28
"RESULTS: Nearly 80% of the 2,876 outpatients in the analyzed sample had chronic or recurrent major depression; most also had a number of comorbid general medical and psychiatric conditions"Brilliant deduction, I must say.
The STAR*D seems to present itself logically and simply to me; its results consistent such that they beg me to take them at face value.
Only a simple mind such as my own would find such a simple study to be so simple.
- Scott
Posted by Racer on January 5, 2008, at 21:09:34
In reply to Re: STAR*D confirmed what patients already knew » Racer, posted by SLS on January 5, 2008, at 19:20:14
>
> I would say that you have indeed - and with such eloquence.Thank you.
>
> How you have grown so smart, I still can't figure out.
>
> :-)
>
>
> - Scott
>
>That part's easy: it's because I have friends who share their smarts with me. You're one of them, and you are a blessing to me.
xoxo
Posted by Dr. Bob on January 6, 2008, at 0:31:18
In reply to Blocked » LostBoyinNCBecksDark, posted by Deputy Dinah on January 4, 2008, at 17:39:56
> I'll set the block length at twice the length of the former block length and ask Dr. Bob to review it.
On review:
duration of previous block: 6 weeks
period of time since previous block: 2 weeks
severity: 2 (default) + 1 (uncivil toward particular groups) = 3
block length = 16.98 rounded = 17 weeksBob
Posted by Dr. Bob on January 6, 2008, at 0:31:23
In reply to Re: STAR*D confirmed what patients already knew, posted by linkadge on January 5, 2008, at 19:53:31
> > most of us can point to effects of these medications.
>
> Placebos with a buzz.Please don't exaggerate or overgeneralize or jump to conclusions about others.
But please don't take this personally, either, this doesn't mean I don't like you or think you're a bad person.
If you or others have questions about this or about posting policies in general, or are interested in alternative ways of expressing yourself, please see the FAQ:
http://www.dr-bob.org/babble/faq.html#civil
http://www.dr-bob.org/babble/faq.html#enforceFollow-ups regarding these issues should be redirected to Psycho-Babble Administration. They, as well as replies to the above post, should of course themselves be civil.
Thanks,
Bob
PS: According to the new formula:
duration of previous block: 1 week
period of time since previous block: 26 weeks
severity: 2 (default)
block length = 1.48 rounded = 1 week
Posted by Jamal Spelling on January 6, 2008, at 1:16:06
In reply to Re: correlation does not imply causality, posted by SLS on January 5, 2008, at 21:05:34
> I thought the STAR*D claimed a success rate of 70%. Where can I find a reference stating that it was 67%? Just curious. Thanks.
On page 63 of the article you have on your website, they give the following cumulative remission rates:
Level 1 - 33%
Level 2 - 57%
Level 3 - 63%
Level 4 - 67%> Nearly 80% of the 2,876 outpatients in the analyzed sample had chronic or recurrent major depression
Indeed, it may be true that nearly 80% had chronic *or* recurrent major depression. But when you break that down, the study shows that the bulk of this figure was recurrent depression, not chronic. In fact, the rates for chronic depression were 30% and 21% respectively for the primary care and psychiatric patients. So this does not invalidate my observation the 70% remission obtained after 56 weeks of treatment may have simply been regression to the mean.
I am not disputing the claim that the majority of depression sufferers can obtain relief when following the STAR*D algorithm. My observation is merely that the remission cannot necessarily be attributed to following that treatment algorithm.
Posted by Jamal Spelling on January 6, 2008, at 3:05:42
In reply to Re: Psycho-Babble practises intellectual fascism, posted by Jamal Spelling on January 6, 2008, at 2:55:11
It is interesting to note that 33% of STAR*D participants failed to remit after 56 weeks of treatment while between 21% and 30% of participants were chronic sufferers. I have no factual basis for making this claim, but it might be that the non-remitters were precisely the chronic sufferers, whereas the remitters were the patients with episodic depression. If this were true, that would enforce the possibility that the observed remission was just regression to the mean, i.e. people eventually getting better on their own.
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