Thursday, April 30, 2009
Right in front of our eyes, and we don't even see it. Recent study shows SSRI withdrawal leads to suicidality.
These pharma-sponsored researchers have the evidence right in front of their eyes that SSRI, or SSRI withdrawal, leads to suicidality, but they absolutely fail to put their finger on this horrible phenomenon (just to get you started, Google "SSRI" and "suicide", or cf.:
The study is in the April edition of the American Journal of Psychiatry (v. 4, pp. 418-426). "Predictors of spontaneous and systematically assessed suicidal adverse events in the treatment of SSRI-resistant depression in adolescents (TORDIA) study."
Lead author is Brent, who in the COI section seems to have no COI. However, other authoers pretty much cover the landscape of pharmaceutical funding.
OK- there has recently been a few notbale comments indicating that talk therapy is valuable and critical for depressed teens. Never mind all that. "Failed" treatment means that a teen did not get better on SSRI, which in other reseaerch has been shown to be modestly effective, and largely due to non-specific factors including placebo response.
Now, withdrawal from SSRI has been extensively noted by many to lead to suicidality. Thoughts and acts.
So, for the kids who did not respond to SSRI, the authors stopped the SSRI, and assesssed level of suicidality.
Level was shocking, at least to me: 20%.
Uh, folks, hang on - maybe we should go to plan B: talk therapy.
Another recently emergent study, the TADS study (John March, found similar results:
15% of depressed kids treated with SSRI had suicidal thoughts; of those treated just with talk therapy, only 6%. Less than half.
Nonetheless, the Brent study has no indication that the suicidality may have been provoked by the "treatment." It possibly reverses the causal relation and indicates that the suicidality has something to do with the subsequent poor treatment response.
Their solution? Keep family conflict and illicit drug use from interfering with the SSRI effect.
How about if we simply do what we can to get these kids into talk therapy, and heed the black box warning that SSRI leads to suicidality in teens?
right in front of our faces, and they totally re-interpret this result to sell more pills. Shameful.
Monday, April 27, 2009
“Reconcile” is doggie Prozac: fluoxetine hydrochloride in chewable, flavored tablets for dogs, which have been tested to make dogs less uproarious when you leave them at home all day alone. Labelled “pet separation anxiety" (as opposed to: "lively social animal left in apartment all day five days a week" syndrome).
The website, plus the package “insert,” indicate that this SSRI should be taken as treatment for the separation anxiety, and that behavioral therapy should also be delivered as the primary mode of treatment. The doggie Prozac brings successful treatment rates from 50% with behavioral therapy alone, to 70% when doggie prozac is added.
Doggie prozac seems to speed treatment response, also. So, this fits with one bit of clinical knowledge: talk therapy works for a range of mental health problems, and adding a psych med can help bootstrap things and quicken the pace of recovery.
The website and “insert” are very clear that the meds are supposed to accompany behavioral therapy. This is quite different from much of the research and the pharmaceutical marketing for antidepressant medications. These sources, such as the cartoon ads with the frowny faces, profile the simple need for a pill to correct some brain chemical imbalance, with no therapy needed.
I guess that dogs are not very susceptible to the placebo effect of pills, so delivering a pill is just not enough to get some favorable response in a drug trial.
We could learn something from man’s best friend.
Friday, April 24, 2009
Fishing with No Hook: With Sample of Only 50 Pregnant Women, Pharma Researchers Declare No SSRI Risk of Birth Defects
I recently blogged my blog for Peripartum Depression Awareness / Melanie Blocker Stokes Act support. when looking at that topic, I noted that there is an active question regarding the safety the developing baby in utero, or the baby when breastfeeding, if mom is taking SSRI.
I noted just one study showing increased risk, just to make the point that this is a problem we need to be concerned about. Especially since there is an alternative - talk therapy.
In that effort, I came across a recent study that seems like it was trying to evaluate whether mom taking ssri posed risk in pregnancy or in the "neonatal" phase. What I discovered was just another piece of Big Pharma marketing, masquerading as clincal research.
The article is from American Journal of Psychiatry, March 16, 2009: Major depression and antidepressant treatment: Impact on pregnancy and neonatal outcomes. Lead author is Katherine Wisner. The paper is "brought to you by" NIMH funding, so by psychiatrist standards, it is totally free of bias from Big Pharma. Wisner, however, has developed a long history of collaboration with pharmaceutical companies, and this is noted at the end of the article. So, if you were a cynical person, the needle on your suspicion-o-meter for lousy research might start moving.
Now, here is the big deal about this type of study:
This is a surveillance study. You are looking at a bunch of people to see if some condition or event happens to occur in some group, or in one group compared to another group.
The whole deal with a surveillance study is the "base rate." This is the number of people, out of a bigger population of people, that have the characteristic of interest.
Let's say your friend is a professional photographer, and your friend has a job taking pictures for some new eyedrops advertising campaign. They want people with brown eyes, blue eyes, and green eyes using the eyedrops. Well, people with green eyes are not so common. So, your friend asks you to go find a person or two with green eyes, and ask if they want to be america's next top eyedrop model.
If you suspect that 1 out of 10 people have green eyes in your neighborhood, you figure that you will have to go out and meet 10 neighbors before you find the 1 person with green eyes.
Now, it makes sense that if you want to detect at least 1 person with green eyes, you are going to have to talk to at least 10 neighbors. Because you have some idea of the "base rate" you might expect.
You also understand that you might luck into finding a green-eyed person in the first 2 or 3 neighbors you encounter, just by chance. People do not go places in your neighborhood and wait in some organized fashion, according to eye color. So, you know there will be some randomness, and variation. So, you figure if you are not very lucky, you might have to encounter 20 people before you encounter a person with green eyes.
Now, if the 3rd person you encounter has green-eyes, you are not going to decide that the prevalence of green eyes is 1 out of 3. No, you are gonna conclude that you were lucky that day: the randomness favored you that day.
The next day, the ball might bounce the other way.
Knowing this, you set out to do your surveillance sufficient for any given day, by being over-prepared: you are gonna plan time to encounter 50 neighbors. That number seems good to overcome the random variations that might happen day to day.
The point is: if you are going to conduct a surveillance study for something, and you have a fair idea it is out there in the neighborhood, you need to plan to do your surveillance on enough people to overcome this randomness.
It also makes sense that you have to pay attention to demographics: the portion of people with green eyes will, obviously, be greater in the anglo people in your neighborhood, compared to the non-anglo people: when you encounter Asians, Hispanics, and African-Americans, you are not going to discover anything close to 10% of people with green eyes.
So, the number of people you plan to encounter will have to go even higher.
So, demographic composition matters. And that, obviously, will depend on your neighborhood.
Now, it makes sense to us that, in this example, if for whatever reason we really are not going to be happy to just encounter 10 people, and check eye color.
So, now, on to this study at hand, where the researchers claim they are trying to detect whether taking SSRI antidepressant medications in pregnancy leads to any pregnancy or birth outcomes.
Low birth weight. Early delivery.
Now, this is similar to looking for the green-eyed people: we know that low birth weight is gonna happen in some births. we know that early delivery happens some of the time. We know that physical anomolies / birth defects happen some of the time.
Do they happen because mom was taking SSRI?
Well, now that we have had our discussion about encountering green-eyed people, it is plain old flat-out obvious that we are going to need find a decent number of pregnant women, then see how the delivery goes.
And, how will we be able to answer whether the SSRI had anything to do with any unfavorable outcome: with low birth weight, birth defect, etc.?
Well, we could compare birth outcomes between women taking SSRI, and women not taking SSRI.
And we will have to have a big enough number to overcome the other randomness - like our neighborhood trips, which we saw might be good one day - finding our green-eyed neighbor after only 3 people on one day, and on another day, after encountering 20 people.
So, with this NIH-funded study, how many pregnant women were in the SSRI group, and how many in the no-SSRI group?
But wait - you cleverly note: what if the depression - not the pills - leads to the low birth weight? We might falsely conclude that SSRIs lead to bad birth outcomes, but the real culprit is the depression.
OK, so we will look in a group of depressed women, some taking SSRI, and some not.
OK - now - how many pregnant women will you want in each group in order to test whether SSRI meds are associated with bad birth outcomes?
Well, here is the answer, for Wisner and colleagues.
Depressed women taking SSRI: 48.
Depressed women not taking SSRI: 14.
Yes: forty-eight, and fourteen. I write this twice so you don't think that I am mis-representing this study by a typo.
Wisner and colleagues believe it is OK to answer the question of whether SSRI is associated with birth defects by looking at 50 births.
Now, people, let's get serious. This is ridiculous.
Unless you are a pharmaceutical company, and you want to promote your pills by encouraging routine surveillance for depression in pregnancy ("prepartum depression," AKA "antepartum depression"), and by declaring that SSRI are safe for the baby. No risk of early delivery. No risk of low birth weight. No risk of birth defects.
Are you kidding me?
I am not even going to discuss the FINDINGS of this study, since our reasonable minds can safely declare that the study is either plain old nonsense, or propoganda, and therefore worthless regarding the question of whether SSRI antidepressants leads to birth defects.
And people, this is your tax dollars at work. NIH funded study.
We can maybe see why Wisner and colleagues signed on to the study. Profit motive, or to get a publication in a major journal to advance their researcher careers.
But this was approved by someone's "IRB" institutional review board / ethics review board. And, it found favor in the NIH, which is quite an accomplishment.
And, the Am J Psychiatry editorial staff and their article reviewers favored the article.
Am I crazy, or is it the rest of the world?
So, in my opinion, they slanted this study, in advance, to fail to find SSRI risk if there is any risk.
This makes me scared, and makes me wonder if they know something we don't know. Like are they actually afraid that if they actually surveyed, like, 100 women, they might actually find a woman with green eyes / find birth defects at a greater rate in the SSRI group, comapared to the non-SSRI group?
Now, if you have followed me this far, you may be able to see that a surveillance study takes a lot more people than a treatment study.
In surveillance, you have to winnow through many study participants to find the rare events: green eyes, birth defects, low-birth-weight babies, etc.
In a treatment study, let's say hypothetically that you were going to see if you could successfuly TREAT postpartum depression. Well, you are going to need to guess your expected success rate, and guess what randomness might happen: who might get better just by luck, who might not get better just by bad luck, etc.
So, in that kind of study, you might consider 14 in a treament group and 48 in the control group.
Maybe. But still you would have to have a "surveillance" type aspect to your treatment study. In this case, that is called "recruitment." You need to screen through lots of pregnant women to discover the depressed women. Then, you provide treatment and see who gets better. Obviously, the number of screened women will need to be much greater than the number treated. So, a surveillance study, in general, will have a sample of people much greater than a treamtent study. Generally.
So, in any treatment study, you hypothetically have a surveillance study built in. If only you conceptualize it that way. And if you report that info, then people reading your treatment study can glean the recuitment data from the treatment study.
The point being: suveillance bigger number than treatment.
At the same time, Dr. Wsner has a detection-and-treatment grant listed in CRISP, the data base listing federally funded studies. Two groups: usual care for postpartum depression, or a more organized "chronic disease management" model, with more case managment and monitoring, plus some emphasis on patient choice.
Sample size for each of these two groups? 231 each.
Yes, for Wisner, you only need 48 patients to conduct surveillance for birth defects, but a treatment study needs four times as many patients in each of the two treatment groups.
That just does not add up. Unless you consider: 1. maybe they really did not want to find birth defects? Why not? Here's a wild idea: profit motive: Big Pharma has been funding Wisner for a long time. When considering meds versus therapy for prepartum depression, she has a reason to favor meds, maybe?
There are other funny things with this surveillance study. Maybe I will ge to them later. But this is plenty enough to: 1. cast suspicion on the reuslts, and 2. wonder how this ever got published.
Thursday, April 23, 2009
I have a lot to say, but I am going to stick to one point. I may get readers who otherwise would never look at my blog, so I really want to get my point across. (Well, no one reads my blog anyway, so I might actually get some readers with this PPD MBS blog week 2009).
Here is my point: Because there are very serious, grave issues with psych drug treatment of depression, including postpartum depression, as we advocate for detection and treatment of postpartum depression, we should strongly consider psychotherapy, and other psychosocial interventions, as FIRST-LINE treatment for depression, before resorting to any psych meds.
OK, thanks for reading. If you are interested in the evidence base for my opinion, please read on.
I have personally looked at MOST of the published empirical evidence (that means actual published, peer-reviewed scientific evidence versus opinions from anyone, professional, patient, pharmaceutical company representative, political activists, legislators, etc.) regarding the actual treatment (not just detection, just demographics, natural history, consensus statements, clinical guidelines, etc.) of postpartum depression.
I have three conclusions, as of this point in time, subject to change (I try to base my opinions on actual evidence, which can change as new studies emerge, etc.). Here are my three conclusions:
1. The evidence overall is just as promising, if not more so, for psychotherapy and other psychosocial interventions (such as fitness walking AKA “pram-walking”);
Example of evidence, talk therapy for PPD: Published by Grote and colleagues, in "Psychintric Services," March 2009: "A randomized controlled trial of culturally relevant, brief interpersonal psychotherapy for perinatal depression;" "participants in enhanced IPT-B, compared with those in enhanced usual care, displayed significant reductions in depression diagnoses and depressive symptoms before childbirth (three months postbaseline) and at six months postpartum and showed significant improvements in social functioning at six months postpartum."
2. There is the risk of harm from medications to the developing fetus or the breast-feeding baby (and I don’t trust the pharmaceutical companies to be perfectly honest and forthcoming about these risks, since there is documented lawsuit evidence that they have hidden and suppressed side effect harm in antidepressant studies as well as other studies).
One example of bad outcomes associated with SSRI, simply to make the point that there is reason for concern, despite ALL the reassurance from the pharmaceutical companies and the researchers they bankroll: Risk for birth defects: Alwan and collegues, and the National Birth Defects Prevention Study, published in New England Journal of Medicine, June 28, 2007:
"Maternal SSRI use was associated with anencephaly (214 infants, 9 exposed; adjusted odds ratio, 2.4; 95% confidence interval [CI], 1.1 to 5.1), craniosynostosis (432 infants, 24 exposed; adjusted odds ratio, 2.5; 95% CI, 1.5 to 4.0), and omphalocele (181 infants, 11 exposed; adjusted odds ratio, 2.8; 95% CI, 1.3 to 5.7)." How to read these results? In plain English, if a fetus had anencephalopathy, the chances are three times as good that the mom was, versus was not, in the group of women taking antidepressants. You pay your money and you take your chances. You pick. Meds vs. therapy.
3. It is becoming increasingly apparent that for some people, antidepressants, or withdrawal from antidepressants, contribute to the person becoming impulsively violent, including murder, suicide, and murder/suicide. For more information, look at my other posts, or google “antidepressants” and “suicide”, or look at, just to begin, these websites:
Point 3, and Melanie Blocker Stokes: It is my opinion, based on limited information from her story on the web, that this phenomenon of antidepressant side effects, NOT postpartum depression itself, may have led to this mother’s suicide. This guess is limited, since Melanie Blocker Stokes’ problems were not typical depression, but also included psychosis, which is NOT typical of the majority of PPD cases. So, this is a limited guess. I recognize that for the family, this young mom’s death is a highly profound and painful issue. I don’t know any of these people, but I only mean to HELP anyone I might help by sharing evidence-based, well-reasoned ideas regarding how to MAXIMALLY help ANY person with problems such as depression, including PPD. By my OPINION, I do NOT mean to diminish the cause of the MBS Act, or say ANYTHING bad about MBS or her family. For them, I say: Philippians 4:8. And any other scripture that might bring comfort.
However, I believe that as WE believers in postpartum depression, who believe ALSO that more needs to be done, we have to be careful that we are not promoting something that seems good but is actually bad: we should be wary of promoting, directly or indirectly, the increased prescription of antidepressants **when a perfectly acceptable, empirically supported, well-recognized alternative exists.**
There are MANY unanswered questions in the topic of PPD. We do need more research. What we DON’T need is more research of this pill versus that pill. Any such research needs to be done WELL: blinded, and against placebo, and also against psychotherapeutic interventions.
Well, that is what I have to say about peripartum depression, on this blog-about-peripartum-depression week 2009. Let’s avoid pills, and look to psychosocial treatments.
The rest of this blog post is technical details regarding how to evaluate pill studies for PPD. You have to become familiar with how the drug companies shape studies to make the benefits look better than they truly are, and to minimize the side effects.
So, if you have read this far, and have heard my points above, I greatly appreciate the attention. Wish me luck in my endeavors to understand and improve care for peripartum depression.
If you are interested in those technical details, which are important in the question of “meds versus therapy” (hence the blog name), read on. (Or, if you have insomnia, read on). -MVT
Here is an important technical detail to examine in any studies testing pills to treat peripartum depression: Was there a “control group”?
To get a group of 10 women with postpartum depression, and give them antidepressants, and to find at some follow-up point that depression scores were, on average, lower, is NOT sufficient to establish that medication as being effective for postpartum depression.
1. Because we don’t know where the scores would have gone without the medication being given. For example, what all of us know from our familiarity with anyone experiencing peripartum depression, it can last for months, or it can wax and wane across a few weeks. So, the overall change could have happened because of the med, or some other things, such as the “naturalistic” ebb and flow of the depressive symptoms.
2. Because the delivery of meds includes other aspects that can help, such as the increased activity, social involvement, and the “installation of hope.”
There are two pre-eminent psychologists who have defined the ways that psychotherapy works. There is a great deal of subsequent research supporting these principals of how psychotherapy works. We are talking back to the 1950s up to the present day, LONG before Prozac ever made it to the market. I believe these factors are worth looking at, since you can then begin to see how the process of seeing a physician and staff, being assessed and diagnosed, being prescribed a med, and being monitored as you start the med, can deliver, along with the med, some curative psychosocial factors.
Here are these factors, or principles.
Irwin Yalom: how does group psychotherapy work, for depression as well as other problems:
Installation of Hope; Universality; Imparting Information; Altruism; The Corrective Recapitulation of the Primary Family Group; Development of Socializing Techniques; Imitative Behavior; Interpersonal Learning; Group Cohesiveness; Catharsis; Existential Factors.
Carl Rogers: what are the "necessary and sufficient" ingredients of change in psychotherapy:
1. Two persons are in psychological contact.
2. The first, whom we shall term the client, is in a state of incongruence, being
vulnerable and anxious.
3. The second person, whom we shall term the therapist, is congruent or
integrated in the relationship.
4. The therapist experiences unconditional positive regard for the client.
5. The therapist experiences an empathic understanding of the client’s internal
frame of reference and endeavors to communicate this experience to the client.
6. The communication to the client of the therapist’s empathic understanding and
unconditional positive regard is to a minimal degree achieved.
To review these principals, you can begin to see that when you go through the process of getting assessed and receiving pill treatment, you are also probably receiving these curative factors as well.
Therefore, to determine if a medication works for peripartum depression, you need to have a placebo group who gets all of the social experience, but none of the pill's active ingredient. And, the researchers/pill providers have to be "blinded;" they can't know who is getting the true pill and who is getting the dummy pill, or they can bias the study. And the patient has to not-know, since the belief that you are getting the "real" pill could give "installation of hope," and lead to some benefit simply by this bias.
Psychotherapy studies don't have to "control" for these alternate effects because these are part-and-parcel of what psychotherapy is. Psychotherapy is partly the specific techniques, questions explored, skills taught, etc., but it is also curative through this special type of relationship. A relationship ultimately described as "unconditional positive regard." Sure you can get this from your Grandmother. And you probably should. If you don't, then I think that says something.
The pharmaceutical companies have dollar signs in their eyes, so they can really influence the design of a study to make their pill look good. So, we need to be wary of them.
On review, the medication studies overall are not at a very high quality level. The evidence for psychotherapy, and other things such as social support, is at a minimum just as promising for pre- and postpartum depression. Plus, there is a frightening aspect of birth defect risk with meds, but not with psychotherapy. So, what do you prefer? MedsVsTherapy.
Wednesday, April 22, 2009
"Wood, 34, also suffered from depression and anxiety and had been prescribed four anti-depressant medications, Sheriff Chuck Jenkins said during a Tuesday afternoon press conference.
Because toxicology reports will not be available for several weeks, detectives do not know if he was taking his medication at the time of his death. The drugs seized were Cymbalta (duloxetine), alprazolam, paroxetine, and buspirone, officials said."
Cymbalta is a SNRI antidepressant. Alprazolam is a plain old anti-anxiety drug. Paroxetine is an SSRI. Buspirone doesn't fit too easily in these types of categories, but acts upon serotonin system, as does any SSRI or SNRI, but has different effect, with more anti-anxiety effect, and less bothersome side effect profile.
SNRIs seem less linked to these violent deathly acts, but still linked, while any SSRI is strongly linked. "ssristories.com" and other sites have overflowing information. Simply google any of these terms, and "suicide," and you are on the trail.
Yes, the guy had half a million in debt. OK, maybe the guy feels hopeless, and wants a way "out." And for some reason wants to have his family die, also.
But look at how gruesome the whole murder was. Killed the wife, AND the kids? Shot THEN butchered people with a knife? Something was messing with this guy's head.
It was a Trojan Pill. He was prescribed these pills, thinking they would help him. Then, like the Trojan horse once inside the walls of Troy, the bad appears, invited through the pathway of good.
Why these 4 different prescriptions? Was this guy so messed up that one, or two, were not sufficient? No.
It is very unlikely that this successful, gainfully employed family man walked into a doc's office and walked out with 4 prescriptions.
These were all seized from the home, at the same time, but they were all part of the meddy-go-round.
Likely, one was initially prescribed as treatment for depression. AND likely NO talk therapy was pushed, referred, delivered, etc. Maybe an antianxiety was also rx since the guy may have mentioned sleeplessness.
Well, he was not depresssed because of a "brain disorder." He was not having poor sleep because of a "sleep disorder."
The docs can try to convince us all they want that these are just biological, genetic illnesses to which we are pre-disposed. Hi, you have sickle cell. Sorry about that. It is genetic and you got it from your folks. Hi, you have cystic fibrosis. It is genetic and you got it from your folks. I will help you get treatment.
We know better. Why do we go along with these pills? I don't know.
Talk therapy also works. And works better. And does not have the range of side effects, such as ED or suicide, as these pills. For this guy, talk therapy may have worked. Also, financial counseling may have helped. Marriage therapy if it looked like the couple was having a challenging time facing the financial problems, and was not working well as a team.
Overall, it seems clear: to improve sleep ,the guy needed to get somewhere on his financial problems, not take a pill. The pill did not help his financial picture.
Likewise, the pills did not improve his hopelessness in the face of financial problems. Actual financial strategies, perspective-taking, etc. would have helped. A pill does not reduce your debt.
So, why 4 meds? I have painted a picture to show WHY the meds failed. The pills do not improve your financial picture. So, the depression and sleeplessness continues.
He goes back to the doc, who believes in a simple idea despite tons of evidence regarding the actually quite limited effect: "pills cure depression." So, the doc switches from one to another. Probably from paroxetine to cymbalta. For anxiety, maybe from buspirone to alprazolam.
Cuz the anxiety pills have not made the worry, or the sleep problems, go away. Why not? because they did nothing to help him address the unsold house in Florida.
This is what the doc is saying about the world: if you give someone a pill, it will work by helping their house to sell more quickly. That does not make sense.
So, the guy goes to switch from paroxetine to cymbalta. And so he gets hit with SSRI withdrawal syndrome. And tries to mask it with alprazolam (AKA xanax).
That is how 4 Rx end up in the home.
I hate to be right about this.
Plus, I hate how the media and eveyone frame this as a "mystery," or a "financial stress" story.
Stable, successful church-going family guys do not brutally slaughter their entire family because of 450k in debt.
Sure, there is always the exception. But this pattern is scary. This is a pattern, not an exception.
Look down the road: down I-70 to 695, and around to Towson, to see what is going on at the family murder / suicide scene in Towson. Maybe Michael Phelp's mom is on the scene to advocate for more psych drugs...
"Family's murder-suicide deaths baffle friends.The Long Island family was found dead in a suburban Baltimore hotel room"
"TOWSON, Md. - They seemed like an ideal Long Island family: William Parente was a lawyer, his wife Betty a stay-at-home mom active in the community. Their daughters were well-liked by teachers and classmates.
Friends and neighbors said they never suspected anything was amiss and were dumbfounded to learn the Parentes had died Monday in an apparent murder-suicide in a suburban Baltimore hotel room."
how can we explain all of this?
"Kremer, the Parentes' next-door neighbor and a clinical social worker, said she saw nothing to indicate the family was having financial or psychological problems. She did note that William's parents and Betty's mother had died somewhat recently."
And you know what we will eventually discover, if only someone has the heads-up to ask: either the husband or the wife was recently prescribed SSRI to help the person cope with the recent losses. I have not yet seen this on the radar in the family murder / suicide of Chris Wood and family down the road in Frederick, Maryland.
Here is how tragically clueless the general America public, and the media, are: even though there is no evidence of economic problems, that is the scenario hypothetically trotted out.
Now, the media may be totally off-track, or I may be totally off-track.
We will see. Because at some point, which apparently is well beyond the thousands of murder and suicides where SSRI has been the common denominator, SSRI will finally get on the radar, and will be trotted out as one of the usual suspects, along with "the economy."
Then, maybe, things will start to change.
Monday, April 20, 2009
An autism blog ran a commentary on the psych pharamceutical issue. One commenter claims to have specific, recent info from the wife, now murdered, that her huband was on SSRI.
Here is the link to the web page with the comment:
And here is the comment:
"Posted by: Rosiecee April 20, 2009 at 10:19 AM
Regarding the recent murder/suicide in Maryland.....
Francie (the wife) was a member of one of my online groups. My "imaginary online friends" as I liked to call them. She was always pleasant and very sweet. I remember reading the birth story of her daughter who was born at home.
She hadn't posted in awhile, maybe the timing coinciding with her move to MD. But some members kept in touch with her.
Apparently some of the members kept in touch with her outside the group....and posted this morning that her husband was on antidepressants. I can't confirm this though but it wouldn't be shocking at all."
Now: what level of evidence would you say this is? Sure, it can be dismissed as "word-of-mouth," or rumor. But then again, it seems sincere and authentic. If it were conveyed by a reporter who happened to interview this woman, we would regard it as fairly credible.
That is where I put it, for the time-being.
We will see. Often, these news stories do not ASK, or REVEAL, the pharma connection. So, as these SSRIs may be posing a terrible threat to many of us - they have been prescribed to an astonishing level for the past 2 decades - the media have not quite caught up enough to ask about psych meds in these events, the way that they apparently will ask about "stress" or "psychological difficulties" or "illegal drugs" or "guns" or "family problems."
why not? we need to be open-minded to this great body of evidence. when we hear: "the murderer / the suicider was on SSRI," we can't just think: oh, well, that explains a lot - they were having mental difficulties," --we also have to think: "I wonder if the SSRI influenced them, to prompt a bad situation or circumstance to go even worse - far worse."
His wife has had a blog in which she noted his stress, including financial stress. So, now, the media and the rest of us will believe the stress, including maybe financial stress related to the economic downturn, caused this guy to slaughter his family.
Do you buy it?
People, we need to begin thinking like this: with a suicide, or murder/suicide, first suspect some big problem with illicit drugs: a person with a long-term alcohol, cocaine, etc. problem finally got impulsive enough to make the aggressive act;
Second: suspect SSRI.
This guy was a provider. He and his family were solidly involved in their normal, everyday house of worship community, and his wife was a stay-at-home mom, raising the kids. The man had accepted a promotion, and was trying to succeed. Early stories indicate the couple may have been looking for another home.
So, this is not some absent father, or overgrown adolescent. This man was a provider. A family man.
So, by my thinking, we should be very suspicious of SSRI influence, or SSRI withdrawal influence, upon violent aggressiveness.
Here on this 10 year anniversary of Columbine (where SSRIs were involved).
I search the news stories: they are all the same. In fact, they are literally all the same story.
But as news pops up, I finally see the clue:
CNN carries a story, with info from a local sherriff:
"There was a mention of some medication' in that note, according to the sheriff."
The man apparently left five or so suicide / explanatory notes.
So, while most of us are led astray by the "stress" explanation, and while some of us start chiming in with the idea that we should not have the right to arm bears, because it leads to mass murders, A few of us will be quite upset about the primary cause. THe cause right in front of everyone, staring at them, but avoiding detecting.
Psychiatric medications. Specifically, SSRIs.
We think: "oh, psychiatric medication: well, this proves he was mentally unstable."
And we can carry on with our own life, feeling safer now that we undestand that this murder suicide occurred because a mentally unstable person, despite treatment, had access to a gun. And access to knives. So, maybe we add knife ban to our list of rules for a perfect world.
But we are not safer. Because when we buy the mental instability explanation, we buy the SSRI cure. Wow, he should have started treatment sooner.
What we see is the opposite of what we should see:
The common thread in so many inexplicable murders and suicides is: SSRI.
Like Angela Lansbury showing up on "Murder, She Wrote." As soon as she shows up, or as soon as Agatha Christie's Miss Marple shows up, you know someone will be dead soon. Or has just died.
Likewise, SSRI is there for all of these incidents. Let's start using logic, and be wary that SSRIs are contributing to these impulsive acts.
Because if SSRIs are part of the solution, like everyone seems to believe, then that indicates one thing.
But if SSRIs are a major part of the problem, we will not get a handle on this problem as long as we are foolishly following the influence of Big Pharma as they push these under-studied drugs.
If autopsies are not even systematically screening for SSRI, and if investigators are not asking survivors about SSRI, and gathering med records, we will continue to allow this phenomenon to escape detection. If this issue is not posted in the actual story as each occurs, the way that "stress" is always bandied about as the trigger of violence, then we will never see what is right there.
Monday, April 6, 2009
Spin: change "Seroquel: risky for depression and anxiety, just as it was for schizop, bp" to "Risk for MDD and GAD same as for Schizophrenia, Bipolar"
AstraZeneca has posted the info that they have submitted in conjunction with this hearing (partly cuz FDA mistakenly posted it too soon).
A brief look thru it shows an interesting spin:
The reason for the hearing is because Seroquel AKA quetiapine seem to lead to diabetes in a fair portion of people. Some end up with diabetes; many end up with weight gain. With other atypical antipsychotics, Big Pharma had handled this by saying that the drugs caused increased appetite, and the appetite led to weight gain. Or inactivity. Anything but the drug.
It eventually came out that these drugs have diabetes risk. Why? DK. But this is where the research agenda SHOULD be; not on finding me-too atypicals, such as Seroquel.
Some evidence supports a theory that the atypical antipsychotic drugs may kill some special type of cell in the liver - scary - but this has not been fully studied.
In the meantime -
How does AZ spin its own evidence that within a few months of taking Seroquel, your body gets worse at responding to glucose? Which probably sez you are on your way to diabetes?
page 78, section 4.2.10:
"Evaluation of metabolic data from the MDD and GAD populations did not reveal any metabolic findings or suggest potential long term metabolic risks inconsistent with those seen in the currently approved indications of schizophrenia and bipolar disorder."
No evidence Seroquel will be any different for MDD and GAD as it was for Schizophrenia or bipolar.
I wish I could write like that. Somehow, the way they put it, it isounds like no big deal.
After getting patients with bipolar disorder stabilized for 3 months on seroquel, pts were randomly assigned to either stay on Seroquel, (plus have lithium or valproic acid as augment), or to get placebo Seroquel (along with lithium or valproic acid as augment).
Seroquel was successful at the main outcome: fewer Seroquel-plus-other-med pts relapsed compared to placebo-plus-other-med.
The study humbly presents a full panel of metabolic data, also, relating to body weight.
In the long-term (about two years) follow-up, the group that continued with Seroquel had greater elevations in glucose (not good) compared to placebo, and greater weight gain compared to placebo (not good).
For the glucose issue, it appears that this differs by diabetic status: little difference for those with no diabetes risk, modest but significant difference for those with diabetes risk, and scary changes for those with diabetes. For each of these three sets of people, I am looking at both the average, tellign which group was higher, plus looking at the standard deviation, which tell how orderly or wildly the glucose changes are.
Blood glucose for those with no diabetes risk looks the same between both groups (Seroquel and placebo).
Results diverge for the diabetes-risk group, with greater standard deviations - which means there are a few things going on to make many people have many differnt experiences. This result is probably not statistically significnt, but it is a concernign pattern.
For the diabetes group, the change in glucose is much greater for the group taking Seroquel vs. placebo, and the standard deviation (a measure of how much the typical person has changed) for the Seroquel group is off the chart: Seroquel group has standard deviation of 143 milligrams per deciliter, while the diabetic group taking placebo group has standard deviation that is a third of that (44 mg/dl).
An additional dimension is the effort to manage diabetes in these patients. I am going to talk here about the diabetic group only, so we can maybe figure out what is happening with these people. No "baseline" glucose is given for the diabetic groups (diabetic with Seroquel, and diabetic taking placebo). Now, here is a weird result: at the two-year follow-up, BOTH groups end up with the SAME average glucose level, 125 mg/dl, but how they got there differs:
The diabetic group taking Seroquel have had an average INCREASE (of 30 mg/dl avg) in blood glucose to end up at 125, but the diabetic group taking placebo has had an average DECREASE (17 mg/dl) in blood glucose to end up at 125.
Plus, as I said above, the standard deviation in change across time is much greater for the diabetic group taking Seroquel compared to the diabetic group taking placebo.
Why were baseline glucose measures not reported? DK. That would help make sense of this data. Per the article, it seems that glucose was taken at baseline, since that was used, along with other info, to define the diabetes group.
Demographics are not provided to let us know how many ppl were diabetic (per their defn), and the portion randomized to each treatment group is not reported.
While the reporting of randomization info is barely at the acceptable level for a decent study (there are standards, you know, like CONSORT guidelines), we can't tell if the weird pattern of results is due to very different numbers of ppl in the two groups.
Either way: this study fits in line with other studies, indicating: 1. it may be time, for someone with access to this and other data (i.e., FDA) to declare that diabetics should not be taking Seroquel; 2. somebody needs to figure out what effect Seroquel is having upon the bodies of ppl with high BMI and / or with diabetes.
The results are dramatic, and I don't quite see the fasting issue as explaining the scary difference: if you have diabetes and take Seroquel, it is going to be very difficult to manage your diabetes.
A funny thing about this study:
It is designed to see whether Seroquel-plus-adjunct-med is superior to Placebo-plus-adjunct med.
For the adjunct meds, each was given at the recognized therapeutic dose, not at some sub-optimal dose (as some prescribers probably still give Lithium: typically augmenting some other med with 300 mg lithium - far below clinical dose which will normally start around 900 mg).
But if you flip this study around in your mind, it becomes a test of Lithium versus lithium-plus-Seroquel, along with a test of valproic acid versus valproic acid-plus-Seroquel.
I think that is something to think about: it makes you see: this study is not about efficacy of Seroquel, although that is what the study authors (with a long list of Big Pharma connection$) seem to be trying to convince the FDA.
Update: a bit more info:
was this actually a test of divalproex or lithium, with or without augmentation by quetiapine?
For that, you would actually have to have therapeutic dosing levels of the divalproex and the lithium.
This study notes that blood lithium levels, in both arms of the study, were at mean of about .7 meq/liter. This is the bottom of the therapeutic window range.
Divalproex blood levels were at average of about 70microg/ml for each group. This is the bottom of the therapeutic window.
And these are averages. Standard deviations are not given, so we are lacking a bit of info on what portion of pts may have beem below therapeutic window. It is possible that these levels were controlled pretty tightly - the fact that the averages are similar in both groups would be quite a coincidence, in light of the headroom available that either drug could have been titrated up to - this is both good and bad - if the study researchers actually intently managed blood levels of these to adjunct meds, then they hypothetically have achieved levels that would maximally favor Seroquel - levels of lithium and divalproex that are within the therapeutic window, so as not to draw attention, but at a point that is gonna lack efficay for a decent portion of patients.
Failing to include standard deviations for these values, or ranges, or some measure of the portion of time pts spent within therapeutic range, is a real limit to understanding this study.
I believe it is safe to say that the lithium and divalproex treatment was technically within normal practice, but barely, and it would not be the optimal way to test a trial of either. Contrastingly, quetiapine WAS dosed at a normal, sufficient level - data suggests at least 400 mg for normal tx response, with a window up to 800 (beyond not tested because there is no reaason to - either 400 to 500 seems to work well, or you are not gonna get a response) - and this study had average dose of 500.
So, whether intentional or not, I would say that the dosing of each of these 3 medications happens to be in the pattern that happens to tilt the study to favor Seroquel.
Wednesday, April 1, 2009
With a bit of websearching, I discovered a pdf of a bit of this communication:
-from UCSF drug company document archive. wow, what a source to discover.
Basically, it is old news now that Merck deliberately and knowingly covered up the cardiovascular risk associated with the painkiller Vioxx.
This emerging story indicates that, along with recruiting (paying) "thought leader" physicians to get the word out about Vioxx, as a marketing strategy thinly disguised as "dissemination of knowledge," or "CME," Merck was also working the other direction: trying to figure out how to intimidate-into-silence any reputable critics.
Great news for all of us as we try to figure out whether we should trust the Merck / trust the Gardasil marketing-through-state-mandates activity. Who knows what Merck might be doing currently to quiet opposition to mandated Gardasil shots for teens.
What have we lost, with the withdrawal of Vioxx? Yes, it worked well, but folks, it was just another non-narcotic pain killer. There remain plenty pain management options.
Pills generally win over psychotherapy strategies for pain, although psychotherapy techniques can have some effect - some ppl are able to benefit from hypnotism. Clinically, I have had a little experience trying to hypnotize ppl for pain reduction. It worked with one person, so I believe it can work. I am pretty sure, though, that it is either just some ppl and some cases that can benefit, or it takes a very good hypnotist/clinician (and for some combo of events, this one client may have believed I knew what I was doing).
Becoming mentally calm seems to let the body turn down the sensitivity meter for pain signals, so when pain does flare up, it is only a one-alarm fire versus two- or three-alarm.
Life managment strategies are important for chronic pain: manage stress, do some good stretching such as yoga pilates etc., get decent sleep, and don't 'over-do' it (hard to tell chronic-pain ppl who for some reason seem to be driven ppl who don't like to tackle plans in bite size pieces, but like to work until they drop. Just my observation. Meds really wins this one. Fortunately, plenty of meds besides Vioxx.