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To: Republic_of_Secession.

I have a different take on it. I think that the vocal minority groups push the FDA to approve drugs before they have been thoroughly vetted. Many of the AIDS drugs were put on the market too early due to pressure from the Gay lobby. May be the same here.


12 posted on 06/24/2008 10:24:10 PM PDT by originalbuckeye
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To: originalbuckeye
I have a different take on it. I think that the vocal minority groups push the FDA to approve drugs before they have been thoroughly vetted. Many of the AIDS drugs were put on the market too early due to pressure from the Gay lobby. May be the same here.

I work in the pharmaceutical industry. You're more on track than you know.

16 posted on 06/24/2008 10:43:26 PM PDT by buccaneer81 (Bob Taft has soiled the family name for the next century.)
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To: originalbuckeye; Republic_of_Secession.; Dad yer funny
I have a different take on it. I think that the vocal minority groups push the FDA to approve drugs before they have been thoroughly vetted. Many of the AIDS drugs were put on the market too early due to pressure from the Gay lobby. May be the same here.

That's not a good example. When you don't have much to work with, almost anything is better than nothing.

Vioxx is also a bad example. No one has offered a mechanism for Vioxx causing death that's made the MSM. It could have been from interfering with Aspirin's irreversible inhibition of platelet aggregation. IIRC, all NSAIDs except Aspirin are described as reversible inhibitors of platelet aggregation. If they took the baby Aspirin two hours before the Vioxx or Bextra they might still be alive.

Drug Insight: cyclo-oxygenase-2 inhibitors—a critical appraisal

Consequently, it is plausible that a permanent blockade of COX2-dependent prostaglandins, including prostacyclin, is the (currently) most plausible explanation for the cardiovascular hazard conferred by selective and nonselective inhibitors. In fact, prostacyclin, which is suppressed by over 60% by both NSAIDs and COX2 inhibitors,50 is not only a potent inhibitor of platelet aggregation, but also interferes with processes leading to hypertension, atherogenesis and cardiac dysfunction. In a randomized study, diclofenac, given in a delayed release form, elicits an even more pronounced inhibition of intravascular COX2-dependent prostaglandin formation than rofecoxib and celecoxib.15 It has been suggested in this context that both degree and time-course of intravascular COX2 inhibition might determine the differential profile of cardiovascular side effects associated with NSAIDs and COX2 inhibitors.

27 posted on 06/24/2008 11:38:47 PM PDT by neverdem (I'm praying for a Divine Intervention.)
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