For some reason, the Montreal Gazette has a piece from the Windsor Star on the website this morning, and it freaks me out. The headline runs: "Workforce expert predicts future jobs." Which is a little like a meteorologist predicting that the future will have weather.
Apparently she's been waiting for a long time for appointments in offices that contain 5-year-old copies of The Economist; arguing that economic growth will depend on local people training and upgrading their skills. "You can't deny the importance of the knowledge economy," she is quoted as saying. The article also says she offers the pharmaceutical industry as a growth area for job seekers.
Now we'll leave alone the fact that we have more people with university degrees than our economy knows what to do with, and just point out that last year alone, Pfizer cut 19 500 jobs. This is the 2nd time in three years they've topped the pharma charts; in 2007 they cut another 10 000 jobs. This past year, Merck cut another 16 000 jobs; Johnson & Johnson slashed almost 9 000; and AstraZeneca lost about 7 500. Between the top 6 job cuts in the industry, over 63 000 jobs went to the big market in the sky.
The reason for this is that the pharmaceutical industry is scrambling to make money right now. There are no blockbuster drugs waiting for approval from the FDA, no huge breakthroughs that promise huge profits. Without the ability to provide any goods, big pharma is reduced to making money in the way that corporations usually do it: mergers, acquisitions and cuts. This is bad news for the workers, none of whom have the advantageous situation of, say, a GM employee.
All that to say that big pharma is not a growth industry in real terms, and anything decent in "little" pharma is going to get its intellectual property snapped up by one of the big boys, leaving little but empty infrastructure and unemployment in its wake. Not what I would describe as a strong market.
* * *
A couple of words on prorogation.
Proroguing Parliament is nothing new. Everyone has done it, from Sir John A to Jean Chretien. Normally, however, Parliament is prorogued to start a holiday break or to end a session. Harper's prorogations have been special, certainly in the modern Parliament (last 30-40 years).
Last time, Harper prorogued Parliament because he was facing a vote of confidence that he thought he might lose, and that a coalition of opposition parties might form a government. So he asked the Governor-General if he could buy some time while he talked with various parties long enough to let the coalition run its natural course: failure. This was annoying, but it was smart politics.
This time, however, the reasons for prorogation are less clear. There is a scandal before the government regarding Afghan detainees, the Olympic Games in February, and another vote of confidence coming in March (the budget). However, these issues don't seem overwhelming - not while important bills are waiting before the House (the anti-crime legislation that is an integral part of the Conservative platform, for example).
This prorogation comes during a scheduled break from Parliament. This is pretty much unheard of, and extends the break from 39 days to 76 days. It is disingenuous for Harper to say that this is a routine procedure: the only other prorogation that lasted this long since 1968 (as early as I checked) was Chretien's 82-day prorogation in 2003-2004; executed mostly to avoid Sheila Fraser's report on the Sponsorship Scandal and inquiries into military conduct in Somalia. For the Conservatives to criticize Chretien's move while defending Harper is outright hypocrisy.
Which shouldn't surprise me, I suppose. What does surprise me is that something was worth wasting political capital on prorogation. What's waiting in the wings when Parliament resumes in March?
Showing posts with label big pharma. Show all posts
Showing posts with label big pharma. Show all posts
Monday, January 11, 2010
Friday, December 4, 2009
Pfizer on CIHR board no conflict of interest
Poor Leona Aglukkaq is getting ripped apart in the news these days for appointing Bernard Prigent, vice-president and medical director of Pfizer Canada, to the governing council of the Canadian Institutes of Health Research (CIHR). The CIHR is the major funding organization for life science research in Canada, distributing some $800 million of taxpayers' money to various facilities in the form of tax-free research grants.
It's easy to see why people are upset about this, the kneejerk reaction is to see this as a classic conflict of interest, a fairy tale where the benevolent non-partisan funding organization is corrupted by that most evil of nemeses, Big Pharma - all because of a plot by the Big Bad Government.
The error here is that Pfizer isn't eligible for most of that research money, which makes them ineligible for a conflict of interest. However, over half the CIHR governing council are university professors from research centres that do actually compete for CIHR funding. Part of success on a CIHR grant application is based on how many other grants have been given to your institute. This strikes me as being more of the classic conflict of interest as most people define it.
I don't think the problem is with Big Pharma making its way into CIHR. Business has a place in science no matter how many people - researchers and laypeople alike - wish it weren't so. The perspective on science is different between academia and industry. Both have their pros and cons, and I think that CIHR and academia in general might profit from exploring some of the alternative ways of looking at science.
My problem is that when I look though the CIHR website, I can see that Pfizer has been spending millions on funding CIHR grants over the last couple of years - and now an exec is on the board. This looks like patronage of the basest sort, but it isn't conflict of interest. Even if it does leave the same sour taste in your mouth.
What I don't find immediately apparent is what kind of return Pfizer is getting on their millions of dollars of investment, apart from tax breaks. A single position on a board of roughly 20 members isn't exactly overwhelming power or voice in the policy or direction of CIHR. What's so great about that?
It's easy to see why people are upset about this, the kneejerk reaction is to see this as a classic conflict of interest, a fairy tale where the benevolent non-partisan funding organization is corrupted by that most evil of nemeses, Big Pharma - all because of a plot by the Big Bad Government.
The error here is that Pfizer isn't eligible for most of that research money, which makes them ineligible for a conflict of interest. However, over half the CIHR governing council are university professors from research centres that do actually compete for CIHR funding. Part of success on a CIHR grant application is based on how many other grants have been given to your institute. This strikes me as being more of the classic conflict of interest as most people define it.
I don't think the problem is with Big Pharma making its way into CIHR. Business has a place in science no matter how many people - researchers and laypeople alike - wish it weren't so. The perspective on science is different between academia and industry. Both have their pros and cons, and I think that CIHR and academia in general might profit from exploring some of the alternative ways of looking at science.
My problem is that when I look though the CIHR website, I can see that Pfizer has been spending millions on funding CIHR grants over the last couple of years - and now an exec is on the board. This looks like patronage of the basest sort, but it isn't conflict of interest. Even if it does leave the same sour taste in your mouth.
What I don't find immediately apparent is what kind of return Pfizer is getting on their millions of dollars of investment, apart from tax breaks. A single position on a board of roughly 20 members isn't exactly overwhelming power or voice in the policy or direction of CIHR. What's so great about that?
Wednesday, December 10, 2008
Smarter, faster, stronger
A stunning opinion piece in Nature on Monday encouraging the use of cognitive-enhancing drugs, which has been all over the news and brought me to remember a problem I have with Ritalin. I'll have you know this is completely different from having a Ritalin problem. I'm not saying I don't believe in ADHD, although I do believe it is over-diagnosed, but I'm not getting into that. What I want to get into is Ritalin. And most of what we have in the way of ADHD drugs.
The simple fact of the matter is that these drugs are cognitive enhancers. They're a couple of chemical steps removed from amphetamines (speed), which are well-known for improvement of certain parts of thinking - short-term memory and attention particularly. Now, the ADHD drugs seem to work in a select number of specific areas of the brain whereas the speedball drives an entire neurotransmission system into overdrive (to make a gross oversimplification), but people without ADHD still see an enhancement of performance on tests of cognitive performance when they take Ritalin. That's why people buy it illegally during exam periods.
I'm about to make a brutal analogy here, so cover your ears - this is like letting Special Olympics athletes go to the other Olympics, but doped up on whatever performance-enhancer is big right now. No, really. My problem with Ritalin is that gives improvement on performance of tests that we use to diagnose ADHD in in both controls and ADHD patients. We're not treating ADHD necessarily - just improving performance on diagnostic tests, performance on which corresponds closely to that on academic exams.
Most of us are already users of cognitive enhancers. During my undergrad I smoked 15-20 cigarettes and swilled maybe 2-4 litres of coffee daily (thankfully, I've since cut down on both significantly). Both nicotine and caffeine are clinically proven enhancers of performance on pretty much any cognitive task you could name. We drink Red Bulls and coffee to make us sharper, we take sleeping pills to help us calm down, we take alcohol to enhance our social performances.
Which brings us back to the topic of the editorial that brought me to this piece in the first place. Why shouldn't we use drugs to become more intelligent? In what way is this possibly a bad thing? There are side effects; many not as bad as are present in a large number of other commercially available drugs (especially alcohol and tobacco). Why shouldn't my doctor, my lawyer, my accountant, my Member of Parliament and my future kid's teacher be on these drugs all the time?
Personally, I think that the means here don't require justification by the ends. There's no ethical dilemma about taking vitamins, or antioxidants, or coffee. We already use pharmacology to improve our quality of life in so many ways, and I see this as no different than taking drugs for anxiety, diabetes, or metabolic syndrome. Better living through pharmacology is still better living, and I don't think anybody should have a problem with a better life.
The simple fact of the matter is that these drugs are cognitive enhancers. They're a couple of chemical steps removed from amphetamines (speed), which are well-known for improvement of certain parts of thinking - short-term memory and attention particularly. Now, the ADHD drugs seem to work in a select number of specific areas of the brain whereas the speedball drives an entire neurotransmission system into overdrive (to make a gross oversimplification), but people without ADHD still see an enhancement of performance on tests of cognitive performance when they take Ritalin. That's why people buy it illegally during exam periods.
I'm about to make a brutal analogy here, so cover your ears - this is like letting Special Olympics athletes go to the other Olympics, but doped up on whatever performance-enhancer is big right now. No, really. My problem with Ritalin is that gives improvement on performance of tests that we use to diagnose ADHD in in both controls and ADHD patients. We're not treating ADHD necessarily - just improving performance on diagnostic tests, performance on which corresponds closely to that on academic exams.
Most of us are already users of cognitive enhancers. During my undergrad I smoked 15-20 cigarettes and swilled maybe 2-4 litres of coffee daily (thankfully, I've since cut down on both significantly). Both nicotine and caffeine are clinically proven enhancers of performance on pretty much any cognitive task you could name. We drink Red Bulls and coffee to make us sharper, we take sleeping pills to help us calm down, we take alcohol to enhance our social performances.
Which brings us back to the topic of the editorial that brought me to this piece in the first place. Why shouldn't we use drugs to become more intelligent? In what way is this possibly a bad thing? There are side effects; many not as bad as are present in a large number of other commercially available drugs (especially alcohol and tobacco). Why shouldn't my doctor, my lawyer, my accountant, my Member of Parliament and my future kid's teacher be on these drugs all the time?
Personally, I think that the means here don't require justification by the ends. There's no ethical dilemma about taking vitamins, or antioxidants, or coffee. We already use pharmacology to improve our quality of life in so many ways, and I see this as no different than taking drugs for anxiety, diabetes, or metabolic syndrome. Better living through pharmacology is still better living, and I don't think anybody should have a problem with a better life.
Monday, March 10, 2008
Do the drugs do what now?
I was a little startled to read this editorial in Nature this week, which chides the media for reporting that antidepressive medications simply don't work after the publication of a meta-analytical study finding little-to-no differences in relief from depression when drugs were compared to placebo.
What is special about this paper is that the authors had to file Freedom of Information Act litigation to get the relevant data for the study. A meta-analysis is a study of studies, so to speak (hence meta-), that uses the data from many different experiments and compares all of the results to get a very good idea of whether an effect is really there or not. They literally had to subpoena drug companies and/or the FDA for the results of clinical trials so they could perform their analyses.
What they found wasn't particularly encouraging. They looked at all 47 clinical trials submitted to the FDA for the 6 most "popular" antidepressants from 1987-99. Over 10% (5 trials) didn't even report the improvement scores on psychological tests (Hamilton Depression Index, for example) after drug treatment. Another 7 were incomplete, and knocked 2 drugs out of their study. Happily, in 35 trials covering 4 drugs (including Prozac and Paxil), all of the drug-treated patients showed improvement. However, that improvement was not so much better than the placebo effect that they could be recommended as clinically efficient drugs.
The Nature writers berate the media for "...miss[ing] that the placebo effect can be remarkably strong in psychological and neurological disorders, especially in mild depression." This startled me because it completely misses the point, and I generally expect more from the Nature editorial board. The placebo effect is, in fact, remarkably strong in psychiatric disorders. It may likely be why the concepts of both the double-blind clinical trial and the placebo exist in modern medicine. But if a drug's effects aren't better than a placebo, then the drug doesn't work. It is as simple as that.
If I wrote for Nature I would have attacked from a more different angle, and you can bet the drug companies will: there is nothing simple about these drugs. There is nothing simple about neuropsychopharmacology. Sometimes the drugs work, sometimes they don't. The problem is that depression comes from a wide variety of neuropsychiatric dysfunctions, not just one. Some drugs are going to be efficacious in some of those situations, some will not. Drugs do help a large number of patients suffering from depression, but those who have recovered with pharmacological help will tell you it takes time to find the right drug and dosage. So hoping to respond properly on your first course of a given antidepressive therapy is perhaps ambitious.
But I'll try taking it a step further - the more we talk about "depression," the longer it's going to take us to solve the variety of neurobiological problems that underlie this term. We are talking about of myriad of things when we talk about depression, and until we start being able to devise better correlations between particular symptoms and the biology underlying those particular symptoms - to further develop a knowledge base and a language to talk about depression in a meaningful way - we won't ever have medications that work better than placebo.
I find this most interesting from a population health policy perspective. The study shows that placebos work almost as well as the drugs in all but the most severely depressed patients, and only because those patients get much worse on placebo but improve on medication. What this seems to suggest is that every patient initially presenting with depression should get a placebo (almost the same effect at a fraction of the cost), and those that are severely depressed will get worse rather than better after several weeks. Once you've identified them, they can have the "real" antidepressants. Our health care system would save tens of millions of dollars, and we wouldn't be pulling any more scientific fraud than the FDA has been since 1987...
UPDATE: I spoke with a psychiatrist who runs antidepressant trials, who tells me the 6-week follow-up point used in this study corresponds to the maximal response in the placebo group - scores taken at 10 weeks of treatment would have been much different. Which, of course, continues to beg for the following question: Why did the FDA license the drug on that data?
What is special about this paper is that the authors had to file Freedom of Information Act litigation to get the relevant data for the study. A meta-analysis is a study of studies, so to speak (hence meta-), that uses the data from many different experiments and compares all of the results to get a very good idea of whether an effect is really there or not. They literally had to subpoena drug companies and/or the FDA for the results of clinical trials so they could perform their analyses.
What they found wasn't particularly encouraging. They looked at all 47 clinical trials submitted to the FDA for the 6 most "popular" antidepressants from 1987-99. Over 10% (5 trials) didn't even report the improvement scores on psychological tests (Hamilton Depression Index, for example) after drug treatment. Another 7 were incomplete, and knocked 2 drugs out of their study. Happily, in 35 trials covering 4 drugs (including Prozac and Paxil), all of the drug-treated patients showed improvement. However, that improvement was not so much better than the placebo effect that they could be recommended as clinically efficient drugs.
The Nature writers berate the media for "...miss[ing] that the placebo effect can be remarkably strong in psychological and neurological disorders, especially in mild depression." This startled me because it completely misses the point, and I generally expect more from the Nature editorial board. The placebo effect is, in fact, remarkably strong in psychiatric disorders. It may likely be why the concepts of both the double-blind clinical trial and the placebo exist in modern medicine. But if a drug's effects aren't better than a placebo, then the drug doesn't work. It is as simple as that.
If I wrote for Nature I would have attacked from a more different angle, and you can bet the drug companies will: there is nothing simple about these drugs. There is nothing simple about neuropsychopharmacology. Sometimes the drugs work, sometimes they don't. The problem is that depression comes from a wide variety of neuropsychiatric dysfunctions, not just one. Some drugs are going to be efficacious in some of those situations, some will not. Drugs do help a large number of patients suffering from depression, but those who have recovered with pharmacological help will tell you it takes time to find the right drug and dosage. So hoping to respond properly on your first course of a given antidepressive therapy is perhaps ambitious.
But I'll try taking it a step further - the more we talk about "depression," the longer it's going to take us to solve the variety of neurobiological problems that underlie this term. We are talking about of myriad of things when we talk about depression, and until we start being able to devise better correlations between particular symptoms and the biology underlying those particular symptoms - to further develop a knowledge base and a language to talk about depression in a meaningful way - we won't ever have medications that work better than placebo.
I find this most interesting from a population health policy perspective. The study shows that placebos work almost as well as the drugs in all but the most severely depressed patients, and only because those patients get much worse on placebo but improve on medication. What this seems to suggest is that every patient initially presenting with depression should get a placebo (almost the same effect at a fraction of the cost), and those that are severely depressed will get worse rather than better after several weeks. Once you've identified them, they can have the "real" antidepressants. Our health care system would save tens of millions of dollars, and we wouldn't be pulling any more scientific fraud than the FDA has been since 1987...
UPDATE: I spoke with a psychiatrist who runs antidepressant trials, who tells me the 6-week follow-up point used in this study corresponds to the maximal response in the placebo group - scores taken at 10 weeks of treatment would have been much different. Which, of course, continues to beg for the following question: Why did the FDA license the drug on that data?
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