Tuesday, September 30, 2008
Gabitril was also allegedly marketed as a treatment for pain. I was unable to locate a single controlled study examining the efficacy of Gabitril for pain, though there were a small number of uncontrolled (i.e., not very useful) studies suggesting that maybe Gabitril could be used to treat pain. Regarding sleep, the placebo-controlled trials I located did not suggest that the drug was particularly effective (1, 2). So we're looking at a drug with essentially no controlled evidence of efficacy being pushed for pain, sleep, and anxiety. Well-done, Cephalon.
Some of the supporting evidence about the off-label marketing cases came from a sales rep who wore a wire to collect evidence on the company's marketing practices. Apparently a total of four company whistleblowers were involved. Shades of Peter Rost?
Read more about the case at the Philadelphia Inquirer.
PS. Cephalon published the negative anxiety Gabitril trials in June 2008. As is well-established, companies often fail to publish negative data about their products, so why is Cephalon being so open? A skeptic might note that with the legal case againt Cephalon gaining steam, it would look even worse if Cephalon was sitting on negative data. So perhaps knowing that bad publicity was coming due to the lawsuit led Cephalon to allow the negative anxiety results to be published, as they could state "Look at how open and honest we are." I'm just saying that it's a possibility.
Reference for anxiety trials:
Mark H. Pollack, Jane Tiller, Fang Xie, Madhukar H. Trivedi (2008). Tiagabine in Adult Patients With Generalized Anxiety Disorder Journal of Clinical Psychopharmacology, 28 (3), 308-316 DOI: 10.1097/JCP.0b013e318172b45f
Update: Also read a related post at Health Care Renewal. It mainly discusses Cephalon's opiate-laced "perc-o-pops" (Actiq) approved to treat cancer pain, but marketed in a much broader manner.
Follow-up mini-rant: Let's not excuse the physicians who jumped on board. Docs need to do a much better job of checking the evidence base, though when some of the evidence base consists of publishing the same data repeatedly and when negative trials are often not published, what kind of "evidence base" are we really talking about?
Thursday, September 25, 2008
This post details the duplicate publication of data on the antidepressant duloxetine (Cymbalta). Marketing and "science" collide to produce hideous offspring: an experimercial that pimps Lilly's bogus "Depression Hurts" marketing for Cymbalta using the exact same (weak) data twice. Data were published in the Journal of Clinical Psychiatry (JCP), and then the same data were published a second time in the Journal of Psychiatric Research (JPR), a blatant violation of JPR policy. Oh, and Alan Schatzberg, president-elect for the American Psychiatric Association is involved in the story.
The study: Lilly conducted a rather uninteresting study of Cymbalta, in which patients who had not shown a treatment response to an SSRI were then assigned to either a) Direct switch: Switch to Cymbalta and immediately discontinue the SSRI medication or b) Start-Taper-Switch: taper the SSRI over a 2 week period while also starting Cymbalta. Note that there was not a control group of any sort, an issue that the authors dance around (i.e., essentially ignore) in the papers based on this study's data.
Publication #1 -- Journal of Clinical Psychiatry: Data from this study were published in the January 2008 issue of the Journal of Clinical Psychiatry. The findings were that, in essence, there were no notable differences between patients who were directly switched to Cymbalta as opposed to those who did the start-taper-switch method. But what do the authors conclude?
Publication #2 -- Journal of Psychiatric Research: Data from the same study were published online (to appear in print soon) in the Journal of Psychiatric Research (JPR). And I mean the exact same data appear again in this paper. This is a huge scientific no-no. Findings are supposed to be published once, not over and over again. Journals are struggling to find space for new and interesting findings, so there is no need to waste space on duplicate data. In fact, to quote from JPR's website
Submission of a paper to the Journal of Psychiatric Research is understood to imply that it is an original paper which has not previously been published, and is not being considered for publication elsewhere. Prior publication in abstract form should be indicated. Furthermore, authors should upload copies of any related manuscript that has been recently published, is in press or under consideration elsewhere. The following circumstances indicate that a paper is related to the manuscript submitted to the Journal: a) any overlap in the results presented; b) any overlap in the subjects, patients or materials the results are based on.So it's pretty clear -- don't submit data that has already been published. Here is a figure from the Journal of Clinical Psychiatry (JCP) article mentioned above:
Authors: The JCP paper was authored by David Perahia, Deborah Quail, Derisala Desaiah, Emmanuele Corruble, and Maurizio Fava. The JPR paper was "authored" by Perahia, Quail, Desaiah, Angel Montejo, and Alan Schaztberg. So to re-publish the same data, it was out with Corruble and Fava -- in with Montejo and Schatzberg. Why Schatzberg? We're almost there...
JPR describes the contributions of each author. For these two authors (Schatzberg and Montejo) who were not credited in the JCP paper, they were both described as "involved in data review and interpretation, including the development of this manuscript." How could they have been involved with data review and interpretation -- the vast majority of the data were already analyzed, interpreted and written up by other researchers in the JCP paper? Did they write the paper? Apparently not, since the JPR article mentioned that "Dr. Desaiah worked with Dr. Perahia to draft the manuscript..." So Montejo and Schatzberg could not conceivably have played any significant role in data analysis, interpretation, or writing the paper. It seems that if Desaiah and Perahia "drafted" the manuscript, then the most Montejo and Schatzberg could have done is to maybe review the paper.
So why is Schatzberg on the paper? Well, it just so happens, I'm sure by sheer coincidence, that Schatzberg is the co-editor in chief of JPR. So he'd be in a good position to help a paper that essentially republishes data from JCP with only minor additions make it into publication against his own journal's policies.
Nice work, Schatzberg. That's pimpin' it hard. That, my friend, is worthy of nomination for a coveted Golden Goblet Award. Congratulations. It is not the first time Schatzberg's "scientific" behavior has been noted. He has been stumping (in the face of much contradictory data) in favor of his pet drug RU-486/Corlux in the treatment of psychotic depression for some time. Between the bad science surrounding Corlux and Schaztberg's myriad conflicts of interest, much has been written (1, 2, 3, 4, 5) -- add another chapter to the chronicles of the storied American Psychiatric Association Leader. This reminds me of an earlier incident involving Charles Nemeroff.
Discussion: As I've noted previously, the discussion section of a journal article often contains key marketing points, science being relegated to secondary status at best. The JPR article provides a few good examples of Cymbalta's talking points:
The current paper focuses on pain-related outcomes, demonstrating that a switch of SSRI non- or partial-responders to duloxetine was associated with a significant improvement in all pain measures including six VAS pain scales, the SQ-SS and its pain subscale, and the SF-36 bodily pain domain.Where do I start? How about by mentioning that JPR states:
Switch of SSRI non- and partial-responders to duloxetine resulted in mean improvements on all pain measures regardless of the switch method used.
Duloxetine, an SNRI, has previously been shown to be effective in the treatment of PPS associated with depression, and it is also effective in the treatment of chronic pain such as diabetic peripheral neuropathic pain (DPNP) for which it is approved in the US, Europe and elsewhere, so duloxetine’s effects on pain in our sample of SSRI non- or partial-responders was not unexpected.
Patients with MDD present with a broad range of symptoms including those related to alteration of mood and PPS, all of which may contribute to global functional impairment. Effective treatment of both mood symptoms and PPS associated with depression may therefore optimize the chances of functional improvement. Recent findings that residual PPS in depressed patients may be associated with impaired quality of life (Wise et al., 2005, 2007), decreased productivity and lower rates of help seeking (Demyttenaere et al., 2006) and a lower likelihood of attaining remission (Fava et al., 2004), further demonstrate the importance of effective treatment of PPS in patients with MDD, so duloxetine’s effects on PPS are reassuring.
Improvements in pain are consistent with previously reported studies demonstrating duloxetine’s efficacy for pain, either as part of depression, or as part of a chronic pain condition such as DPNP.
7. Discussion: The results of your study should be placed in the appropriate context of knowledge, with discussion of its limitations and implications for future work.So maybe if there was research that questions Lilly's talking points about Cymbalta relieving pain in depression, such research should be discussed. Well, it just so happens that there is research, which analyzed Lilly's own clinical trials and found that Cymbalta was no better than a placebo or Paxil in treating pain in depression. This meta-analysis of Cymbalta trials was published in January 2008, yet the JPR article, which was originally received by JPR on March 26, 2008 did not mention the negative data. Hmmm, that doesn't exactly sound like placing the findings "in the appropriate context of knowledge," does it? All this talk about Cymbalta's fantastic analgesic effects despite Lilly's own data showing that Cymbalta is at best close to useless in treating pain among depressed patients. Another study that claimed to show Cymbalta was a helluva painkiller was also smacked in a letter to the editor a few months ago -- and the authors of the Lilly-sponsored trial conceded defeat by refusing to reply to the critiques of their study.
Better Than "Weak" SSRIs (Not Really): In the JPR study, it was mentioned that the evidence for SSRIs in treating pain is "weak." No disagreement on my end. But see, once SSRI patients switched to Cymbalta, their pain magically went away because Cymbalta, unlike SSRIs, relieves pain. Never mind the lack of control group, which was allotted a grand total of 15 words in the discussion as a potential limitation of the study. The authors also failed to note that prior research showed that Cymbalta was no better than Paxil in treating pain in depressed patients. And Perahia, the lead author of the JCP and JPR "studies" is certainly aware of the research showing that Cymbalta works no better than a "weak" SSRI, since he was the lead author on one such study! So he is quite aware that Cymbalta has never been shown superior to Paxil in treating pain, yet he accurately describes research indicating that SSRIs are "weak" pain treatments, but then neglects to mention that Cymbalta failed to demonstrate superiority to Paxil in treating pain in depression. This is called lying by omission.
I may pass along my concerns to the Journal of Psychiatric Research. My prior experiences in passing along such concerns to journals via my blog identity is that they either a) ignore my concerns entirely or b) instruct me to write a letter to the editor which would be considered for publication, with the stipulation that I use my real identity. Sorry, but a published letter to the editor is not worth blowing my cover.
Call for Action: Rather than my running into point b. from the last paragraph, how about one or more scientifically inclined readers submit your concerns to the journal, under the following condition: Make sure you read the original papers first to judge if my concerns are valid. Then, if you feel similarly, why not send a letter to the editor? This is bad science which does nothing to advance patient care -- it seeks only to advance sales of Cymbalta by pimping it as a painkiller in depression while ignoring all contradictory data. So let's try a little research of our own -- see if JPR is willing to address these issues or if they will be swept under the rug.
Reference to JPR article:
D PERAHIA, D QUAIL, D DESAIAH, A MONTEJO, A SCHATZBERG (2008). Switching to duloxetine in selective serotonin reuptake inhibitor non- and partial-responders: Effects on painful physical symptoms of depression Journal of Psychiatric Research DOI: 10.1016/j.jpsychires.2008.07.001
Update: Also see an excellent follow-up post on the topic at Bad Science.
Tuesday, September 23, 2008
In the meantime, check out another hot, hot psych blog: The MacGuffin. This fellow anonymous mental health blogger hates bad science. We're peas in a pod that way. And he's willing to diss research on both psychotherapy and meds. Dripping with sarcasm and with a sharp eye for spotting scientific shortcomings, I wholeheartedly encourage all readers to add the site to your list of faves.
Also, Danny Carlat is continuing to get into scrums with the CME industry and it's fun to read about.
Furious Seasons updates us on the FDA and child bipolar disorder.
As per usual, the Scientific Misconduct Blog has items related to scientific misconduct. Questions surrounding the behavior of a so-called regulatory agency and drug safety are brought to the fore yet again.
Findings from my latest investigations will hopefully be unveiled soon. Stay tuned!
Thursday, September 18, 2008
Interestingly, a group of researchers has claimed that olanzapine (Zyprexa) has "neuroprotective" qualities; it's good for your brain. Um, color me skeptical. Their research was based on rats, whereas Andreasen's work is on humans. Andreasen's latest work is not yet published, making it difficult to judge the quality of the findings. But research on monkeys exposed to antipsychotics found that:
In conclusion, chronic exposure of non-human primates to antipsychotics was associated with reduced brain volume.I am not a neuroscientist, but if both sets of findings were accurate, then we'd have people taking antipsychotics who have smaller but better brains. The more neuroscientifically inclined may wish to comment on this possibility, because it seems a little odd to me.
Monday, September 15, 2008
The Diagnostic and Statistical Manual of Mental Disorders (the current edition is referred to as D.S.M.-IV) describes bipolar disorder as a condition whose average age of onset is 20, but virtually all the leaders in the field now say they believe it exists in children too.Well, then. I found two psychiatrists whose opinion appears to differ. Jon McClellan seems to disagree that bipolar exists in young children, as does David Healy. I could probably find others without much difficulty. Maybe they are not "leaders in the field?" But ok, let's say that it does exist in young kids. I'll grant Jennifer Egan that most agree that bipolar exists in adolescents (but toddlers???), though at what rate is a matter of debate. And more importantly, who gives a rat's behind what people think? Um, maybe we should be more concerned about what the actual science has to say about it. And in that regard, there are some serious unanswered questions, as I've described before.
1. Does child bipolar really exist in substantial quantity?
2. Does treatment help kids with this "disorder"?
But to be fair to Egan, maybe I took the last quote out of context, because she adds a somewhat more balanced view by stating that:
Many clinicians say the illness looks significantly different in children than in adults, but the question of how it differs, or what diagnostic terms like “grandiosity,” “elevated mood” or “flight of ideas” (all potential symptoms of adult bipolar disorder) even mean when you’re talking about kids, leaves room for interpretation. For example, it’s normal for children to pretend that they are superheroes, or believe that they can run faster than cars, whereas in an adult, these convictions would be signs of grandiosity. Equally unclear is whether a child who is identified as having a bipolar disorder will grow up to be a bipolar adult. Work on the D.S.M.-V is under way, and discussions have begun on how to address the issue of bipolar children.OK, that's better. But in general, the article focuses on the proponents of the child bipolar paradigm rather than those who raise concerns. And Egan discounts a big study in a pretty odd way...
As Ellen Leibenluft, who runs the pediatric bipolar-research program at the National Institute of Mental Health, told me, “There definitely will be — and needs to be — more description of what bipolar disorder looks like in children, how one diagnoses it and some of the challenges.”
A study last fall measured a fortyfold increase in the number of doctor visits between 1994 and 2003 by children and adolescents said to have bipolar disorder, and the number has likely risen further. Most doctors I spoke with found the “fortyfold increase” misleading, since the number of bipolar kids at the beginning of the study was virtually zero and by the end of the study amounted to fewer than 7 percent of all mental-health disorders identified in children.Huh? So it's misleading to say that for every one treatment visit for bipolar in 1994, there were 40 in 2003? No, that's exactly what the study found. Let's try an analogy. The rate of suicide among kids and teens, on an absolute scale, is very low. Very few children and adolescents actually commit suicide. So if the suicide rate went up by a factor of 40 in the next 10 years, would we then say, "Well, that's misleading because suicide was very rare in 2008, when the study began?" That makes no sense whatsoever. And to say, hey bipolar is now only 7% of kids diagnosed with mental disorders, so it's no big deal -- ??? What treatments do you think these kids get? Play therapy and lollipops? Uh, try antipsychotics, often in combination with anticonvulsants, antidepressants, and who knows what else? If you think this is all based on science, go take a spin over to Pubmed and see what you can find. What, there's no evidence that carpet bombing developing brains with a wide variety of psych drugs is effective for "bipolar"? Count me as shocked, shocked, that medications would be prescribed so widely in the absence of supporting evidence. Sure, maybe if you provide highly tranquilizing medications, they mellow out bad behavior a bit in the short-term. Is that an effective long-term solution? And at what cost?
In Leibenluft’s studies at the National Institute of Mental Health, only 20 percent of children identified with bipolar disorder are found to meet the strict criteria for the disease. Breck Borcherding, a pediatric psychiatrist in private practice in the Washington area, said: “Every time one of my kids goes into the hospital, they come out with a bipolar diagnosis. It’s very frustrating.”OK, so a study that finds that bipolar diagnoses have shot through the roof is "misleading," but at the same time, other Egan then discusses research suggests that bipolar is being misdiagnosed at a high clip. Am I the only one who is confused?
Then there is “The Bipolar Child,” a successful book published by the psychiatrist Demitri Papolos and his wife, Janice, in 1999, and referred to by more than one parent I spoke to as a “bible.” The Papoloses’ description of pediatric bipolar disorder was amassed partly by using responses to an online questionnaire filled out by hundreds of parents on an electronic mailing list, who said they believed their children were bipolar (and who often had strong family histories of the disease). The Papoloses’ diagnostic criteria include some idiosyncratic items — a severe craving for carbohydrates, for example — that are found nowhere in D.S.M.-IV. Nevertheless, many parents walk into doctors’ offices having already read “The Bipolar Child” and concluded that their children are bipolar. Because doctors rely heavily on parental reports when diagnosing disorders in children, these “prediagnoses” may have an impact on the outcome.
Well, if that isn't the most airtight method for a study that I've ever heard. Put up an online questionnaire, have people who insist that their kids are bipolar fill it out, then use whatever these parents say as criteria for the disorder. And... severe craving for carbs? Nope, I've never ever seen a kid who really, really wants candy before. But if I do see such behavior, I'll turn on my bipolar radar; I'll be keeping my eyes peeled at the candy store.
And of course, there are pressures and blandishments from the pharmaceutical industry, which stands to profit mightily from the expensive drugs — often used in combination — that are prescribed for bipolar illness, despite the fact that very few of these drugs have been approved for use in children.
You mean like the part where key opinion leaders sign on for Big Bucks to give talks for psych drugs in treating kiddie bipolar? No, you won't find discussion of that anywhere in the article. Because we are making progress in understanding the biological disease of bipolar disorder and how to treat it. Progress is slow but everything is headed in the right direction -- the time-honored narrative of the academic-pharmaceutical complex always making progress in mental health. There is a sentence dedicated to discussing the influence of Big Pharma. One. Off-label marketing of antipsychotics for kids is never mentioned, despite Otsuka/Bristol Myers Squibb settling a federal lawsuit for pimping Abilify for kids. I suppose mentioning such shenanigans might poke a bit of a hole in the idea that we are making perpetual progress.
And here comes the hammer. Sure, bipolar might be overdiagnosed, but of course the biggest problem is the undertreatment of bipolar kids:
For all the possible overdiagnosing of pediatric bipolar disorder, however, many in the field also say that a lot of truly bipolar children who could benefit from therapy are falling through the cracks. This is a critical issue; studies clearly show that the longer bipolar disorder goes untreated, the worse a person’s long-term prognosis.
If you are so into "studies clearly showing" things, then maybe you could point to studies that clearly show benefits of treating bipolar disorder in children. I'm waiting. In fact, I've been waiting for years. As the rate of drugging kids for bipolar has increased drastically, the research showing treatment benefits is... where? And if you're telling me that kids behaving very badly, which seems to be fit roughly 100% of kids who wind up diagnosed with bipolar disorder, are not getting treatment, I think you aren't paying attention. Desperate parents want a solution, and whether the diagnosis is opposition defiant disorder, conduct disorder, ADHD, autism, pervasive developmental disorder, WTF NOS, or bipolar, I'm pretty sure that these kids are getting treated in droves. But maybe I'm wrong.
Gabrielle Carlson, the director of child and adolescent psychiatry at the Stony Brook University School of Medicine, has studied childhood mania for many years and says bipolar disorder is uncommon in children under 10, revealing itself in the same discrete episodes of mania and depression that we see in bipolar adults — not in chronic irritability. According to Carlson, a large group of aggressive and explosive children, who in fact are “diagnostically homeless,” are being relabeled as bipolar, which is a development she says is unhelpful both to the children and the field. “Diagnostically it ends up being a very important consideration of what the kid really has,” she told me. “If he really has A.D.H.D. and it’s not mania, then you give him medication for his A.D.H.D. You also give him behavior modification.” One patient she saw that day, who was thought to have bipolar disorder, actually had autism, she said. “If you say, ‘Hey, his problem is bipolar disorder,’ then you’re not going to treat his language disorder, you’re not going to give the social-skills treatment he needs,” she said. Problematic conditions in a child’s home life are also less likely to be addressed if the child’s behavioral issues are attributed to bipolar disorder, Carlson said. “Many people, when they hear bipolar disorder, their brain slams shut.”After including quotes from Janet Wozniak of the ever-present Harvard bipolar child team, it was nice to see comments from someone who has a bit more skepticism. A harsher critic could have been included in the story, but was not. No, I'm not going to quote Wozniak because you already know what she said, which is that we discovered that bipolar disorder in kids is way, way, way, way, more common than previously thought.
The most basic question about bipolar kids remains a mystery: Will they grow up to be bipolar adults?No, four of the most basic questions are, in no particular order:
- How many of these kids labeled as bipolar have been misdiagnosed?
- What are the benefits and risks of treatment, in the short-term and in the long-term?
- What happens if we try nonmedical interventions aimed at changing discipline strategies, proving more structure at home, etc.
- Is child bipolar at least partially a medical term for bad behavior? And where does the bad behavior stem from? Could social problems have anything to do with it? Think of things like poverty, absent parenting, violent TV programming and video games, vastly unequal income distribution, gangs, unemployment/underemployment, and the list goes on... In other words, our society ain't exactly ideal and some of these problems will impact mental health. Isn't throwing pills (or even therapy) at these problems a little shortsighted? This ain't the place to discuss how to improve society; I'm just saying that many of these problems discussed on the site probably arise from more than just intrapsychic issues or troubles with an alleged (not proven) "chemical imbalance." Do you think there is a reason, for example, that foster kids are so frequently on antipsychotics? As written by The Last Psychiatrist: "A 20% increase in therapy visits will be interpreted by psychiatry as a 20% increase in depression and anxiety. It will say depression has a prevalence of X, it will say it is underdiagnosed and undertreated, etc. And it will creep into the social consciousness that these are pre-existing diseases with triggers, not the consequences of external events. Society needs that illusion, it needs that lie, because it has created unrealistic expectations in people and no way of fulfilling them."
Think my question 4 is a little weird, that it's wild speculation? Well, if you want some wild speculation that exceeds mine, try a few slices from the NYT mag piece:
Some studies suggest that bipolar disorder may actually be on the rise among young people. One intriguing hypothesis involves a genetic phenomenon known as “anticipation,” in which genes become more concentrated over generations, bringing a stronger form and earlier onset of an illness with each successive generation. Another theory is “assortative mating,” in which a more mobile and fluid society, like ours, enables the coupling of people whose mutual attraction might be partly due to a shared genetic disposition to something like bipolar disorder, thus concentrating the genetic load in their offspring.Yeah. That's the ticket. We've had how many thousands of generations of human existence and now, suddenly, bipolar is becoming more concentrated in kids. Intriguing hypothesis? Wouldn't such a trend be gradual, not sudden? Same story with "assortative mating" -- is it just now that bipolar folks would choose to mate with each other? Presumably, this would have happened throughout human existence, so pulling this kind of thing out of a hat now makes absolutely no sense. But there's an answer to that -- we're living in a "more mobile and fluid society." So now that we're "mobile," bipolar folks breed with bipolar folks, but before cars and planes, they couldn't breed with each other. Huh?
Kiki Chang, director of the pediatric bipolar-disorders program at Stanford, has embraced the kindling theory. “We are interested in looking at medication not just to treat and prevent future episodes, but also to get in early and — this is the controversial part — to prevent the manic episode,” he told me. “Once you’ve had a manic episode, you’ve already crossed the threshold, you’ve jumped off the bridge: it’s done. The chances that you’re going to have another episode are extremely high.”Oh boy. Preventive psychopharmacology. If you are a hyper kid, we'll give you antipsychotics because they might keep you from becoming bipolar later. Trust us, your son is fine in our hands, ma'am.
Also see Furious Seasons' take on the matter. And give him some $$$ to help with his fundraiser. If you ever wanted to give me money, don't. Pass it his way.
Monday, September 08, 2008
Oh boy. Here we go again. A study published online ahead of print at the Journal of Clinical Psychiatry notes that among Oregon Medicaid patients who received a prescription for an atypical antipsychotic:
- 52% had a depression diagnosis
- 34% had an anxiety diagnosis
- 15% had a PTSD diagnosis
But only 15% had a schizophrenia diagnosis and 27% had a bipolar diagnosis. So... the majority of atypical scripts were written off-label. Seroquel was the most frequently prescribed atypical, followed by Zyprexa, then Risperdal.
Doses less than what are typically given to treat schizhophrenia or bipolar disorder (subtherapeutic dosing) were quite common. As in 86% of Seroquel scripts were subtherapeutic, 59% of of Risperdal scripts, and 48% of Zyprexa prescriptions. Wait, am I calling for higher doses of these drugs? That doesn't sound like me at all, right? Don't worry, I haven't lost my mind (I think).
Here's the deal. The authors suspect that a lot of these low-dose prescriptions are being written to manage agitation and as sleep aids. The authors note that there are likely less expensive/more effective medications for such conditions. Not to sound too cavalier, but one could also recommend behavioral treatment to help with sleep as well. Nah, that's crazy talk -- not enough money to be made in that.
Primary care docs were more likely than psychiatrists to dish out low-dose antipsychotics. I guess that the Viva Zyprexa marketing blitz was a success after all. Thanks to Daniel Hartung and collagues for their study, which provides another insight into the wonderful world of atypical antipsychotics as a treatment for everything imaginable. Sorry to beat a dead horse with my zillionth post about the topic of atypicals, but isn't this getting just a teeny bit out of control?
Daniel M Hartung, Jennifer P Wisdom, David A Pollack, Ann M Hamer, Dean G Haxby, Luke Middleton, Bentson H McFarland (2008). Patterns of atypical antipsychotic subtherapeutic dosing among Oregon Medicaid patients Journal of Clinical Psychiatry DOI: ej07m03658
Friday, September 05, 2008
I would also like to go on the record as saying that I am totally against banning books from libraries, which might make me a poor candidate for higher office.
Hat Tip: Respectful Insolence
Wednesday, September 03, 2008
The authors, who incidentally are not exactly in the Peter Breggin camp, opine that: "The widely held – and probably erroneous – belief that the placebo response in depression is short-lived appears to be based largely on intuition and perhaps wishful thinking." Ouch. Wishful thinking about psychiatric medications? Hmmm, that is giving me Effexor flashbacks for some reason...