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Hippocratic psychopharmacology


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Hippocratic psychopharmacology

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A Hippocratic psychopharmacology of bipolar disorder would emphasize the use of the only proven agent in the prophylaxis design, lithium, followed by those agents shown effective in the relapse prevention design, lamotrigine and divalproex. Carbamazepine is likely also effective, though not proven in placebo-controlled designs. Atypical antipsychotics are not proven effective in maintenance designs yet, though they have continuation phase benefit, and likely are useful as adjuncts, but not as mood stabilizers used in monotherapy.

A Hippocratic approach would emphasize agents with the most proven benefit (Holmes

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Also, prophylaxis is the prevention of disease. So, if I had taken Lithium since I was born, I wouldn't have BP I? If he's saying that Lithium is the only drug proven to show effect in the treatment of Bipolar, well that's just wrong.

And what's his difference between prophylaxis and relapse prevention? Relapse? WTF?

Again, if he's using "relapse prevention" to mean "maintinance" I believe he's flat-out wrong again.

So in my mind, that whole paragraph is based on two incorrect premises.

InfoNut's rule: Don't let your patient die because you're afraid the drug is harmful. It's considered bad form.

While it's true that dead patients don't need to worry nearly as much about adverse side effects, you do have the whole "aw shit... they're dead" thing to worry about.

(edited to continue ranting)

And how is the use of mood stabilizers NOT treating symptoms? Help me out here. Is the premise that Bipolar is caused by mood swings? Then... what causes the mood swings? If mood swings are indicitive of the disease, not the cause, then you are still simply treating symptoms with mood stabilizers. Screw Osler. The reason many mood stabilizers are not used in monotherapy is that they usually don't do much to aliviate depression.

okay... I'm done.

IN

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And what's his difference between prophylaxis and relapse prevention? Relapse? WTF?

Again, if he's using "relapse prevention" to mean "maintinance" I believe he's flat-out wrong again.

So in my mind, that whole paragraph is based on two incorrect premises.

In the context of the article "relapse prevention" refers to collecting data only from responders, .ie. no random treatment comparisons. So if Depakote was an effective anti-manic drug for a subject, the time to relapse was was recorded. The problem with with this type of design is that it is unfairly weighted. Lets say that 30% of people who were acutely manic responded to Depakote. Now if 60% of those responders went on without an acute episode for six months ( or what ever the design study may have as an end point), the conclusion would be that Depakote would be 60% effective in prevent relapse. The problem with this is that it is really 60% of 30%, which is 18%.

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And what's his difference between prophylaxis and relapse prevention? Relapse? WTF?

Again, if he's using "relapse prevention" to mean "maintinance" I believe he's flat-out wrong again.

So in my mind, that whole paragraph is based on two incorrect premises.

In the context of the article "relapse prevention" refers to collecting data only from responders, .ie. no random treatment comparisons. So if Depakote was an effective anti-manic drug for a subject, the time to relapse was was recorded. The problem with with this type of design is that it is unfairly weighted. Lets say that 30% of people who were acutely manic responded to Depakote. Now if 60% of those responders went on without an acute episode for six months ( or what ever the design study may have as an end point), the conclusion would be that Depakote would be 60% effective in prevent relapse. The problem with this is that it is really 60% of 30%, which is 18%.

Actually, in my mind the conclusion that Depakote is 60% effective for preventing relapse is true.

60% of the people who responded to Depakote didn't relapse.

The 18% comes in when you put both parts together.

i.e. Depakote was only 18% effective in the amelioration and "relapse prevention" of acute mania.

Or am I just splitting hairs?

IN

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Actually, in my mind the conclusion that Depakote is 60% effective for preventing relapse is true.

60% of the people who responded to Depakote didn't relapse.

The 18% comes in when you put both parts together.

i.e. Depakote was only 18% effective in the amelioration and "relapse prevention" of acute mania.

Or am I just splitting hairs?

IN

It is all in the way you read the data. The makers of Depakote will always refer to the 60% figure. The point Dr. Ghahemi was trying to make was that Lithium's "relapse prevention" response rate was not based solely on Lithium responders but on the much larger total participants number.

NB. the numbers I used were made up to explain methodology. They are not actual ones.

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It is all in the way you read the data. The makers of Depakote will always refer to the 60% figure. The point Dr. Ghahemi was trying to make was that Lithium's "relapse prevention" response rate was not based solely on Lithium responders but on the much larger total participants number.

NB. the numbers I used were made up to explain methodology. They are not actual ones.

I understood your numbers were simply conveniences... no worries.

I even understand somewhat the spirit behind the article.

But I think by mentioning specific drugs as the only true treatment for Bipolar, he invalidates most of what he says.

Lithium is not the only proven drug for short term treatment of Bipolar Disorder.

IN

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And how is the use of mood stabilizers NOT treating symptoms? Help me out here. Is the premise that Bipolar is caused by mood swings? Then... what causes the mood swings? If mood swings are indicitive of the disease, not the cause, then you are still simply treating symptoms with mood stabilizers. Screw Osler. The reason many mood stabilizers are not used in monotherapy is that they usually don't do much to aliviate depression.
A version of Ghaemi's point that I might a gree with is that a true mood stabilizer isn't the medication that t necessarily treats the symptoms du jour. Rather, it is prophylactic in that prevents further acute episode from occuring (or delays their course).

However, it seems that Ghami is taking up Osler's line that we should only use agents that have been shown beneficial in prophylaxis and largely disregard the current symptoms. And I, too, just can't agree with this in a country without much of a social safety net. (And where you are seen as deficient and morally weak if you can't work.) Yes, it's possible that the mood stabilizers, by Ghaemi's definition, reduces further episodes, once the initial one subsides. But what are we to do until then? We have to be functional and work. And it's not that common to achieve complete and utter prophylaxis. So what do we do when a new episode crops up, or if there are residual symptoms?

I mean, where the hell are the patients in Ghaemi's discussion? InfoNut has a good point about the risk of suicide with unchecked acute symptomology. Even more the issue: I think that many of us go through the cost-benefit calculus explicitly. And you know what, even with the weight gain and lipid ugliness from the AAPs is well established now, look at the number of people on Zyprexa and Seroquel. This, to me, reveals our need for acute treatment, despite the risks. Granted there might be other unknown long-term side effects, but we also know that .. and are still willing to take them. Or we choose not to. For fuck's sake: give us some agency here!

~cache-monkey

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And how is the use of mood stabilizers NOT treating symptoms? Help me out here. Is the premise that Bipolar is caused by mood swings? Then... what causes the mood swings? If mood swings are indicitive of the disease, not the cause, then you are still simply treating symptoms with mood stabilizers. Screw Osler.

I disagree here. The mood swings, or acute episodes, are caused by the disease. So by treating the disease with medications that have proven efficacy you are in effect treating the symptoms.

However, it seems that Ghami is taking up Osler's line that we should only use agents that have been shown beneficial in prophylaxis and largely disregard the current symptoms. And I, too, just can't agree with this in a country without much of a social safety net. (And where you are seen as deficient and morally weak if you can't work.) Yes, it's possible that the mood stabilizers, by Ghaemi's definition, reduces further episodes, once the initial one subsides. But what are we to do until then? We have to be functional and work. And it's not that common to achieve complete and utter prophylaxis. So what do we do when a new episode crops up, or if there are residual symptoms?

The context of the article is prophylaxis. The point Dr. Ghaemi is making is that some current studies are equivocal in outcomes WRT the benefits of certain agents used for such.

I mean, where the hell are the patients in Ghaemi's discussion? InfoNut has a good point about the risk of suicide with unchecked acute symptomology. Even more the issue: I think that many of us go through the cost-benefit calculus explicitly. And you know what, even with the weight gain and lipid ugliness from the AAPs is well established now, look at the number of people on Zyprexa and Seroquel. This, to me, reveals our need for acute treatment, despite the risks. Granted there might be other unknown long-term side effects, but we also know that .. and are still willing to take them. Or we choose not to. For fuck's sake: give us some agency here!

Again I would wager that Dr. Ghaemi would have no troubles giving Zyprexa during an acute episode. The issue is should it be used long term. All in all I think that all he is trying to do is inject some rationality into the treatment (long term) of BD. Also keep in mind that treatment decisions may also be influenced by the health care system. As you noted, there is a lot of pressure to end an acute episode fast. The pressure is both internal ( the patient) and external (who ever is footing the bill). Such influence may allow for a pharmacological regime that is geared towards ending the episode but will not help prevent new ones. So unless the management strategies change after addressing the acute episode there may be nothing in place to prevent further ones. Which should be the number one priority.

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  • 3 weeks later...

Please do NOT ask me why, and herrfous is going to be OT here again (!), but this somehow somewhere reminds me of a discussion I had yesterday with Mom, over the phone:

Mom: "It says here [on the PI sheet] that Lamictal has driven a few people psychotic! You need to stop taking it!"

Me: "Uh mom, way more bipolars have found it effective... didn't you read the part that talks about efficacy?"

Mom: "It's still not worth it!!! You need to stop taking it!!"

Me: "Do you not remember how I'd probably be dead by now had I not looked for therapy and meds?"

Mom: "Oh. Good point."

*rolls eyes* as usual,

--herrfous

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This is all very scary for me. Yesterday, I got a letter in the mail from Blue Cross/Blue Shield stating that they will pay for medications that they believe to be the most effective before the more expensive ones the pdocs prescribe. Yikes! I can understand their reasoning. I'm sure they don't make enough money as it is with those premiums and co-pays and deductibles. ( I meet my 500$ deductible in a little over a month!).

I'm sure they REALLY don't like me too much. I think w/ my meds alone, they are dishing out-aboout 1500$ per month-every month.

I would hate to think some beaurocrat in BC/BS would read articles such as this one to determine what meds they in their expertise deem suitable. mel1

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Exactly mel. Hubby tried the lithium and later, the depakote. He was miserable.

The Lamictal is working. He is no longer psychotic nor is he suicidal. Side effects are so minimal as to be completely discounted. Occassional use of zyprexa or seroquel is still necessary, but he is doing fantastic. 2 year ago he was planning his own death.

How about Wifezilla's law... If it aint broke, don't fix it!

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I would hate to think some beaurocrat in BC/BS would read articles such as this one to determine what meds they in their expertise deem suitable. mel1

You are misconstruing what is being said. At no point does Dr. Ghaemi suggest using only Li or Depakote. He is suggesting that they are the most proven, along with carbamazepine, to offer the long term help. And for other agents like the AAP's the evidence is tenuous. It is his opinion that a successful six week treatment does not mean that it will work for one or more years, as has been shown with the first line treatments. But that very same standard is what is used by the drug industry to suggest that it does. I have read the article and have yet to find anywhere where it is suggested that second or third line agents should not be used if necessary. In the book Polypharmacy in Psychiatry he clearly states that disorders like BD are difficult to treat and usally require more than one med.

Ghaemi also devotes much attention to defining polypharmacy, distinguishing between rational and irrational polypharmacy. Some disorders (for example, bipolar disorder [bD]) historically require 2 or more drugs for adequate treatment of the disorder and its associated symptoms. In such cases, polypharmacy is not only rational but may be standard treatment
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