Monday, November 30, 2009

Okay, I'm immature.

Science Daily has a story titled:
Small Hairy Balls Hide Foul-Tasting Healthful Enzymes
It has nothing to do with the brain or with neuroscience, but how could I ignore reading an article with that title? And now sharing it with you... Basically, it looks like a Dutch group has figured out a way to package enzymes so that you don't have to taste them, and so they don't break down or lose potency before they get to your stomach or small intestine (or, as flight attendants like to say, wherever their final destination may be).  Could be a cool new tool for drug delivery, but then, you'd have to be okay with putting small hairy balls in your mouth.

Saturday, November 28, 2009

Facilitated Communication

It's like a Ouija board only much, much worse.  Here's a link to give you some idea of what I'm talking about.  Basically someone is claiming this guy is not brain dead because they can pick up his hand and use it to type words on a keyboard.  I, like PZ Myers, would like to see how well he answers the questions being asked when the "facilitator" is blindfolded.  Anyway, hopefully now the cartoon makes sense.

Wednesday, November 25, 2009

Tryptophan and Turkey (Again)

So, I likely won't get to post anything tomorrow what with traveling and then eating and drinking followed by more eating and drinking and then some more eating for good measure.  Since I won't be posting anything, enjoy this lovely e-card from, and the blog version of a rebroadcast in the form of a link to my post from a few days ago explaining how tryptophan in turkey is not the culprit for your thanksgiving day drowsiness.  If anything is to blame, it's the booze and all the "carbage".  Here's the link to the turkey/tryptophan post, in the meanwhile...

Brain size: is bigger better? or, Of mice and men (and elephants)

What would you say if I told you there may be a way to increase your brain size?  Would you be interested?

If you are, you're probably not alone, but would having a bigger brain make you smarter? Or would you just be throwing your money away?

Sadly, most of the evidence suggests that overall brain size is not a critical determinant of intelligence or cognitive function, and in some cases, having a bigger brain can actually be a bad thing.

Now, I was planning on writing a nice long post about how bigger is not always better when it comes to the brain, particularly when we look at different animals, but, I just read this article on ScienceDaily ( that sums things up pretty well.  I'll just give a quick example that I think is quite convincing:
the brain of an Asian elephant is obviously larger than that of your average human (about 7.5 kilograms, where the human brain is, on average, a little less than 1.5 kilograms).  Though, I think we will all agree that humans are smarter than elephants (if only slightly).  To get around this blatant difference between humans and elephants, some people have argued that proportional brain size is what matters. That is, if you take the size (or mass) of the brain and divide it into the size of the whole animal, you get a ratio that describes the size of the brain in proportion to the the rest of the body.  This works well when you look at humans and elephants, where, in humans, the mass of the brain over that of the body gives a ratio of about 2.1%, and in Asian elephants, about 0.15%. And to some extent, this approach works for other comparisons, where there are several examples that make sense (the ratio is larger in "smarter" animals),  HOWEVER... there are definitely many examples where this doesn't work, for instance, when you look at mice, the ratio of brain weight over bodyweight is 3.2%, about one and a half times more than the ratio in humans.  So, if bigger is always better, then either mice or elephants are smarter than people... which, despite the popularity of Sarah Palin's new book, is still highly doubtful.

So, comparisons across different species suggest that bigger brains don't equal smarter animals (even when you take overall body size into account).  But what about if you compare humans to other humans?  Here, there is some evidence that bigger is better (that's what she said), though again there are many exceptions and reasons for questioning that evidence (he retorted defensively).  For example, when we look at the fossil record, we see that, as humans evolved, our skull cavities got bigger, suggesting that our brains got bigger as we got smarter (though, again there are exceptions, like Neanderthals whose brains may have been bigger than our own).  When we look at more recent evidence in humans, we see some interesting things.  For example, boys have larger brains (on average) than girls (which remains the case in adulthood as well).  But does that mean boys are smarter than girls?  Well, if we look at average SAT scores, boys do tend to score higher than girls, BUT, if we look at grades (in co-ed institutions) girls get better grades than boys do.  So where does that leave us?  It leaves us with no clear evidence that one sex is any smarter than the other, despite the difference in brain size.  (The funny thing is, when we look at brain size as a proportion of total body size, girls actually have bigger brains than boys do, of course that still doesn't help us).
If we try to ignore the confusion of comparing men and women (or boys and girls as the case may be), there are some reports (based on data from MRI scans) that suggest bigger brains do correlate with higher IQ scores (which are certainly a limited, and perhaps biased measure for intelligence, but still interesting, and not completely irrelevant).  However, these are weak correlations, and they do NOT demonstrate a hard and fast rule (see the very end of this post for a more detailed explanation of what I mean).  For example, though he wasn't included in the MRI studies, one famous exception to this idea is Albert Einstein.  When pathologists examined Einstein's brain after his death they found that it was not any larger than your average human brain, though I'd be willing to bet he would score pretty high on an IQ test. 
In addition to the fact that these correlations were weak, there are a couple other points that make this evidence questionable (as to what it really means, if anything)...
1. several variables can change brain size over short periods of time.  For example, drinking alcohol temporarily shrinks the brain, which means if anyone in these studies was hungover, they would likely appear to have a smaller brain and also probably wouldn't do so well on the IQ test.  Other factors that are known to affect brain size include diet, exercise, marijuana, medication, and even meditation.  Given the relative ease with which these things can alter brain size, it seems more difficult to tie any measure to absolute brain size since brain size is obviously not absolute.
2. IQ tests may not indicate a person's overall intelligence.  That is, someone with a smaller brain may not have done as well on an IQ test, but they may be much more skilled in some other form of intelligence, like art (painting, sculpture, or music, etc.).  We all know that Mozart was a genius (whose music can actually make you perform better on IQ type tests) and yet, he would probably not score so high on an IQ test.
3. Correlation is not cause.  I have talked about this before.  Even if we assume the data is unequivocal (that is, an almost perfect correlation, where 100 percent of the time a bigger brain is associated with greater intelligence) we still can't say that having a bigger brain causes people to be "smarter".  Perhaps, brains get bigger with use, and therefore, people who study more or who have more years of education (and can therefore score higher on an IQ test) have slightly larger brains. For example, a study conducted about a decade ago with London cab drivers suggested that, at least a part of the brain might be able to get bigger with use.  The study showed that the hippocampus (which is important for remembering where things are located) was bigger in cab drivers than in regular commuters, and cabbies who had been on the job for many years had larger hippocampi than cabbies who had only been working for a shorter time.  While this isn't definitive, and doesn't say anything about other parts of the brain, it does suggest that brain growth in response to use or practice is a reasonable hypothesis.

So, what's the answer?  Are bigger brains better? I think, despite the correlations between brain size and IQ, we still have to say NO.
One final piece of evidence I would like to offer is the presence of a condition (in humans) called megalencephaly, which literally means "large brain".  Megalencephaly is characterized by a brain that is unusually large or heavy when compared to average brain size, and while it is suspected that the causes are genetic, they are not fully known.  Interestingly, megalencephaly often results in decreased intelligence and mental retardation, which seems pretty convincing evidence that simply having a bigger brain does not confer any improvements in cognitive abilities. Of course, another condition known as microencephaly, or "small brain", also results in mental retardation and, often, early lethality.  Together, these extreme conditions suggest that our brains work best within a range of sizes that are reasonably close to average.  So if you have an average sized brain, be grateful, and know that, you're in good company (with Einstein), and while there may be other factors determining how smart you are (environmental factors like education level, or diet and exercise, or genetic and biological factors, like how many receptors for neurotransmitters your nerve cells make), brain size is likely not one of them.


The statistical measure for a correlation is the r value.  In the MRI studies the r values ranged from 0.35 to 0.51, which may be statistically significant, but suggest a fair amount of deviation (what we would call a "weak" correlation).  "r" values range from -1 to +1, with -1 being a perfect negative correlation (one thing gets smaller while the other gets bigger), +1 being a perfect positive correlation (two values get bigger together), and 0 being no different from random chance (the two variables don't seem to be related to each other at all). While getting an r value of 0.4 or 0.5 is definitely meaningful (what we call "statistically significant"), it suggests that there are a fair number of people who break from the trend. "Significance" in terms of statistics, signifies that the relationship being studied (in this case between brain size and IQ score) is not random, or likely doesn't reflect measures you would get by chance.  To give you a simple example of what it means to be non-random, or not by chance, think of the simple comparison between two individuals where chance for a given variable is 50 percent (like flipping a coin, 50 percent chance of heads, 50 percent chance of tails).  If you come across two people with different brain sizes, the MRI data suggests it is likely that more than fifty percent of the time, the person with the bigger brain will score better on an IQ test than the person with the smaller brain.  However, a greater than 50 percent chance is NOT a hundred percent certainty.  So, some of the time (less than 50 percent, but still greater than 0 percent), the person with the smaller brain will be "smarter" than the person with the larger brain (at least when measured by IQ).

Sunday, November 22, 2009

Mad cows and cannibals...

A new article in the New England Journal of Medicine (1) shows the recent evolution of a mutation in a population of people in Papua, New Guinea that is protective against the degenerative brain disorder known as kuru.  Kuru is a prion disease which is a disease (specifically a transmissable spongiform encephalopathy) that is caused by proteins that act like viruses.  That is, the proteins are transmissable (i.e. contageous) and though they don't replicate themselves like viruses or bacteria would, they somehow seem to be able to cause all the other similar proteins in their host/victim to misfold in a way that then causes the build up of neurodegenerative plaques which are often fatal.  Mostly, these diseases are transmitted through the eating of meat, as in Mad cow disease (which is known as Bovine spongiform encephalopathy, or BSE, in animals, the mutated form of which, in humans, is called Creutzfeld-Jakob Disease, or CJD).  Kuru is a lot like CJD or BSE, and was passed on in the tribes of Papua New Guinea by the practice of the eating of dead relatives in memorial services.  Though this practice was ended in the 1950s, the populations of people in this area experienced kuru epidemics that shaped the evolution of their tribes.  One tribe in particular seems to have a high prevalence of a mutation (G127V) that protects them against kuru.  Since kuru is fatal (killing many women and children in these populations), it makes sense that this mutation would be selected for, and its prevalence would increase in the population.  This is particularly exciting because, not only is this a great example of evolution in action (in humans no less!), but as of yet, there are no treatments for CJD or kuru, and these diseases are often, almost always, fatal.  The discovery of this mutation in a population that has evolved a resistance to a prion disease will offer insights into how we might go about protecting the brains of those who haven't evolved a resistance to prion diseases, and hopefully save some lives.

1. Mead, Simon, Whitfield, Jerome, Poulter, Mark, Shah, Paresh, Uphill, James, Campbell, Tracy, Al-Dujaily, Huda, Hummerich, Holger, Beck, Jon, Mein, Charles A., Verzilli, Claudio, Whittaker, John, Alpers, Michael P., Collinge, John. A Novel Protective Prion Protein Variant that Colocalizes with Kuru Exposure. New England Journal of Medicine, 2009; 361 (21): 2056 DOI: 10.1056/NEJMoa0809716

Monday, November 16, 2009

You may feel sleepy on Thanksgiving... but it's not the turkey.

Since Turkey-day is around the corner, I thought I would bring up the very popular myth that tryptophan in turkey is what makes us all feel groggy on Thanksgiving.  In an earlier post, I talked about how the amino acid tryptophan gets converted into serotonin, and then melatonin.  Melatonin, as you may or may not know is the "sleep hormone". It is secreted by the pineal gland to help regulate our sleep/wake cycles which follow a circadian rhythm of about 24-25 hours.  During the day, when it is bright and sunny we feel awake, then, as the day turns into night, we start producing more melatonin, and we get sleepy.  Considering this, it's not too hard to see why tryptophan became the scapegoat for our Thanksgiving day sleepiness, but the truth is tryptophan, or really turkey in general has gotten a bad rap.  First, tryptophan is a fairly prevalent amino acid, and there is actually plenty of it in most of the protein containing foods that we eat.  Furthermore, turkey does NOT contain a higher level of tryptophan than most other common meats, fish, and poultry.  For example, per 200 calorie serving, duck, pork, chicken, soy, sunflower seeds, several types of fish, and turkey all have about 440 - 450 mg of tryptophan, with turkey being the lowest in the group.  Of course, that being said, even if turkey did have significantly more tryptophan than other meats, it is still questionable as to whether normally consumed levels of tryptophan can make you sleepy.  While at first glance, the research seems to back the idea that tryptophan has sedative effects, these studies have used very large quantities to test for effects. For example, one study from 1975 suggested that consuming 5 grams of tryptophan (so, about 11 servings of turkey) did increase self-reported drowsiness, and a study conducted in 1989 found that a dose of 1.2 grams of tryptophan did not increase measures for drowsiness, but a dose of 2.4 grams did.  These studies suggest that you would have to eat a lot of turkey (like, over a pound and a half) to get an effective dose.  So, while it is possible that you may eat that much turkey on our most hallowed of gluttonous holidays, it is more likely that thanksgiving day drowsiness is the result of a coming together of many factors, a perfect storm if you will, of:
1. lots of food (which diverts bloodflow to the digestive tract),
2. much of the food is carbohydrate heavy stuffing and sweet foods like cranberry sauce, sweet potatoes, and desserts (which can cause an overproduction of insulin resulting in low blood sugar, and thus sleepiness, later on),
3. and then of course there are usually a couple of alcoholic beverages involved (with obvious sleep inducing effects). 
Add all of that up with being  in a nice, warm home, on a comfy couch, with football or parades or a fire flickering in the background, and what you have is a recipe for a nap.  I'm kinda sleepy just thinking about it.
Have a Happy Thanksgiving!

Wednesday, November 11, 2009

I'm a "No" man... oh, and alcohol doesn't kill brain cells.

So, I've been reading Randy Olson's new book Don't be such a scientist: talking substance in an age of style, and in it, he talks about the disconnect between the general public (in our modern overly stimulated society) and scientists (who cloister themselves in their labs and ivory towers).  A large part of the communication breakdown he posits comes from the nature of science itself which is a bare bones, take no prisoners, purely data and fact driven culture that breeds overt skepticism at all costs.  This is important for how science works and for maintaining integrity in research, and it can actually be quite helpful in making your experiments better, but when you are trying to convey your findings to a broader audience they tend to find all the negativity and information overload to be, well, boring.  Partly this is because the attention of the average person is now a hot commodity, and the marketplace for the average joe's attention is filled with advertisers, marketers, politicians, television, music, movies, you tube, and on, and on.  Spend a few minutes going on about the role of bone morphogenetic proteins, wnt-beta catenin signaling, hedgehog singnaling, and several other factors in the differentiation of stem cells in the development of different aspects of the central and peripheral nervous system, and zzzzzzz.....  Of course, I don't know if its the training, or if people of a certain mind set just gravitate to science, but a lot of us are like that.  We go off on our research as if its the most important thing in the world, and we are obsessed with facts and with being accurate, and, we are very negative, we are always questioning the validity of what we're seeing or being told (it's what we do, we get paid to be skeptical). And so, as I've been reading this book, I've realized that I am no different, and that even this whole blog is devoted to negativity.  I have set out to debunk, demystify, and disprove many common misperceptions about neuroscience.  I am a "no" man.  That's not how this works... That idea is wrong... I have become the person who constantly annoys everyone by correcting their grammar, escept I do it with neuroscience.  Well, I can't help it.  It's who I am, and part of my nature as a scientiist. BUT... despite my obsession with factual accuracy and my desire to negate the myths that are out there, it doesn't mean I always have to be the bearer of bad news.  For example, today, the myth I want to debunk is the myth that drinking (alcohol) kills brain cells.  As it turns out, there is very little (if any) conclusive evidence to suggest that drinking alcohol kills brain cells.  So where did this myth come from?  Well the obvious memory loss and headaches that come from binge drinking suggested that some sort of brain damage was occuring.  And more recently, MRIs have shown that the brain shrinks after drinking.  Don't worry, it's only temporary, but apparently it shrivels like a prune.  Also, alcohol can damage parts of cells known as neurites that form synapses which are the connections between cells that allow them to communicate.  Synapses are critical for forming new memories, and it appears to be this aspect of alcohol's effects that result in the short term memory loss we've all experienced at some point or another.  Of course all that being said, overdosing on alcohol (or alcohol poisoning) can most definitely cause cells to die (and could cause you to die).  Also, drinking and driving could kill brain cells by smashing them into the windshield at 60 miles per hour.  But if your just going to have a few drinks with some friends, live it up, and relax, confident in the knowledge that your brain cells aren't lightweights, but they're actually tough enough to handle a couple beers, and maybe even a shot or two.  Hey, some studies have even suggested that moderate drinking can improve mental abilities.  So maybe a glass or two of wine a night is the way to go (since it's good for your heart too).
Normally I link to a bunch of stuff to back up what I'm saying, but I am off to Wisconsin, so these links will have to suffice....

Sunday, November 8, 2009

More BS from people trotting out PhDs

The proponents for creationism (or intelligent design, as the names are really interchangeable) at the Discovery Institute (DI) have a new campaign going on where they aim to expound upon 95 theses that, they claim, will make you reconsider Evolutionary theory. At least, I think it's the work of the DI since the only thing on the page right now is a link to a DI document that lists the names of scientists and other academics who have assented to the statement:

“We are skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged.”

First, I love that the 95 theses are a tribute to Martin Luther's seminal work which he tacked to cathedral doors to ignite a reformation of the Catholic church. And they say intelligent design isn't religious in nature?
Second, I love that there isn't anything on the page. I am sure this is the calm before the storm, but for now it just points out that there is no evidence to disprove any facet of evolutionary theory as it stands today. Most likely, these 95 theses will be things that argue against Darwin's ideas of 150 years ago or will just point to gaps in our understanding and say, "since we can't explain this (yet), God must have done it". Same old crap, new marketing and PR.  Or, it will just be some crazy ideas that are unfounded and unsubstantiated by any factual evidence (like this one)
Next, I would like to point out that the statement above is pretty reasonable. First, it's not asking anyone if they denounce evolutionary theory, of even whether or not they think it fails to explain the origins of species, it just asks if they are skeptical about random mutations and natural selection being the SOLE cause of the complexity of life, and if they would encourage people to pursue further inquiry into evolutionary theory. It is cleverly worded so that a scientist would read it and think, "of course, why wouldn't we want to further investigate the theory that underlies ALL of the major findings in biology for the last 150 years. Surely there are nuances to be expounded upon, and our understanding of the natural world will likely never be complete, as new species arise everyday." Of course a non-scientist would read this, and if they were already skewed to favor creationism, would accept this as evidence that there is a major conflict amongst academics over whether or not evolution is true. Let me be plain, THERE IS NOT. The OVERWHELMING majority of scientists recognize that evolution is a fact.  Those who don't, I suspect, are lying out of some misplaced sense of duty to their religious beliefs, or for some monetary or political gain.  Asking whether or not you agree with such a statement is a trick question... ask any evolutionary biologist, and my bet is that all of them would agree. Why? because if they didn't think that evolutionary theory should be "carefully examined", they wouldn't be able to justify their own jobs! I mean, why would you spend your whole life and career studying something you didn't think needed a more "careful examination"  And as for being skeptical, that is what scientists do. I am skeptical too! Particularly when you ascribe something like ALL of life's complexity to just 2 processes: random mutation of DNA, and natural selection. Especially when we already know that artificial selection, sexual selection, and genetic drift can drive evolution as effectively (if not more so) than natural selection.

And as for random mutation, it is a wonderfully exciting hypothesis to suggest that there might be changes to DNA, that could be selected for or against, that are not random, and actually, I think you could already make a case for it. More and more evidence suggests that our environment interacts with our DNA at the molecular level. As a common example, UV radiation from the sun preferentially targets thymidine molecules in our DNA, more specifically, pairs of thymidines that happen to be next to each other. When UV light mutates our DNA, more often than not, it causes two of these molecules to fuse together, forming a thymidine dimer (see figure above, copyright 2004, Steven M. Carr). These are the mutations we worry about with sun exposure because they can lead to skin cancer, and these mutations are obviously not random: the chemical structure of thymidines in DNA lends them more to an energy induced change in bonding than other molecules in the DNA (the C, G, and A nucleotides). Of course, this example is more of an analogy because, in order for a mutation to be passed on to one's offspring, it has to occur in cells that will ultimately give rise to either a sperm or an egg cell, and, hopefully, your spermatagonial cells and ovarian follicles aren't getting sunburned. However, this analogy suggests that it is possible for mutations to be non-random, which means it may be possible for mutations that get passed on to be non-random as well... for example, molecules from the food we eat and the air we breathe enter the blood stream and are thus trafficked to all of the cells in our bodies (including sperm and egg cells). These molecules may introduce mutations in a manner similar to UV radiation from the sun, that is in some preferential, non-random way. This is a fascinating idea! And it can be tested experimentally and thus scientifically, and thus, should be "more closely examined". And then we will obtain evidence either for or against non-random mutations being an agent of evolutionary change. And, if we find it's possible, then we can futher "examine" different species for more examples of non-random genetic changes.

But there are even more hypotheses and predictions we can generate based on the evidence we already have, which lead us to "examine more closely" these aspects of evolutionary theory. Previous mutations could make it more or less likely for specific types of mutations to occur in the future. And DNA, by its very chemical nature and structure may lend itself to certain types of changes over others (like the suburn and thymidine example, except possibly without the need for a mutagen). Also, we know that mutations at the sequence level aren't the only things that can bring about change at the phenotypic level. Whole genes sometimes get duplicated when the processes of meiosis and mitosis go awry.  We can further "examine" these duplication events to see how often they occur, or how important they are for different types of traits. Sections of chromosomes cross over during meiosis to introduce genetic variability, and mechanisms have arisen to vary phenotypes at the RNA and protein levels as well.  These areas all need further "closer examination" to see what role they play in evolution, if any.

The point is, this statement that seems to indict so many scientists as "dissenting from Darwinism," is actually quite weak and not up to date with much of what has been discovered about evolution and genetics in the past 50 or 60 years. Many biologists would admit to not only being skeptical, but to claiming that the statement "random mutation and natural selection account for ALL the complexity of life" is actually false, (since we already know that random mutation and natural selection are not the WHOLE story of evolution). Basically, the poorly named discovery institute has trotted out some old ideas about evolution and asked, "who thinks we should investigate further?", NOT, "who disagrees?", but "who thinks we should investigate further?" Well, of course scientists are going to want to investigate more closely, that's what we do! But the DI just wants you to read that statement, and think that there is massive "dissent from Darwinian theory", and that we should all pack up our books and go home. Agreeing to the statement they have written only means you dissent from an antiquated and un-updated theory of evolution. You may as well ask physicists if they are skeptical of the ability of Isaac Newton's ideas to explain ALL of the things we see in the universe. I imagine they would all say no, his ideas have been updated and expounded upon by others like Einstein to fill in the gaps where Newtonian physics fail and to explain what's going on at the sub-atomic level, or in black holes, or at the beginning of the universe. Does this mean that ALL of Newtonian physics is wrong? No. In fact, it is still the basis for most of our knowledge of physics in the world we live in (where everything is at least as big as an atom and things move slower than the speed of light). The same is true for Darwin's ideas.  Are they perfect and all-inclusive? NO. Do they still provide the framework that explains almost everything we observe in biology? YES.

The main difference here is, ID propoents use this statement to claim that scientists support so called "intelligent" design because ID, so they claim, further investigates evolutionary theory.  But that is a lie.  Scientific investigation allows us to more closely examine evolutionary theory.  ID, while helpful in its ability to point to some of the unanswered questions and interesting examples, does nothing to find out anything new about those instances.  The whole basis of the idea is this: some divine being who we cannot see or know in any objective or natural way put everything here and that was that.  This idea is the opposite of further examination, it is fatalism pure and simple.  It is saying that things like the origin of species are too complex to figure out, we should just say god did it, give up, and go home.  In fact, I should think that while most biologists would affirm the statement put forth by the DI, most creationists would not (at least if they were to read it the way scientists do).  In fact, I suspect that most of the fellows at the DI don't really want to examine evolutionary theory any further because everytime we do, their claims are disproved and evolutionary theory is further verified (like the evidence for the evolution of the bacterial flagellum which I talked about here).

This is just another example of how the DI and other proponents of creationism manipulate people and information to cloak themselves in this false air of credibility when really they are being flat out deceitful. They don't really want to "examine" evolutionary theory "more closely" they simply want to tear it down in the eye of the public. ID is a smear campaign plain and simple.

I don't yet have a PhD, but when I do, maybe they'll ask me to sign their petition as well?  I think I would have to refuse on moral grounds. I agree with the statement, but not the spirit of it, and not the dishonesty that went into crafting and disseminating it. Questioning evolutionary theory is great! It's what good biologists do everyday. And I encourage everyone to question it, to find out more (from reputable sources), and to test their theory over and again, scientifically.  The difference is, the DI doesn't want you to carefully examine evolutionary theory, at least, not in any productive way. They want you to learn FROM THEM the specific examples of things that haven't been explained yet. And the things they point to, like old ideas, and say they've been proved wrong when really they've just been updated. And they want you to think that numerous scientists disagree with evolutionary theory, when really the true scientists just want you to understand it better.

Wednesday, November 4, 2009

A little late for Halloween, but...

you want to see something that will freak you out?  at least as freaked out as you can be by something that is uber nerdy and neurosciencey?  Check out this video of the McGurk effect.  Watch the video, and try to identify the one syllable sound that is being repeated.  Then, watch it again, but close your eyes, or look away from the screen.

Did the sound change?
What happened?
The McGurk effect is an auditory illusion that demonstrates how our brains process the information we get from our senses. Generally, these pathways have some overlap which we often take for granted. For example, the same coordination of auditory and visual information being exploited in the illusion here is actually useful when you are in a bar or crouded party and you can't really hear the person you're talking to. Luckily, in real life (unlike in the video) the auditory and visual cues match up and your brain can use the visual information to help you "hear" the person next to you in that loud party. Though not exactly the same, a similar overlap occurs with olfactory (smell) and taste pathways which is why food tastes different when you have a cold or pinch your nose.

Here's another video that includes an explanation of the McGurk effect, and after that, a video showing the reactions of some viewers on a Japanese television show.

Sunday, November 1, 2009

What do Autism and Milli-Vanilli have in common?

Very little as you might have guessed, but recent popular media articles with clever titles like "Autism: Blame it on the Rain" I get the feeling I'm going to be just as disappointed as when I learned those guys were lip syncing the whole time.  Anyway, the articles go on to talk about an epidemiological study that shows a correlation between counties in west coast states that get a lot of rainfall and increased incidences of autism.  And as I suspected, I am disappointed, not in the research that inspired the popular press articles, but that most of the popular press articles seem to gloss over the fact that this study is VERY PRELIMINARY.  The authors of the study are not saying there is a definite link between living in a rainy area and the chances that your kids have autism.  Here's what I mean.  Before anyone gets too agitated and starts thinking of moving to the Arizona desert, let's consider one of the most famous adages in science: "correlation is not causation".  What that means is: just because two things are correlated doesn't mean they have anything to do with one another.  A great example of this comes from the website, home of the church of the flying spaghetti monster, which has a figure correlating the decline in the number of pirates with the global increase in average temperature. 

Does this mean that we should assume global warming is responsible for the decrease in piracy we've seen since the 1800s?  No, it is simply a correlation, and there is no good evidence to suggest that increases in the average yearly temperature have any affect on how many pirates there are.  Or that pirates somehow cool the globe, and their absence is what has caused the world to get warmer. Given what we know of history and climate science, it is much more likely that the increases in technology and industry since the 1800s led to increased air pollution (and increased levels of greenhouse gases) which has led to steadily increasing average temperatures. Conversely, technology also allowed for improved national navies and merchant marines that have had more success in capturing and imprisoning or killing pirates, or evading them.  Additionally, the development of air travel meant less and less people and valuables were transported by sea.  As the cost to benefit ratio of being a pirate became more costly than beneficial, less and less people opted for it as a career.  (And of course, if we look at the recent increase in pirates coming out of Somalia, we see no decrease in temperature to account for this absurd relationship, but the dire circumstances in Somalia and the millions of dollars in ransom these pirates have been able to amass suggests there is something to the cost/benefit idea.)  Anyway, the fact that the only thing this study shows is a correlation with no evidence of causality is not the only strike against an argument for relating rainfall to autism.  Apparently, there were several issues with the methodology of this study that make its results sketchy at best.  An article at actually does a great job of explaining everything, but just to give the highlights here:
Despite the statistically significant findings, a careful reading of Waldman’s article published in the November issue of Archives of Pediatrics and Adolescent Medicine results in more questions than answers.
Could the rain-autism correlation be an artifact of another relationship? Traveling through Oregon or Washington, for example, a distinct trend emerges: the further east, the more rural and dry. It may be that urbanized counties do a better job of reporting autism cases, and that these simply happen to be the same counties with more rainfall.
Teasing out other causes, like ruralness, is difficult in an epidemiological study. This is one reason why Waldman’s research design is the “weakest type of epidemiological study,” according to Irva Hertz-Picciotto, an environmental epidemiologist at the University of California, Davis, also uninvolved with the study. Rather than examining exposures of individuals, ecological studies compare whole groups, which means information that could help decipher the true cause-effect relationship is lost.

Further, the grouped data in Waldman’s study came from a combination of sources — from state agencies to regional health centers — leading Hertz-Picciotto to suspect the numbers are not comparable within or between states. “Often the [agency or center] will put the children into the categories that they know they can provide services for,” Hertz-Picciotto says, “even though the categories may not be the best description of the child’s diagnosis.”
All of that aside, does this study tell us anything important?  Despite my somewhat rough treatment of it here, the answer is actually yes.  The finding that the incidence of autism may be correlated to the amount of rainful an area receives could lead to the discovery of some other factor that is related to both autism and rainy days, and thus, provide an explanation for the correlation.  For example, there is a psychological disorder called Seasonal Affective Disorder (SAD) which is more commonly known as the "winter blues".  When the days are shorter, and we are exposed to less natural light, and it is hypothesized that people with SAD produce less melatonin and serotonin (a hormone and neurotransmitter, respectively, the former most notably characterized as helping to regulate sleep/wake cycles, while the latter is the neurotransmitter most often enhanced by antidepressant medications).  It may be possible, that children who have a genetic predisposition to autism spectrum disorders may be sensitive to getting less light in a similar fashion as people who have SAD, these kids may have brains that produce less serotonin or melatonin, and this may, in turn affect the development of their brains.  Alternately, it may be that kids who fall on the spectrum may become more antisocial or have a more difficult time with vocal development because they are forced to stay indoors more, watching tv and playing video games rather than interacting with other kids.  Both of these ideas are completely speculative and are not substantiated by any hard evidence.  But it is important in science not to discount any ideas until they have been tested, and disproven.  And the benefit to the study mentioned in these articles is that it gives us a reason to hypothesize about the role of light exposure or time spent isolated indoors as factors that could affect autism, and better still, reason to test these ideas so that we will one day know for sure whether or not, and to what extent, where you live, or how you live, affects the chances your kids will be autistic or not.