Archive for the ‘science education’ Category

From Salon: Doctors need to be aware of widespread health misinformation on the Web, because patients are going to find it.  Although the article is pitched as “Internet information is good for patients and doctors”, the misinformation aspect it its major point.

And a good point.  This is a basic tenet among the people who study end users of software and web applications, who do user-centered design, human-computer interaction, usability studies, etc:  You have to design your approach for what people are going to do.  Designing (whether it be software/web applications or any kind of information delivery) for what you think they ought to do is an approach destined for failure.

And you can’t stop the Internet.  It spreads information, and misinformation, like nothing else.

(On the other hand, calling doctors who don’t get this – like the article does – ow.  Good way to piss people off.  Doctors are end users of information, too, and starting off your approach with an insult, maybe not so effective.)

This is an awesome idea. I hope the execution is just as good. (I’ve linked to the MindHacks article because the original site plays noises at you.)

Michael (who comments here a lot) lent me a book on educational videogames, which I have yet to read, but am looking forward to. Educators can learn a lot from the cognitive psychology principles involved in videogame design. I had a conversation at lunch today with a fiction writer who is trying to get into manga, about how science fiction writers complain that no one is interested anymore. The popularity tells you where people are at. And how to reach them.

Several summers ago I spent six weeks in another country, doing research in collaboration with autism researchers there.  We traveled around by subway, train, and cab, visiting multiple schools with autistic children.  Some were regular schools that had an autism unit; others were boarding schools for special-needs children or for children with autism specifically.  We worked with the higher-functioning kids with autism (who had at least some language) and with younger mental-age-matched kids without autism (because mental retardation is very common in autistic kids – up to 74% although I read something non-peer-reviewed on the Internet that claims as low as 50% – to compare autistic and non-autistic kids on cognitive stuff you need to equate them on mental age, not chronological age).

We did a variety of tasks with the kids, involving stuff like sorting cards, or hearing stories and answering questions, or pushing buttons in response to pictures of faces on a computer screen.  One of the weirder tasks, which was something for our collaborators, not for me and my prof, involved measuring kids’ heads with a measuring tape.  I thought it seemed kind of an odd approach at the time – most of what I was involved in was heavily cognitive.  And so I’ve been surprised to see that line of research actually panning out.

Here’s a recent instance of it (citation below).  Researchers found that, very clearly, children with autism had larger head circumferences.  What I thought was interesting was that head circumference above the 75th percentile was  “associated with more impaired adaptive behaviors and with less impairment in IQ measures and motor and verbal language development.”

So something strongly associated with autism was also associated with less mental retardation (but mental retardation is strongly associated with autism).  There’s some interesting stuff in there…  I’m tempted to hypothesize beyond the data, but I’m not going to.

Larger head circumference was also associated with allergy/immune disorders in the kids and their first-degree relatives.  The researchers speculate that this relates to immune dysfunctions that themselves cause or are associated with increased cell cycle progression (cannot dredge what that means up out of my brain) and/or decreased apoptosis (deliberate, clean cell death).

At the time of my first couple years in grad school, it was being speculated that for the quarter or so of autistic kids who have a noticeable period of skill loss (coincidentally around the time of the MMR shot, which has led to a whole lot of bad crap) lose their skills around the time that the brain undergoes a major reorganization in which unnecessarily neuronal connections are “pruned” or cut back.

So: Maybe immune dysfunction leads to lack of cell death in pruning and maybe outside of it too, and thus autism and larger head circumference?

That and a dollar will get you one-quarter of a latte, or almost a small iced tea, or a tiny little bit of the funding necessary to gain actual knowledge, or a fair bit of annoyance from someone more educated who already knows why you’re wrong.   Speculation is tasty and rampant, but actual knowledge comes from eliminating the untrue theories with evidence, and hammering on the true ones until we decide there’s not much point in continuing to do so.

Sacco, R., et al. (2007) Clinical, Morphological, and Biochemical Correlates of Head Circumference in Autism. Biol Psychiatry.

Often studies only give you snapshots of a population – what one set of people looks like at hospitalization. What a different set looks like five years after hospitalization at a different hospital and in a different region. What fifty-year-olds look like right now, and what twenty-five-year-olds look like right now.

We often infer information about the course of a disorder based on who we can pick up at different points in life. But there’s no guarantee that the people we catch when they’re fifty were, at twenty-five, like the twenty-five-year-olds we’re catching now. We might have used recruiting techniques that caught (say) twenty-five-year-olds who are heavy drinkers, and fifty-year-olds who are drinkers now but were teetotalers at that age. There are a lot of ways these problems can come up, and researchers work diligently to do what they can with what is actually feasible to do, and we do our best to check on that knowledge in a variety of ways.

But it’s always good to have extensive longitudinal research to address questions about course of illness. Here’s an article (cite at bottom of entry) reporting on a large longitudinal study of people with bipolar I. I wanted to get ahold of the article to go into more depth, but my university doesn’t have it and it appears to be in either Portuguese or Italian, and since the closest thing I have is some Spanish my translation would be highly questionable.

This is from a decade-long project, the McLean-Harvard First Episode Project & International Consortium for Bipolar Disorder Research which followed people with bipolar disorder and psychotic disorders from their first hospitalization. This abstract only looked at data for bipolar I.

There are several findings I would prefer not to be true, but if we don’t consider the possibility, we can’t plan for them. People usually do not recover fully from their first episode, and they are very likely to have more episodes in the first two years (and to switch from depression to mania or vice versa),

Some conditionally good or bad stuff: Most people have the most problems early on with depression/dysphoria, and they tend to have a worse course. Initial mania or psychosis shows a better prognosis (interestingly enough). Very high rates of suicidal behavior accidents occurred early but not as much later on (this finding is pretty extensively reported). Early substance-use and anxiety go together. Prodromal symptoms (stuff indicating you’re about to have an episode) predicts bipolar disorder better than non-affective psychotic disorders (good for bipolar, bad for others).

Some good stuff: Most people didn’t cycle more and more over time (but if I’m reading the abstract right, they didn’t stick to a single steady cycle length, either). Also, how long people waited and how many episodes they’d had was unrelated to their response to mood stabilizers.

Salvatore, P., et al. (2007). Longitudinal research on bipolar disorders. Epidemiologia e psichiatria sociale, 16(2), 109-17.

 

The more mood swings, the more deterioration. They only looked at people with 1 to 6 swings over four years. The news story doesn’t say whether they looked at frequency of mood episodes versus total number of days, so we don’t know whether someone with long, infrequent episodes would have the same damage as short, frequent ones (something of concern to people who rapid cycle). (I unfortunately don’t have access to this article.)

They did not find a decline in intelligence, although the article talks about declines that weren’t significant. That just means the scientists want to say they found a decline, so they’re putting it forth even though the rules of science designed to keep that kind of thing under control say it isn’t sufficiently certain for people to count it as a finding. (We have this kind of rule for a variety of good reasons, but mostly to keep people from overstating their findings.)

The lead author of the study says medication didn’t appear to be making the deterioration worse. He doesn’t say that helps, although both he and the writer of the news article hope that it does (as do I, and I hope someone follows up and tells us whether that’s the case).

What you can actually conclude from the news article is that people with infrequent episodes in bipolar disorder show gray matter loss in proportion to the number of episodes they have, and that we don’t have any evidence showing that this is harmful. My money is on yes, we will find it’s harmful, and maybe we’ll find that medication averts it (instead of, for example, finding that it’s related to the tendency to have more frequent episodes, rather than to the actual episodes). But we don’t know that right now. The news article (and possibly the lead researcher) are constructing a logical story around how things work, and telling that; and it makes sense. But real life is often less intuitive than our stories.

On a related topic, I hope to post about kindling tomorrow.

Study Shows People Can Suppress Bad Thoughts

People can get better at suppressing negative memories over time, and the prefrontal cortex (a part of the brain known to be involved in executive control, i.e. planning, carrying out plans, and inhibiting impulses) is involved. They would like this to point toward directions for therapy in post-traumatic stress disorder.

The article is somewhat misleading (although I’m fairly certain the research is much better):

Research by neuroscientists shows that, with practice, people can suppress emotionally disturbing memories. Investigators say the finding could lead to therapies for individuals suffering from post-traumatic stress disorder.

It’s not hard to read into this the notion that what works for normal people will work for disordered people if they just work at it. I.e., people with post-traumatic stress disorder just need to work at suppressing them harder; people with bipolar disorder just need to cope with their emotions better; people with AD/HD just need to concentrate harder; people with depression just need to take a shower and get out of the house for a bit, etc. But the problem isn’t that people with disorders are failing to employ normal coping techniques – it’s that those normal coping techniques do not fix the disorder, because the dysregulation you see in a functioning system – brief unpleasant memories from seeing a photograph – is not the same kind of dysregulation as in a disordered system, such as vivid, disabling reliving of memories of a situation that occurred personally to you in which you thought you would die.

The article isn’t saying that people with PTSD will be fixed by practicing suppression harder, but it’s not doing a good job of explaining the relationship between research on normal self-regulation and treatments for disorders. Humans have have very intuitive, unquestioned frameworks for thinking about other (normal) people, and in the absence of being told that those frameworks don’t apply (and having that pounded into our heads repeatedly until it overrides the intuitions), we frequently jump to the conclusion that everyone is a normal person so of course what works for everyone else will work for the person at hand, and if it doesn’t, then they’re probably just not doing it right. (And should be blamed, etc.)

The APA has argued that when you treat mental disorders, you don’t need to spend as much on physical healthcare, for a variety of reasons.

The linked article contains references to a bunch of studies, but is remarkably not like an APA paper in that it doesn’t mention and address any studies that were not favorable to its conclusion (something you have to do in science). It’s not possible to tell from reading it what the obstacles are to implementing better psych treatment, and it doesn’t seem targeted – i.e., it doesn’t mention and probably doesn’t address the concerns of the people it’s aimed at.

I really wish it did. I would much rather be writing a blog entry about how APA was carefully attempting to address the issues involved in convincing insurance companies (hospitals? other healthcare providers? the government?) to offer cheaper/better mental health treatment.

It’s so easy to do advocacy focused on showing you’re right, and so hard to do advocacy focused on removing the obstacles preventing your target audience from doing what you want them to do. But you don’t have to go all out to acknowledge why they aren’t taking your position, and to address those reasons.

I do think APA is probably right – and even if they’re not, I believe that appropriate mental health care (and physical health care) should be available to everyone, everywhere.

I’m updating early because I’m moving apartments this weekend, but my general plan is to post every evening by nine-o-clock meds time (EST).

Nash Suggests Schizophrenia May Serve Adaptive Function

On the mental illness side: schizophrenia is not associated with genius or creativity. None of our evidence says it’s anything but severely impairing. Bipolar is associated with creativity despite fucking everyone over, but schizophrenia mostly just fucks people over, although there are people who do well at times. John Nash is a genius, but that’s not necesarily due to schizophrenia. People who are geniuses can also be crazy without a causal link. People who have bipolar are more likely to be creative, and not necessarily actually more creative. Inability to think clearly or concentrate, or being depressed or manic, can really do a number on your creativity.

On the evolutionary side: the detrimental effects of adaptations sometimes get undermentioned. An “successful” adaptation can severely impair most of the people who have it if, on average, there’s enough benefit for at least some people to “balance that out”. It doesn’t have to benefit an individual person. It doesn’t even have to benefit any of the people who actually have it! It might benefit copies of their genes that reside in their kin, instead. This is where schizophrenia may come into play – family members of people with schizophrenia display increased creativity (can provide cite later, seriously supposed to be packing my remaining crap right now).

Take-home point: If serious mental illnesses are adaptations (I’m not convinced they are, but I’m open to the possibility), they’re not beneficial for most affected people. If they were, we wouldn’t call them mental illnesses – a major requirement in the DSM is that a mental disorder cause marked impairment in functioning. It’s nice to think we’re all geniuses, but that stereotype covers up the crappy reality of just trying to make it day to day, let alone hold down a job or have good relationships.

New study shows five subtypes of alcoholics: young adult, young antisocial, functional, intermediate familial, chronic severe. This seems to be getting a fair bit of media attention.

Here’s a 1983 study with six subtypes. Here’s a 2006 review finding as many as four subtypes. Here’s a 2004 study with four subtypes. There’s also a type 1/type 2 distinction from 1988, and a type A/type B distinctions. This is just from a quick google search and a non-exhaustive search on PubMed.

Ahistorical science news is pretty common – everything’s a big new finding, a new development, the first of its kind. I’m not sure how much this has to do with science writers not having much background, how much it has to do with news not selling unless it’s new, and how much it has to do with the fact that if you don’t have to give people historical perspective it makes you able to do your job – writing stories people will want to read – much more efficiently.

I still wish that science news would come with more information on what this has to offer over similar previous findings, and more information on how those previous findings (for work with applied implications) were useful or not useful. Is this really a shiny new finding, or just another variation? That kind of thing. (At least it’s not yet to the point where people are still reporting it as news months from now.)

I’m agnostic about whether this specific study in a shiny new finding or not – it may be a useful improvement on previous studies, it may not; I don’t know enough about that area of research to tell. The point I want to make, though, is that a lot of science-related stuff hyped as news isn’t, and it often gets oversold because it’s presented without the research context.

Yesterday I went to the Chattanooga aquarium almost all day, and it was awesome. When I got home I was too tired to think straight, and briefly posted something on psych meds and creativity that was inaccurate – oops. It may make another appearance later on. In the meantime, here’s something more off-the-cuff.

First, the media and anecdotes:

People with serious mental illness have problems using glucose efficiently in the brain

Okay, I find this completely fascinating and intuitively plausible. When I was around twelve – the first time I remember having mood problems, although probably not the first time I started having them – I started eating sugar excessively. Not just at dessert, but during the day. I’d take powdered sugar from the cabinet and put it in a tupperware and hide it in a drawer in my room and eat it straight. Among other things. I felt awful about it, but just stopping never seemed to work, even though I tried frequently. (If you can get addicted to video games, why not a substance that has immediate lifting effects on mood and energy, followed by a crash?)

When I was seventeen and working in a bookstore, I ran into a book with the badly-chosen title “Potatoes Not Prozac” which argued that sugar could be addictive, that it was related to alcoholism (I have alcoholism running on both sides of my extended family, and there’s a plausible evolutionary argument related to this I’ll share some other time), and that you could go off of it and get a drastic improvement in mental and physical health through a diet that can be summed up as sufficient protein and whole grains (similar to what later became very popular as the South Beach diet). This worked very well for me; it was like suddenly getting a stable personality, and was very similar to the first time I went on an antidepressant. Neither of those effects lasted, but they were amazing and gave me hope that life didn’t have to be the way it was most of the time.

Interestingly enough, when I’m stable on medication I can have a relationship with sugar that’s about what regular people have – it’s nice sometimes but I can drop it without a problem (unless I start eating dessert more than occasionally; I still have to watch for that).

Further anecdotal information: When I mention to psychiatrists that sugar affects my mood, they’re never surprised, although I don’t think any psychiatrist has ever suggested this as a factor up front. It’s pretty common in the patient literature, though.

So that’s the media and the anecdotes. Here’s some stuff to notice about the article (and the anecdotes):

1. There’s no mention of a published article. If it had been published, that would have almost certainly have been mentioned. That strongly suggests that this research has not been peer reviewed. (The list of articles on the lab’s website does not appear to refer to the research mentioned in the article. There’s something about glutamatergic dysfunction in schizophrenia that may be a precursor to this work.)

2. This is the only reference to that research I can find on google news or on google. I don’t have a way to cross-check the accuracy of the reporter’s take on what’s going on (I’ve seen enough errors in science reporting that I don’t want to trust an individual article, and this one appears to confuse “inefficient glucose processing” with “not enough glucose” and “lack of sugar” with “not enough glucose in the brain”).

3. I’m telling this anecdote where I’m linking my own personal screwed-up relationship with sugar to this brain glutamate thing, but I’m not sure they’re even related. I’m not sure what the relationship between ingested sugar and glucose in the brain is, but I doubt it’s all that straightforward, and anyway the article is suggesting it’s lack of sugar that’s the problem, right? And I actually felt better when I stopped, even though there was probably a reason I was eating it to begin with. (I’m pretty sure the “lack of sugar” thing doesn’t actually mean “go eat more sugar, it’ll make you feel better”, though, even if it’s possible to take that away from the article.)

4. Anecdotes aren’t data. Lots of anecdotes collected in a careful, systematic way using random sampling are data, but my telling you this stuff off the cuff isn’t data. I could be wrong about a connection between my craving sugar and my mood problems. I’ve been flat-out wrong about myself before – I thought some major issues I have following lectures and other extended verbal information would turn out to be due to an auditory processing problem, but they turned out to be due to ADD and disappeared with stimulants. (This is what we have highly trained medical professionals for – to save us from some of our best guesses.)

So what does this mean? Well, it doesn’t mean the researcher’s conclusions are incorrect. The article has some problems, like the “lack of sugar” bit giving the false impression that not getting enough sugar in diet = lack of glucose in brain, and that in turn giving the impression that the problem is lack of glucose in the brain when the research appears to implicate inefficient glucose processing.
But it doesn’t mean they’ve hit the status of widely accepted fact. It’s more of a back pocket kind of finding – very interesting, tuck it away, pull it out again later when you hear more – like another article mentioning a publication (or a publication itself), or another researcher’s work.