Away from Nervewracker for a little while, and looking for a chance to rev up and return when nothing less than a New York Times op-ed arrives to fortuitously bonk me over the head with a subject. In this column Nicholas Kristol, a writer I like, turns to a couple of researchers who looked at reactions to the Obama candidacy based on a test of "implicit associations." And it turns out, according to the researchers that college students are less likely to see a black candidate as "American." Subconsciously, that is.
You can take the kind of implicit association test this is based on here. I've taken it before, and just took it again now. And in my experience, the results are plain nonsense. And the problem here is that it is insidious nonsense, because as a test of unconscious biases any objection can be answered with, "Oh, but you're just in denial," or some more technical sounding version of that. Better to just say nothing, because if the test shows you have an unconscious bias that you don't think you have, you're a two time loser, a bigot who just can't accept it.
Well, let me tell you my results over several tests. When I first tried a series of these tests a couple of years ago, I showed an unconscious association of blacks with guns and violence (the assumption of the test, by the way, seemed to be that guns have negative associations--though frankly, for me I'm not really sure they do). I also, according to more tests, believe that women are better at math and science than men. Have no preference for thin people over fat people. And, according to the test I took now, have a slight preference for gay people over straight ones. All this basically makes me say, "Huh?" Really? Well, okay, maybe I'm an unconscious bigot. And ... gosh ... could I be gay and not know it? But what am I supposed to make of the idea that I think women are better at math and science? No amount of introspection lets me make sense of this. I really have no idea either way, though when I was younger I knew a number of folks with a truly spectacular talent for math--all, as it happens, men.
The dumbest part here, though, is the test of attitudes about people who are overweight. Because here I think I'm pretty in touch with my automatic impulses, and (unfortunately) they're not what the test shows at all. My ex-wife once told me that when she wanted me to dislike someone, she took care to drop in that he was fat. This is a stupid prejudice, that I'm not proud of. But it's one that I have trouble shaking. And this test utterly misses it. The bottom line is that I see no more reason to beat myself up over a supposed fear of blacks than I do to pat myself on the back about my inclusive attitudes about women in science or my comfort with different body types. I have no doubt that prejudices exist. But as a journalist I can tell you that it's easy enough to make them come out just by asking.
What I find distasteful about the test is that it is ultimately a bizarre inversion of the great Freudian project of self-understanding. For all the problems with Freudian analysis, the basic principle that our inner thoughts are something worth bringing out and examining is a worthwhile one. At its root, the Freudian project assumed that we have thoughts that we don't want to admit, and this accords with all of our experience. The premise of the implicit association test, on the other hand, is that our thinking is just not subject to introspection or examination, and can be brought out only by measuring the speed with which we press a sequence of keys. This would be a depressing idea if it could be proved true. It is an insidious and scary one when presented in a way designed to make sure that it can't even be proved false.
10.13.2008
The High Price Of Remembrance
Some readers might recall a small wave of publicity about a study by UC-Irvine researchers led by Elizabeth S. Parker of a woman identified as "AJ" with an uncanny memory for everything that had happened over a period of years. I read the study, A Case of Unusual Autobiographical Remembering this weekend, and it's blow-away fascinating.
AJ had spectacular recall of dates and events both in her life, and was able to bring back news events, her schedule, and even details such as how her house smelled for years back. What the news reports didn't make clear was what a big cognitive cost this memory seems to come with. The authors propose that AJ's memory could be called a disorder, and when you look at the details you see why. AJ has preternatural autobiographical recall, but that does not translate to a memory for, say, numbers or patterns.
More strikingly, she has serious impairments in tests of concept formation and executive function--way below average (the study gives some fairly technical statistical results, but they translate to numbers in the bottom 5 percent of normal scores on these tests). AJ--whose kindness in cooperating with the researchers was really great, so it's a little painful to say this--just doesn't think very clearly.
The paper doesn't really settle on a biological hypothesis for what's going on in AJ's brain. Understandably so, since one person just isn't going to give you a set of definitive answers. I won't try to formulate one here, or bore you with technical details. But for the biologically inclined, you might consider looking into some of the studies of scopolamine (once thought of as "truth serum"--maybe more on that in a future post) and apomorphine. Apomorphine clearly clobbers executive function and working memory, with much less certain effects on "episodic memory." Scopolamine, on the other hand, has hugely negative effects on memory formation while leaving most other functions intact and, interestingly, increasing verbal fluency--a profile that's pretty close to the opposite of AJ's.
The paper doesn't really settle on a biological hypothesis for what's going on in AJ's brain. Understandably so, since one person just isn't going to give you a set of definitive answers. I won't try to formulate one here, or bore you with technical details. But for the biologically inclined, you might consider looking into some of the studies of scopolamine (once thought of as "truth serum"--maybe more on that in a future post) and apomorphine. Apomorphine clearly clobbers executive function and working memory, with much less certain effects on "episodic memory." Scopolamine, on the other hand, has hugely negative effects on memory formation while leaving most other functions intact and, interestingly, increasing verbal fluency--a profile that's pretty close to the opposite of AJ's.
An Easy Way To Misunderstand Addiction
I keep running into studies that that promote "likeability" as a measure of how likely psychotropic drugs are to be abused, studies that are loved by makers of drugs like Strattera and Provigil that score low on this measure. The idea is that if they don't get you high in a pleasant and immediate way, they will not create what we think of as addiction. This is a weird conclusion to draw, for a couple of reasons. One is that and the problem with, say, methamphetamine is not that it is likable. It's that it will eventually cause mania, delirium and basically drive you crazy in a bunch of ways. Likeability tells you nothing about this.
Worse, however, is that likeability tells virtually nothing about dependence, because much of what we've learned about addiction is that addiction and likeability are two very separate things. Addiction involves repetitive, stereotyped, compulsive behavior. The pattern absolutely doesn't have to involve something that's likeable--think of some young women's compulsive self cutting. In fact, the general direction of work on drugs like cocaine and amphetamines from both human and animal studies points to the repetitive behaviors increasing with higher doses or extended use even as the high ("likeability") decreases or disappears. I'm not willing to do the experiment myself, but my bet is that anybody who stays up for three nights popping Provigil is going to be just as just as anxious and agitated as any speed addict--and will be looking around for the next dose.
Worse, however, is that likeability tells virtually nothing about dependence, because much of what we've learned about addiction is that addiction and likeability are two very separate things. Addiction involves repetitive, stereotyped, compulsive behavior. The pattern absolutely doesn't have to involve something that's likeable--think of some young women's compulsive self cutting. In fact, the general direction of work on drugs like cocaine and amphetamines from both human and animal studies points to the repetitive behaviors increasing with higher doses or extended use even as the high ("likeability") decreases or disappears. I'm not willing to do the experiment myself, but my bet is that anybody who stays up for three nights popping Provigil is going to be just as just as anxious and agitated as any speed addict--and will be looking around for the next dose.
10.09.2008
Anxiety, Attention, And The Value Of Dark Glasses
Everybody knows that you'll never make a free throw in basketball if you let anxiety take over. But what's less obvious is why you can't make one by just shutting that anxiety down—say, pop a Xanax? It'll certainly make you less anxious. And it'll pretty much guarantee you'll miss.
In the last post I wrote about the neurotransmitter norepinephrine, and the range of disparate effects it seems to produce. In the brain, anxiety and attention are linked in a way that is not obvious when you're experiencing them. Norepinephrine raises some signals and the brain and dampens others; the effect it produces depends on what else is going on. And while it is clearly associated with anxiety, it's linked to concentration, too. An experienced therapist I know (quite well, actually—she happens to be my mother) points out that changing the word “anxiety” to “worry” brings out the natural—and perhaps evolutionary—link. To be worried is to be anxious, but it's also to be attentive to your surroundings.
One example of this relationship comes from studies of the eye in decision making. The release of norepinephrine makes the pupils dilate—it's why someone can be “wide eyed” with surprise. The dilation that marks surprise or shock also, as this study from Caltech shows , marks key moments of concentration and decision making. You can't just shut down the rush of norepinephrine—it has to be there in the right moment. Though sometimes in competition it pays to hide it, which is why, as the authors of the study have pointed out, poker players wear dark glasses (why they wear bolo ties is beyond the scope of any scientific investigation).
In the last post I wrote about the neurotransmitter norepinephrine, and the range of disparate effects it seems to produce. In the brain, anxiety and attention are linked in a way that is not obvious when you're experiencing them. Norepinephrine raises some signals and the brain and dampens others; the effect it produces depends on what else is going on. And while it is clearly associated with anxiety, it's linked to concentration, too. An experienced therapist I know (quite well, actually—she happens to be my mother) points out that changing the word “anxiety” to “worry” brings out the natural—and perhaps evolutionary—link. To be worried is to be anxious, but it's also to be attentive to your surroundings.
One example of this relationship comes from studies of the eye in decision making. The release of norepinephrine makes the pupils dilate—it's why someone can be “wide eyed” with surprise. The dilation that marks surprise or shock also, as this study from Caltech shows , marks key moments of concentration and decision making. You can't just shut down the rush of norepinephrine—it has to be there in the right moment. Though sometimes in competition it pays to hide it, which is why, as the authors of the study have pointed out, poker players wear dark glasses (why they wear bolo ties is beyond the scope of any scientific investigation).
Back To Those Knockout Mice
I can write about knockout mice—that means mice genetically engineered to lack individual genes, I mentioned them a few days ago days ago in a post about ADHD—pretty much endlessly I'll try to keep this from turning into the Knockout Mouse Blog, but I chanced on a study by researchers at Vanderbilt University that has some more counter-intuitive results that are worth recounting.
Norepinephrine, is a hormone and neurotransmitter that is associated with anxiety and anger—and also with attention, and protection from depression. In the Vanderbilt study, mice were bred to lack the norepinephrine transporter, meaning they had a persistently high level of the hormone in their brain and nervous system.
This had two very different, and essentially opposite, effects. On the one hand, when placed in a stressful environment, the mice had lower heart rate and blood pressure than ordinary mice. They functioned well under stress—to a point. But they also had an extreme reaction to shock, with their heart rate shooting up dramatically, the equivalent of panic in humans. This makes a lot of sense. The operation of norepinephrine is complex. One thing that it does is vary the frequency and amplitude of signals in the brain, making some signals stronger and others weaker—you can imagine it as working a little like the dials on a higher end stereo.
What I find especially compelling here is how useful this kind of study is in modeling human behavior. Just as a malfunction in the dopamine transporter may be associated with hyperactivity and attention problems, so we can see patterns in the norepinephrine transporter deficient mice eerily reminiscent of those that we see in humans—surprisingly complicated patterns. Sometimes the very same people who seem to do well in real world stressful environments will have mysterious panic attacks, or choke under pressure. What looks like a confusing and hard to explain set behaviors can get traced back to a change in a single gene that affects levels of a single molecule in the body.
Norepinephrine, is a hormone and neurotransmitter that is associated with anxiety and anger—and also with attention, and protection from depression. In the Vanderbilt study, mice were bred to lack the norepinephrine transporter, meaning they had a persistently high level of the hormone in their brain and nervous system.
This had two very different, and essentially opposite, effects. On the one hand, when placed in a stressful environment, the mice had lower heart rate and blood pressure than ordinary mice. They functioned well under stress—to a point. But they also had an extreme reaction to shock, with their heart rate shooting up dramatically, the equivalent of panic in humans. This makes a lot of sense. The operation of norepinephrine is complex. One thing that it does is vary the frequency and amplitude of signals in the brain, making some signals stronger and others weaker—you can imagine it as working a little like the dials on a higher end stereo.
What I find especially compelling here is how useful this kind of study is in modeling human behavior. Just as a malfunction in the dopamine transporter may be associated with hyperactivity and attention problems, so we can see patterns in the norepinephrine transporter deficient mice eerily reminiscent of those that we see in humans—surprisingly complicated patterns. Sometimes the very same people who seem to do well in real world stressful environments will have mysterious panic attacks, or choke under pressure. What looks like a confusing and hard to explain set behaviors can get traced back to a change in a single gene that affects levels of a single molecule in the body.
10.06.2008
A Depressing Debate About Antidepressants
A much publicized study released earlier this year purported to show, based largely on the results of the drug makers' own research, that anti-depressants such as Prozac and Paxil don't work much better than a placebo at ameliorating depression. I don't like the study very much, in part because even the authors' own engineering of the numbers actually shows that the serotonin reuptake inhibiting drugs are in fact effective in cases of major depression. That's something you may not have caught if you saw articles about the study by writers who didn't get past the press release.
One question that studies like this raise for me is whether say more about the drugs or about the criteria for the illness the drugs are supposed to address. Folks who read that antidepressants are not more effective than a placebo pill come away with the idea that these drugs don't do anything. But this is obviously untrue. Anybody who has taken antidepressants knows that they have dramatic effects. They certainly are not always the effects that you might want—they can be bad effects—but that they do something is very clear.
The gap between the results of studies that show little effect from drugs and the experience of people (some of whom swear by antidepressants, some of who detest them) who have used them underlines a more profound split between drugs and the criteria againt which they are tested. The expectation that a drug will have effects that neatly line up with the definitions of the DSM-IV yields the preposterous conclusion that the drugs have little effect when the problem of something like “depression” is so badly defined that it may well be made better or worse by the very same drugs in different people—or in the same people at different times.
Oddly, this situation benefits both critics of drugs such as antidepressants and their developers. Critics can point to studies that show unclear or unpromising results. Drug companies, on the other hand, feel little pressure to explain exactly how the drugs work or what they do, as long as they can come with a study that shows some difference in some condition that fits the DSM-IV standards. With each new antidepressant the endless debate about whether the drugs "work" continues, and we grow barely closer in understanding how they work and no closer at all in defining what we want them to do.
One question that studies like this raise for me is whether say more about the drugs or about the criteria for the illness the drugs are supposed to address. Folks who read that antidepressants are not more effective than a placebo pill come away with the idea that these drugs don't do anything. But this is obviously untrue. Anybody who has taken antidepressants knows that they have dramatic effects. They certainly are not always the effects that you might want—they can be bad effects—but that they do something is very clear.
The gap between the results of studies that show little effect from drugs and the experience of people (some of whom swear by antidepressants, some of who detest them) who have used them underlines a more profound split between drugs and the criteria againt which they are tested. The expectation that a drug will have effects that neatly line up with the definitions of the DSM-IV yields the preposterous conclusion that the drugs have little effect when the problem of something like “depression” is so badly defined that it may well be made better or worse by the very same drugs in different people—or in the same people at different times.
Oddly, this situation benefits both critics of drugs such as antidepressants and their developers. Critics can point to studies that show unclear or unpromising results. Drug companies, on the other hand, feel little pressure to explain exactly how the drugs work or what they do, as long as they can come with a study that shows some difference in some condition that fits the DSM-IV standards. With each new antidepressant the endless debate about whether the drugs "work" continues, and we grow barely closer in understanding how they work and no closer at all in defining what we want them to do.
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