51–60 of 93 posts
The other thing to keep in mind is that if this was a pivotal trial study, the FDA had the complete data set yet failed to recognize the increase in suicidal ideation as well.
So why isn't there some sort of post-approval monitoring system for drugs? With aircraft and cars we have enough data captured that problems can be identified and traced.
Earlier quoted context omitted.
> Now let's find out if this anti-depressant really helps anyone, or is it just another terrible drug with horrid side effects? If it doesn't help better than placebo; take it off the market? The claim that SSRIs are no better than placebo is increasingly popular on the internet and among some researchers eager to make headlines, but the claim is not backed by the data. At best, it represents a misunderstanding of ho…
How can we really be sure that they're more efficacious than placebos (which can be quite efficacious) when we aren't allowed to see negative data generated during clinical trials? We have absolutely no aperture into the internal studies that weren't submitted as proof of the drug being effective. Sure, administering these drugs will make some patients report fewer negative symptoms-- typically the worst hit patients…
The monoamine hypothesis of depression (the idea that all depressions are directly attributable to negative alterations in monoamine dynamics) has been known to be inadequate for a decade or two now in the scientific community. The idea that researchers are still operating on this basis is totally false at this point, but anti-pharma crusaders still hold it up as a convenient straw-man because it's so easy to discredit now using (ironically enough) all of the latest research that the scientific community actually uses for our current understanding of depression.
We're all very well aware that depression isn't caused by "low serotonin levels" or other such completely wrong marketing-speak of the 90s. In fact, there are quite a few very promising anti-depressants in the pipeline and stage III clinical trials that don't directly manipulate monoaminergic systems at all.
Finally, your suggestion that the monoamine hypothesis is the theory behind the actions of SSRIs is completely false. We've known for a very long time that the therapeutic effects of SSRIs lag the near-immediate alterations of monoaminergic. You can't equate discrediting the monoaminergic hypothesis of depression with discrediting SSRIs.
Earlier quoted context omitted.
I'm sorry, but one can't "just use a lot of question marks" without completely destroying whatever meaning they're trying to get across. I don't give a rat's ass if someone confuses "their" with "there", or "it's" with "its". The meaning is entirely left intact. But ending every single sentence with a question mark is very confusing to the reader. I still have no idea if marincounty is agreeing with the parent, calli…
It helps if you read it in an Australian accent?
This is an egregious violation on many levels. It highlights a massive gap in the clinical trials process (companies can stop trials without reporting negative results) that really should be addressed. I think everyone (outside of drug companies) can agree on that much. I would like to say a few words on SSRIs (the class of drugs that Paxil is in) and their risks in general, because articles like these tend to cultiv…
I have some experience as a patient with Escitalopram (an SSRI) and can only say: indeed. The first two weeks it was utter confussion (I feel so worse) but reading the prospect (a very good one in Spain) and talking to my doctor clarified the situation. After some weeks the "new normal" settled and to me, the medication helped. It is good to have your doctor handy anyway.
I'm still surprised that more doctors aren't taking a proactive approach to telling their patients what to expect. I suspect part of it stems from lack of education, but I think some doctors are afraid to tell depressed patients that they might get worse before they get better because that suggestion alone might make them not take the medication in the first place.
I use to work in pharma research (at the data acquisition and analysis side, blinded from treatment) and the fact that pharmas are able to start clinical trials and then shut them down without reporting result is a problem. The folks who make those decision usually have access to unblinded data and in the least objectionable case they do it due to lack of efficacy but you never know. Maybe they found a side-effect an…
"I use to work in pharma research (at the data acquisition and analysis side, blinded from treatment) and the fact that pharmas are able to start clinical trials and then shut them down without reporting result is a problem." This Cherry Picking should become a felony? Spit out the data you have on hand, even if incomplete? Give the results of the studies to the FDA, or make whatever data you have available to the sc…
So why isn't there some sort of post-approval monitoring system for drugs? With aircraft and cars we have enough data captured that problems can be identified and traced.
There is, post market monitoring.
Earlier quoted context omitted.
I have some experience as a patient with Escitalopram (an SSRI) and can only say: indeed. The first two weeks it was utter confussion (I feel so worse) but reading the prospect (a very good one in Spain) and talking to my doctor clarified the situation. After some weeks the "new normal" settled and to me, the medication helped. It is good to have your doctor handy anyway.
Thanks for sharing your experience. I'm still surprised that more doctors aren't taking a proactive approach to telling their patients what to expect. I suspect part of it stems from lack of education, but I think some doctors are afraid to tell depressed patients that they might get worse before they get better because that suggestion alone might make them not take the medication in the first place.
Depression runs in my family. Please be considerate in your replies here to me. I think in US every available antidepressant has that 'suicidal thoughts' warning right at the top of the list yet antidepressants have been a very valuable tool for our family for young and old alike. I do not believe that any causation has been determined for currently commonly prescribed medications. This is Reuters article reprinted a…
What we have, at least in the US, is too many pharmacological solutions and not enough CBT.
It was once explained to me that depression and anxiety are like a top spinning out of control. There's too much momentum throwing it off, no amount of self-effort will correct it and eventually it will probably crash. Meds are like resetting the top, and talk therapy equips you to keep it spinning correctly. Then once you're properly equipped with strategies to keep your top spinning straight you can taper off the 'crutch'.
But it's way, way easier to write a prescription and say 'come see me again in 8 weeks when the meds take effect', leaving the patient to suffer for 2 months.
Earlier quoted context omitted.
How can we really be sure that they're more efficacious than placebos (which can be quite efficacious) when we aren't allowed to see negative data generated during clinical trials? We have absolutely no aperture into the internal studies that weren't submitted as proof of the drug being effective. Sure, administering these drugs will make some patients report fewer negative symptoms-- typically the worst hit patients…
> Then there's the academic problem: the monoamine hypothesis (the underlying theory behind the actions and use of SSRIs etc) is at best a crude approximation with precious little in vivo data to support ideas that are known to be inaccurate and incomplete. The monoamine hypothesis of depression (the idea that all depressions are directly attributable to negative alterations in monoamine dynamics) has been known to b…
I think it's fair to say researchers are still operating loosely within the framework of monoamine imbalance, given the predilection of pharmas to releasing new drugs which operate via modulation of monoamines rather any other action. Paradoxically if they were stepping away from the monoamine hypothesis, they would produce polymonoamine regulatory drugs which would more subtly manipulate multiple monoamines in order to get the desired modulation of maloperating neural circuits, the target du jour.
I guess we have to disagree on the science here regarding your last point... the therapeutic effects of SSRIs are certainly (100% with no wiggle room, a settled fact) a result of subtle neural circuit modulation to get therapeutic effect via monoamines.