Scientific Chick

Live from the sky, somewhere over the prairies

2011-05-29T22:55:00.000-07:00

It’s been a while, science-loving friends, and I apologize. I could list all the things that have kept me away from this blog in the past month, but then I might scare away anyone who is considering the postdoc life. Instead, I will reward your patience with brain news hot off the press: a report from a neuroethics conference I just attended in Montreal called Brain Matters. As with previous conference reports, I will share my insights in bullet-proof format, as my foggy jet-lagged brain cannot write a coherent paragraph at the moment.

The conference brought together a large variety of professionals: neuroscientists, lawyers, bioethicists, philosophers, psychiatrists, you name it. As it turns out, psychiatrists know a joke or two.

We heard quite a bit about how the media handles neuroscience news. The consensus is that in most cases (but not all), the answer is poorly. The blame gets tossed around. Journalists hype research too much, but it’s not their fault, they need to sell papers. Researchers hype research too much, but it’s not their fault, they need to get funding. I voted to shift the blame onto grad students. I also thought we could solve the problem easily by making everybody read Scientific Chick. It didn’t take as well as I had hoped.

We also heard quite a bit about deep brain stimulation (DBS), a potential treatment for a variety of illnesses and conditions that involves sticking a stimulating electrode in the brain and leaving it there. Right now, this works relatively well for treating advanced cases of Parkinson. The problem is that it comes with side effects and that people undergoing this type of treatment are reporting things like “no longer feeling like themselves”. This brings us to an important question: What does it mean to feel like yourself? One of the most fascinating talks of the conference involved an in-depth discussion of personal identity and how it is or isn’t affected by brain interventions like DBS.

There was also a discussion of self-experimentation. Should willing neuroscientists be allowed to stick electrodes in their own brains to advance our knowledge of neuroscience? The speaker argued that we allow people to skydive and bungee jump without having them fill endless forms and run their proposal to do something crazy through an ethics board, so self-experimentation should be no different. I mean, do you want the Nobel Prize or not?

One of the most interesting talks was on placebos. The researcher argued that antidepressants work only marginally better than placebos in most cases (though not all cases), and so we should really ask ourselves whether the small improvement is worth the side effects. I thought of a genius business venture that involves selling sugar pills for every possible condition. Then I remembered that this already exists. It’s called homeopathy.

Speaking of placebos, everyone always assumes that they only work because you think you’re getting an active drug. Some researchers were skeptical about this, and so they carried out this fascinating study that involved giving placebos to people with irritable bowel syndrome, but also telling them that they’re getting placebos the entire time. Guess what? They felt better anyway.

This blog post is already dragging on too long, but these were just a few of all the very interesting topics and discussions we had over two days. I hope to be back with regular science programming very shortly, so stay tuned for the latest and greatest!

Pretty politics

2011-04-10T13:47:00.001-07:00

My Canadian readers are no doubt preparing for the upcoming federal election. Living in a democracy, we have the opportunity to vote for the candidate we think is most competent (even if sometimes it seems like all options are pretty grim). If we choose well, we may be rewarded: there is much evidence that intelligence and competence correlate with effective performance in politics. Unfortunately, research also shows that intelligence can’t be predicted from one’s appearance. Everyone knows that. That’s why we would never choose a competent candidate solely based on what they look like. Or would we?

To evaluate how much looks factor in when choosing a political candidate, Swiss researchers asked over 600 adults to rate which of two faces (in photographs) looked most competent. Little did the participants know, the two faces were actually of two candidates in a past French parliamentary election. As it turns out, over 70% of the participants ended up picking the candidate who had won the election.

To take things a little further, the researchers then carried out a similar experiment in children. They had over 600 children ranging from five to thirteen years old play a computer game that involved a sailing trip from Troy to Ithaca (sounds familiar?). After the game, the children were shown the same two faces used in the adult experiment and were asked to choose who they would prefer to have as captain of the boat. Again, just over 70% of the children chose the election winner.

Interpreting these results can be a bit tricky, but keep in mind that we already know that competent people aren’t necessarily prettier. One thing is clear: the experiments tell us that adult and children use similar types of visual information when judging whether someone is competent or not. The researchers also conclude that voters don’t factor in enough information about the actual performance of candidates when heading to the ballots, relying instead on what candidates look like. While I’m sure they are at least partially right, I think it’s a bit of a stretch to come to this conclusion given the simplicity of the study.

In any case, the results serve as a good reminder to think about our candidates and to take our civic duties seriously. After all, we wouldn’t judge a book by its cover…

Reference: Predicting elections: child’s play! (2009) Antonakis J and Dalgas O. Science 323(27):1183.

But what about clones?

2011-04-04T22:53:00.000-07:00

I feel cheated.

When I heard all the buzz about a recent Canadian study showing that identical twins don’t share the same DNA, I thought: there’s this week’s blog post. Easy peasy. I imagined the title of the article was probably something like “Identical twins don’t share the same DNA” or, even better: “Just kidding: everybody is unique after all”. Instead, to give you the low-down on this moderately exciting finding, I had to read through a paper called “Ontogenetic de novo copy number variations (CNVs) as a source of genetic individuality: studies on two families with MZD twins for schizophrenia”. So don’t ever say that I don’t love you.

The finding is very straightforward and fairly intriguing, but before I dish out the details, I have to remind you about two concepts you may not have heard since high school (but rejoice: it's sex-related): meiosis and mitosis. Meiosis is what happens when one cell with two copies of each chromosome divides to produce gametes – in our case, sperm cells and egg cells, each with a single copy of chromosomes. This process is necessary for sexual reproduction. Mitosis is what happens when one cell generates two separate sets of chromosomes and then divides, leaving each daughter cell identical to the mother cell. This process is necessary during early development.

Now onto the article: the researchers were on the hunt for genes that are involved in schizophrenia, and as is often the case in these types of studies, they were looking at identical twins. The idea is that diseases can arise from genes (for example, Huntington’s disease), from the environment (for example, certain forms of cancer), or from a combination of both (for example, certain forms of Alzheimer’s disease). If identical twins have the same genes but only one of them gets a disease (say, schizophrenia), then researchers typically rule out genetics as the cause and examine what differences in the environment of the two twins may have caused the disease. See how that works?

In this study, the researchers were particularly interested in a DNA alteration called “copy number variations”. You see, DNA is never perfect, and sometimes cells have abnormal copies of big chunks of your DNA. These copy number variations can be harmless, but they can also cause certain diseases, so geneticists are paying close attention to them. In any case, the researchers found that supposedly identical twins had different sets of copy number variations when compared with their parents (meaning they didn’t inherit these DNA alterations from their parents). The cool thing about this finding is that the researchers can now determine when the alteration happened depending on who has the different copy number variation. If both twins have the same copy number variation, then we know it originated during meiosis (when the parents were generating eggs and sperm). If only one twin has the variation, then we know it originated during mitosis (during development).

While the article doesn’t focus all that much on the fact that identical twins have the same DNA (I hate to say it, but we kind of already knew that), this tidbit of information is relevant in two ways. First, it’s going to change how researchers carry out twin studies, because we can no longer assume that identical twins have the same DNA (as if we needed to complicate things further…). Second, this finding might lead to a new way of thinking about genetic diseases.

So there you have it: we are all unique individuals after all. Up next: your parents aren’t who you think they are. Your “parents” are really bug-eyed aliens from Neptune! (as always, bonus points for the correct reference in the comments…)

Reference: Ontogenetic de novo copy number variations (CNVs) as a source of genetic individuality: studies on two families with MZD twins for schizophrenia. (2011) Maiti S et al. PLoS ONE, 6(3):1-13.

Sticks and stones may break your bones but words will break your brain

2011-03-27T22:34:00.000-07:00

“Sticks and stones may break my bones but words will never hurt me.” Sounds familiar? You may have been taught this witty maxim to fend off bullies during the glorious years that are high school. Since then, bullying has become a big deal: its often-devastating consequences are more than ever in the public eye. We already know that childhood abuse in many different forms (sexual abuse, physical abuse, witnessing domestic violence) can have long-lasting impacts. For example, sufferers are found to be more susceptible to depression and suicide, and more likely to engage in fights, do drugs and use a weapon. But what about verbal abuse from peers?

To evaluate the effects of peer verbal abuse on the brain and behavior, a team of researchers studied over 800 young adults who had no history of any of the big confounding factors such as exposure to domestic violence, sexual abuse, or physical abuse. The participants were asked to fill out surveys about how much verbal abuse they experienced from peers at school as well as surveys with more general questions about mood, behavior and psychiatric symptoms.

The results show that the more peer verbal abuse one is exposed to during school, the more likely they are to experience anxiety, depression, anger and drug use. As it turns out, verbal abuse from peers is just as bad as verbal abuse from parents in generating these consequences. As well, researchers found that peer verbal abuse that occurs during middle school years (ages 11-14) has the most significant impact (compared with elementary school and high school). I find that surprising, as I remember high school being much worse than middle school, but apparently it has to do with the timeline of brain development, not my personal feelings about high school.

To dig a little deeper, the researchers selected 63 participants who had experienced varying degrees of peer verbal abuse and had them undergo a brain scan (MRI). They found that participants who had been exposed to a lot of peer verbal abuse displayed abnormalities in their corpus callosum, a big bunch of white matter fibers that connect the left and right sides of your brain. The researchers suggest that this abnormality may explain some of the behaviors and symptoms associated with the abuse (such as depression).

While this study convincingly highlights the impact of bullying on the brain and brain function, there are a few things to keep in mind. Repeat after me: correlation does not mean causation. That undergoing bullying is associated with abnormalities in the brain does not mean that bullying necessarily caused these abnormalities. More studies will be needed to uncover that link. As well, the study is retrospective, meaning the authors “go back in time” by asking the participants to remember events from years ago. This can sometimes lead to faulty recalls or false associations. Lastly, I find it a bit strange that the researchers have not looked at the hippocampus of the participants. You may remember that the hippocampus is a brain region important for memory, but it is also involved in emotions, and it has been shown to be susceptible to other forms of abuse. I’m hoping the bullying-hippocampus link will be looked at in a future study.

Overall, though, the study reminds us that bullying is an important and potent childhood stressor. Sticks and stones it is.

Reference: Hurtful words: association of exposure to peer verbal abuse with elevated psychiatric symptom scores and corpus callosum abnormalities. (2010) Teicher MH et al. Am J Psychiatry 167(12):1464-71.

Who are you?

2011-03-21T10:01:00.000-07:00

It's Scientific Chick's blogiversary! To celebrate two years of sciency goodness, treat yourself to some cupcakes:

I also take this occasion to launch my first-ever "Who are you?" thread. Since I've started this blog, I've been picking science articles that I thought were interesting, and writing about them in hopes that my excitement for science would be contagious. Two years later, it's time for me to think about how to make Scientific Chick better, and how to cater to my readers. This means I need to get to know you! So pretty please, indulge me by answering these easy questions in the comments:

1) Tell me about you. Who are you? Why are you here? Do you have a background in science? An inquisitive mind?

2) Tell me about what you like. What are your favorite stories? What topics are you most interested in? Do you enjoy a meatier science discussion, or are you satisfied with the big picture?

3) Tell someone you know about Scientific Chick. Do you have a friend or family member who you think would enjoy this blog? Let them know! Readership keeps me going. :)

Don't be shy! I can't wait to meet you!

The stress of having an unattractive partner

2011-03-07T19:40:00.000-08:00

Here’s how blog writing usually goes for me: I peruse science journals for a suitable story, read a few articles, pick one, write the blog post, copy the reference, and find a good picture. Then I spend anywhere from an hour to a couple of days trying to come up with a title. For some reason, finding the right title is always the hardest part. So this week, when I saw an article with a title that I could use as is for the blog post, I just knew I had to write about it.

The article, as you can infer from the title of this post, looks into the relationship between attractiveness of a mating partner and stress in female birds. Most birds, like humans, tend to form monogamous pair bonds that last through the course of at least one reproductive event. Because of this “socially monogamous” system, if there are approximately the same amount of males and females around, most birds will be able to find a partner, but inevitably, a big chunk of females will end up paired with males of “below-average” quality (but I’m sure they have lovely personalities). So the researchers wanted to know, how does that make the female birds feel?

As I’m sure you can imagine, rating the attractiveness of one bird over another is no easy feat for human scientists. What’s more, beauty is in the eye of the beholder, but you can’t send out mass emails to female finches to fill out online in their spare time (“On a scale of 1 to 7, 1 being Dwight Schrute and 7 being George Clooney, how would you rate Mr. John Finchy?”). Therein lies the beauty of this study: the researchers picked a very creative model to answer their question. They studied a type of finch that comes in two colors: red heads and black heads. Even though they are the same species, red-headed and black-headed finches are partially genetically incompatible (meaning they have a harder time producing offspring), and so these birds tend to have a preference for mating partners with the head color that matches their own (though if there are slim pickings, they will mate with a bird of the other color). Knowing this, the researchers set up an aviary with a whole mix of these birds (males, females, in combinations of red heads and black heads) that had not previously met, waited until every bird had paired off, and then assessed the females’ satisfaction with their mating partner based on two parameters: how long until she would agree to breed, and how much corticosterone (a stress hormone) she had in her blood (don’t worry, a harmless procedure).

The results show that females that paired with a male of the wrong color laid eggs nearly one month later that the females paired with a male of the same head color. What’s more, females paired with incompatible (“below-average” quality) males had three to four times more stress hormones in their bloods, and this went on for weeks. Who knew that attractiveness could have such an impact on stress levels?

As it turns out, a widespread strategy used by female birds to deal with unattractive mates is to… select alternative, extrapair fathers for their offspring. Dan Savage would have a field day if he knew about these little sneaky females…

Constrained mate choice in social monogamy and the stress of having an unattractive partner. (2011) Griffith SC et al. Proc. R. Soc. B [Epub ahead of print].

Enlarge your brain in only 8 weeks!

2011-02-27T10:58:00.000-08:00

Having a big brain seems like a very desirable thing right now (it certainly wasn't "trendy" when I was in high school, though). Games like "Big Brain Academy" measure your success by the size of your virtual brain. In the real world, scientific studies right, left and center extol the virtues of anything ranging from exercise to learning a new language as ways of expanding your gray matter. It turns out that learning to manage your stress might also do the trick, as I found out from a recent article pointed out to me by my friend Fawn.

The article looks at mindfulness mediation, a practice that involves becoming aware of experiences in the present moment without judging oneself. Many studies have already shown that mindfulness-based stress reduction programs can ease symptoms of anxiety and depression and can improve sleep and attention. But how does it work? To answer this question, researchers studied what mindfulness meditation does to your brain (to learn about what mindfulness mediation does to your pain, see this post).

The study looked at a handful of participants enrolled in an 8-week Mindfulness-Based Stress Reduction course. This course entails one meeting per week, one full day of training in week 6, and daily homework to do at home (meditation exercises). The experiment was very simple: researchers took a picture of each participant's brain using magnetic resonance imaging (MRI) at two time points: before the course started, and once it was over (8 weeks later). They also took pictures of the brains of control subjects who didn't take the course (also about 8 weeks apart).

By now I'm sure you've guessed the results: yup, the participants who meditated had significantly bigger brains. One area of the brain in particular was bigger: the hippocampus, a region known for its role in memory, but also involved in emotions. The researchers hypothesized that the increase in gray matter in the brain of people who mediate may explain the improvement they experience in dealing with their emotions. This hypothesis is supported by the fact that people who suffer from certain emotion-related diseases and disorders like depression and post-traumatic stress disorder often have a smaller hippocampus.

While I'm a big believer in meditation (this blog is so biased!), there are two limitations of this study worth mentioning. First, the researchers only looked at about 14 participants in each group. That's a pretty small sample, so it will be interesting to see what later experiments looking at more subjects come up with. Second, the mindfulness-based stress reduction program is not only about meditating: it also involves social interaction at the weekly meetings, stress education, and gentle stretching, which the control participants didn't get. So it's quite possible that the effect described here (bigger brains) are not the result of meditation per se. At this point we can't tease it out.

Regardless of these limitations, though, the study drives home an important message: the adult brain can change in response to training. I for one find some comfort in that.

Reference: Mindfulness practice leads to increases in regional brain gray matter density. (2011) Holzel BK et al. Psychiatry Research: Neuroimaging, 191:36-43.

A picture better be worth a thousand words

2011-02-16T23:02:00.000-08:00

My friend Michael (a.k.a. this crazy guy – would you please send him to New Zealand?) recently blogged about undergoing what he perceived as an unnecessary medical imaging procedure. He was concerned that this exposure to radiation might impact his fertility. A recent study suggests that Michael should add cancer to his list of concerns.

We’ve known for a long time that radiation is bad news. Scientists studied atomic bomb survivors and found that those who were closest to the blast had a higher incidence of cancer than survivors who were farther from the blast. While the evidence is conclusive, the atomic bomb delivered a much higher dose of radiation than medical imaging procedures. To tease out whether low-dose radiation from medical imaging procedures also increase one’s risk of developing cancer, a team of researchers from McGill University analyzed a group of over 80,000 patients who were admitted to the hospital for a heart attack. They perused the medical records of these patients and noted who received medical procedures involving radiation and who didn’t, and then followed-up by finding out who got cancer later on.

The researchers found that over 10,000 patients developed cancer later on. Interestingly, two-thirds of those cases of cancer were located in the abdomen, pelvis or thorax (presumably the areas that would be subject to medical imaging procedures aimed at the heart). After looking at each patient’s history of procedures, the researchers were able to determine that the more radiation one is exposed to, the higher the risk of developing cancer.

While the study looks at a large number of patients and shows a significant link between radiation exposure and cancer risk, the researchers were limited in that they only had the information available in the medical records. This means that while they controlled for variables like age and sex, they didn’t know everything about the patients: what they ate, how much exercise they did, what kind of environment they worked in. There may be a confounding variable that we don’t know about. As well, the researchers did not assess mortality as an end-point, and even write, “These patients most likely will die of cardiac-related causes”. So it’s important to remember that the scenario is not 1) patient has heart attack, 2) patient undergoes medical procedures, 3) patient gets all better heart-wise but develops cancer because of the procedures, 4) patient dies of cancer. It’s likely much, much more complicated than that.

That said, any medical procedure is all about risks and benefits. We need to weigh the risks of cumulative exposure to radiation (you’ll be glad to know that exposure to radiation from a single test does not substantially increase your risk of cancer) against the value of the information that the medical imaging procedure will provide. Not always an easy task. In Michael’s case, the physician was clear: she was running the test to appease his wife. Now what is that worth to you?

Reference: Cancer risk related to low-dose ionizing radiation from cardiac imaging in patients after acute myocardial infarction. (2011) Eisenberg MJ et al. Canadian Medical Association Journal. [Epub ahead of print].

The Super Bowl: Inspiring traumatic brain injury since 1966!

2011-02-06T22:05:00.000-08:00

It’s Super Bowl Sunday. Most of us spend the day eating nachos and wings, drinking beer, and acting rowdy in front of the television. For those of us who don’t have a television or snack foods in the vicinity (gasp!), we may chose to spend the day looking up scientific articles with a mention of football and writing blogs. I’m going to let you guess what I did.

High school can be a dangerous place: many will go through those few years carefully balancing social life, self-esteem, some sort of learning and the inevitable characterization of every single person into a specific group (you might be surprised to find out that I fit in the “jock” category). For the athletes, high school can also be dangerous for something very precious: their brains.

In a recent study, researchers looked at the incidence of concussions in high school sports over eleven years (1997 to 2008). They wanted to know whether certain sports had higher rates of concussions, and whether the incidence of concussions varied by gender, and over time. So they followed 25 high schools in a large public school district and recorded every instance of concussions for twelve sports: football, lacrosse, wrestling, soccer, basketball and baseball for boys, and field hockey, lacrosse, soccer, basketball, cheerleading and softball for girls.

The researchers reported a few interesting findings. They recorded nearly eleven million instances of a student playing a given sport, and out of those, identified 2651 instances of concussions. While boys accounted for just over half of the instances of students playing a sport, they accounted for three quarters of all concussions. Perhaps not surprisingly, football accounted for more than half of all instances of concussions. Baseball was the boy’s sport with the lowest incidence of concussions. For girls, soccer took the lead with the highest incidence of concussions, while cheerleading had the lowest incidence. Unfortunately for all my Canadian readers, the researchers left out our national sport, so I’m not sure how hockey would compare. But hey, we can talk about hockey when the Stanley Cup rolls around.

What surprised me the most in this study is that the overall rate of concussions increased significantly over time (a 4-fold increase between 1997 and 2008). Football showed the greatest increase in concussion rates over time, but it’s important to note that all twelve sports showed an increased concussion rate over time.

As for sex differences, the researchers found that for sports that are the same for girls and boys (like soccer and basketball), girls had a higher rate of concussions. However, in lacrosse, where the girl’s game has different rules, protective equipment and nature of play when compared with the boy’s game, girls had a lower concussion rate than boys.

There are several factors that could explain some of these results: an increase in concussion rates over time could be explained by a greater awareness of this medical phenomenon, and thus an increase in the reporting of concussions. Girls could be showing higher concussion rates for the sports they share with the boys because evidence shows that girls tend to be more willing to report injuries. However, even when all these factors are considered, the study highlights a need to prevent, detect and treat concussions across all sports, not just football. Concussions can be a serious brain injury, especially if complications develop, and repeated concussions are particularly dangerous, as they can lead to dementia.

In the heat of the Super Bowl, I don’t want to be a complete downer, though: being active during your teenage years can have numerous benefits, and can lead to habits that will last a lifetime and play an important role in preventing a whole load of diseases. So play away, but just make sure to protect that noggin’ (and parents: chose that extracurricular activity wisely)!

Reference: Trend in concussion incidence in high school sports: a prospective 11-year study. (2011) Lincoln AE and al. Am J Sports Med [Epub ahead of print].

A day on Alzheimer's disease

2011-01-31T10:19:00.001-08:00

On Friday I attended a series of seminars on Alzheimer's disease at the University of British Columbia's Brain Research Centre. I think the idea was to showcase Canadian research in the field of dementia to woo politicians (also in attendance) and ask them for more funding. We heard about all aspects of Alzheimer's disease, from its history to its treatment, and in this post I will fill you in on the latest developments.

Alzheimer's disease is the number one public health problem in the developed world, with approximately 35 million cases worldwide. In Canada it represents a very expensive problem, estimated to cost 50 million dollars a day. In the time it takes you to read this post, there will be two more people diagnosed with Alzheimer's in Canada. As there are currently no approved treatments that affect the disease itself, there is an urgent need to keep our heads down and power through (bonus points for whoever can identify this reference in the comments) to find a cure.

The first "official" patient with Alzheimer's disease was a 51-year old woman named Auguste Deter. She was examined by Alois Alzheimer in 1901. She suffered from impaired memory, aphasia (a language disorder) and disorientation. Alzheimer kept meticulous records: we have a very detailed description of Auguste's condition, and even a sample of her handwriting (see picture). Even though the condition was described in great detail, Alois Alzheimer did not know what had caused Auguste's disease. Today, as one of the researchers at the seminar pointed out, we still don't know what causes Alzheimer's disease, but on a much higher level.

We do know that one of the main culprits in Alzheimer's disease is amyloid beta (Abeta), a protein that everybody's brain makes. In the brain of an Alzheimer's patient, though, too much of this protein is being made, and it aggregates in toxic chunks called plaques. The researchers present at the seminar predicted that vaccines against these plaques will fail. However, there are several candidate drugs that could prevent or treat these plaques in clinical trials right now.

Interestingly, researchers are also studying naturally occurring compounds: one of the speakers talked about his research looking at whether natural extracts can block the formation of plaques in a "petri dish" model of Alzheimer's (brain cells grown in a dish). He finds that ginger, cinnamon, turmeric, cranberry, rhubarb, blueberry, pomegranate and blackberry all help prevent the aggregation of Abeta. However, he warns that at this point, it is not practical to focus on eating these foods because the concentrations used in the lab are just not possible to recreate in a diet.

Beyond the molecular and biological underpinnings of Alzheimer's disease, researchers are also addressing the inevitable changes the world will need to undergo to accommodate a growing prevalence of dementia. For example, one speaker pointed out that many public places such as airports and even hospitals are very difficult to navigate for cognitively healthy people: this represents a true disservice to people with Alzheimer's disease. Efforts are also being made to engage the public (as to avoid more bad news like this one), and to provide resources for caregivers (such as the fantastic First Link initiative).

Overall, I'm disappointed to report that I didn't learn of any magical intervention that will rid us of Alzheimer's disease, but it's comforting to know that there is a big research community out there who is taking this problem very seriously and who is tackling it from many different angles.

Not-so-subliminal messages

2011-01-24T22:02:00.000-08:00

For this week’s post, I had originally intended to kick-off the (Vancouver) cycling season with a post about helmets. So I reviewed the recent evidence to see if I could find an interesting paper. Unfortunately, I ran into a problem of the “boring” kind: the evidence out there is pretty much what you think it is: helmets are good, they prevent injuries. While that’s relevant, it doesn’t make for a great post, because, well, you already know this.

Luckily, I stumbled upon a related story that looks at helmet usage amongst… Fictional characters. The study, published in the journal Pediatrics, looks at safety practices depicted in movies over time. This may seem like a silly waste of time (or the project of your dreams, if you're a grad student), but we know that children tend to imitate what they see in movies (and that is why my eventual kids will never see the “Jackass” movies). Given that by age 18 the average child has spent two years in front of a screen, we might want to know a little more about the kinds of influences they may be getting from mass media.

The researchers started by identifying the 25 top-grossing G-rated (general audience) and PG-rated (parental guidance suggested) US movies for each year between 2003 and 2007. Of those 125 movies, they excluded movies that were animated, not set in present day, fantasy, documentary or not in English. That left them with 67 movies. The researchers then analyzed the safety practices in all the scenes that included characters with speaking roles either walking, driving or riding in a car, driving or riding in a boat, or riding a bike (for a grand total of 958 scenes).

The results show that in movies, just over half (56%) of motor-vehicle passengers wear seat belts, just over a third of pedestrians (35%) use crosswalks, three quarters of boaters (75%) wear personal flotation devices (or lifejackets), and a quarter (25%) of cyclists wear helmets.

Compared with similar studies carried out in the 1990’s and early 2000’s, there is a significant overall improvement in the depictions of safety practices. However, about half of the scenes still show unsafe practices. What’s more, movie characters rarely suffer the consequences of unsafe behavior. How many times did you see someone get up after falling off a cliff and think “Come on!”. The depictions of unsafe behavior combined with the absence of consequences for these behaviors may lead children to minimize dangers in real life, so parents, make sure you point it out when you see characters acting unsafe!

Now the study excluded quite a few movies for simplicity’s sake, and ended up with a fairly small sample, so it would be premature to generalize these results to all movies out there. I would be especially interested in finding out how animated movies fare, since they definitely cater to a younger crowd (Simba sure learned the consequences of *his* unsafe behavior). A later post, perhaps, if such a study exists!

Definitely not the crosswalk!

Reference: Injury-prevention practices as depicted in G- and PG-rated movies, 2003-2007. (2010) Tongren JE et al. Pediatrics 125(2):290-4.

Dogs have owners, cats have staff, and children have rashes

2011-01-16T15:38:00.000-08:00

The word "eczema", a skin inflammation that affects 15 to 30 percent of children and two to 10 percent of adults worldwide, is derived from an ancient Greek word that literally means "to boil out". I know firsthand why this word was chosen, as I suffer from contact dermatitis, a form of eczema that is caused by an allergic reaction (to nickel). The itch is not unlike that of bug bites, and this is by far the best depiction I've ever seen of what it feels like to be itchy:

(the ant hill is a nice touch)

As I'm sure you can imagine, having a child with this condition is a bucket load of fun. The ointments, the whining, the scratching, the scabs... (and, in my case, the sowing of little patches of fabric behind *every* jeans buttons... Thanks, mom!). So while eczema is not really a life-threatening condition, researchers are looking into it, because it's very closely tied to parental sanity.

We already know that eczema is not purely genetic: the environment you grow up in can influence your chances of developing the itchy rash. However, what we don't know is what components of the environment play an important role. A recent study attempts to add a piece to this puzzle by researching whether family pets can have an impact on the development of eczema.

Researchers followed over 600 children starting at one year of age. At the start of the study, the parents of each children were asked to fill a survey of their environment, and researchers took a dust sample from each house to test for allergens and such. Three years later, the researchers evaluated which child had developed eczema and which child hadn't, and analyzed what contributing factors might have played a role.

It turns out that owning a dog is not only good for your blood pressure: children who lived in a house with a dog had a significantly lower risk of developing eczema by four years of age. What about cats? The situation was a bit trickier for cats: living with a cat increased a child's risk of developing eczema, but only if the child tested positive on a cat allergen sensitivity test (the skin-prick kind).

So get rid of Mittens and adopt Fido? Not so fast. First, these findings don't hold true for all allergy-related conditions. For example, dogs are thought to contribute to asthma. Second, what this study really does is highlight how complicated these conditions are: several different types of environmental exposures may impact allergies in different ways, so it's very hard to draw clean, straightforward conclusions and guidelines.

That said, I'm still going to blame my eczema on growing up in a dogless home. I wish I would have known this tidbit of information way back when I was a kid: it might have helped me in my campaign to get a pet (admittedly, my heart was set on a horse).

A healthy start!

Reference: Opposing effects of cat and dog ownership and allergic sensitization on eczema in an atopic birth cohort (2010) Epstein TG et al. Journal of Pediatrics [Epub ahead of print].

New Year's resolutions through delayed gratification

2011-01-12T08:26:00.001-08:00

It's that time of the year. That I-will-eat-better-and-exercise-lots time. It's that time when we kick start New Year's resolutions with the best intentions, the best plans, the most motivation. Unfortunately, and I can tell you this from experience, some of us will fail. A recent article published in the journal Obesity sheds light on one important aspect in keeping some resolutions: delayed gratification.

Delayed gratification, as the name implies, refers to the ability to forgo an immediate reward (for example, delicious Cheesy Poofs) for a benefit that will come later (for example, rocking that little black dress). A lot of research shows that the better you are at delaying gratification, the better you do in life in general (you may have heard of the famous marshmallow study). To see if delayed gratification is linked to obesity, a team of researchers set out to test whether children who have a high body mass index (BMI) are less likely to delay gratification.

The researchers looked at data from an educational obesity intervention program. In this program, attended by obese or overweight children along with their siblings (the healthy weight control group), children earn a point if they complete their weekly goals. They then have two choices: either spend that point immediately on a small toy prize (like a pencil) or save the point to use later on a larger prize worth more than one point (like a basketball). The measure of points saved and points spent is thought to be a valid model of delayed gratification. So the researchers looked at the relationship between how many points were saved by a child and that same child's BMI. The results show that a higher BMI is associated with less points saved, meaning the children who were overweight or obese had a harder time delaying gratification.

The strong aspect of this study is that the rewards were not food-related. This allowed the researchers to study delayed gratification as a behavior trait in general, and not specifically as it relates to obesity. However, their sample was fairly small (59 children) and the duration of the study was fairly short (12 weeks). Therefore, it's difficult to say whether delayed gratification plays a role in weight loss.

Overall, the research is relevant in that it suggests that working on delayed gratification (it's possible to "train" to get better at it) may help in obesity interventions. And for all you out there with eat-less-exercise-more resolutions, all I can say is "eyes on the prize"...

Reference: Ability to delay gratification and BMI in preadolescence. (2010) Bruce, AS and al. Obesity [Epub ahead of print].

The year in review

2010-12-28T09:01:00.000-08:00

As the year draws to an end, it’s time to compile the exciting discoveries that marked 2010. Here is a snapshot of my top 5, in chronological order:

Study #5: Communicating with the minimally conscious

In a nutshell: An imaging technique, functional magnetic resonance imaging (fMRI), allowed researchers to communicate with patients in a vegetative state. Researchers asked yes/no questions, and the patients answered by thinking of playing tennis for yes or thinking of a house for no. The resulting brain signals from these thoughts could be imaged, interpreted and used for communication.
The good: This technique gives great hopes for friends and relatives of patients in minimally conscious states.
The bad: The study was heavily criticized: only one patient was tested, and the technique is far from perfect.
What’s next? We will no doubt hear more about this in the near future. The first step will be to replicate these findings with a greater number of patients.

Study #4: The synthetic cell

In a nutshell: Researchers made synthetic DNA and incorporated it into an empty bacterial cell, thereby creating a fully functioning cell with a man-made genome.
The good: This study represents a technical feat and opens new doors in the fields of molecular and cellular biology.
The bad: Like transgenic organisms before this, the synthetic cell re-opens the Pandora box of ethical questions.
What’s next? Human-engineered cells will probably play a role in gene therapy and in the quest to build tissue in a dish.

Study #3: Brain training doesn’t work

In a nutshell: A study of computerized brain training using over 11,000 participants showed that people improved at the tasks they practiced, but this improvement didn’t extend to general cognition.
The good: This study urges caution when buying into the brain training craze.
The bad: The results may be misleading: it’s not because the researchers didn’t see any improvement that there weren’t any. The brain training could have been inadequate or the researchers could have been measuring the wrong parameters.
What’s next? More controlled studies will be needed to determine the effectiveness of the games. Brain training is likely to become increasingly specialized: training for older adults, for children with autism, etc.

Study #2: Optogenetics

In a nutshell: Researchers were able to control brain cells using light, and rescued symptoms of Parkinson’s disease in mice.
The good: I said it before and I’ll say it again: optogenetics has the potential to revolutionize medicine.
The bad: The technique is quite complex and difficult and so far only possible in small mammals.
What’s next? Researchers are already testing in larger mammals and developing new ways to deliver light into the brain.

Study #1: The slut gene

In a nutshell: Researchers found a relationship between a specific version of a gene and promiscuous sexual behaviors.
The good: The study provides new insights into the link between genes and human behavior.
The bad: It’s not that simple.
What’s next? You can expect more studies of the “this gene does that” type. However, researchers are increasingly interested in how the environment can impact the expression of genes, and the story is bound to get even more complicated.

Looking forward to more gems in 2011!

Happy New Year!

Prozac for puppies

2010-12-20T10:43:00.000-08:00

Separation anxiety isn’t just for babies anymore: one in two dogs is thought to suffer from separation-related behaviors when their owners leave the house. These behaviors take many forms, from chewing your favorite pair of Jimmy Choo’s (Santa Baby… I want Jimmy Choo’s) to yapping uncontrollably until the neighbors call the police. Seeing as this may represent a serious problem in animal welfare, a team of researchers assessed the relationship between separation-related behaviors and the overall moods of dogs.

The researchers used 24 shelter dogs and started by measuring whether each dog suffered from separation anxiety. To do this, a researcher played with a dog for 20 minutes in a designated room. The next day, the dog was taken to the same room, played with for a few minutes, then left alone for five minutes. The dog’s behavior during those five minutes was analyzed and graded as a “separation anxiety score”.

A few days after the test, the researchers conducted another experiment to assess whether each dog had a pessimist or optimist outlook. In order to achieve this, they trained the dogs to learn that when in a given room, a food bowl placed at the very left of the room always had a treat in it, and a food bowl placed at the very right or the room never had a treat in it. Once the dogs learned this, the researchers placed a food bowl right in the middle of the room. Presumably, dogs that ran fast to see if this new bowl has a treat in it were anticipating that it had food in it and were considered to be “optimistic”, whereas dogs who either slowly made their way over or didn’t bother to check it out were considered to be “pessimistic”. It’s kind of a dog version of the glass half-full or half-empty paradigm.

The relevant finding of this article is that the researchers found that dogs who experienced separation anxiety were more likely to be of the “pessimistic” kind. Pessimism is thought to be related to negative moods, and knowing this may help in figuring out how to avoid chewed-on Jimmy Choo’s.

While I thought the study was quirky and interesting, I found it a bit of a stretch to label these dogs as optimistic or pessimistic using such a simple experiment. The researchers themselves owned up to this by saying that “the conscious experience of such a state [optimistic/pessimistic] cannot be known for sure”. When I read the article, I thought maybe the dogs who went for the food bowl in the middle were just more curious than others, and I’m not sure how curiosity relates to optimism (for example, I consider myself to be quite curious, but not necessarily optimistic: I browse the Jimmy Choo website to see what the new styles are, but I don’t envision ever owning a pair). As well, I thought the measure for separation anxiety was a bit weak. While it’s a known experiment, it’s not immediately obvious to me that the behavior of these pound dogs relates to the behaviors you would observe in dogs with a stable home.

Still, it’s a good reminder to keep our pets as happy as possible, especially during the holidays when routines are broken and moods are uneven.

Reference: Dogs showing separation-related behaviour exhibit a “pessimistic” cognitive bias (2010) Mendl M. et al. Current Biology, 20(19):R839-40.

Food for thought on thoughts for food

2010-12-11T15:45:00.000-08:00

Christmas party season is officially upon us. The next few weeks are pretty much going to be a long string of turkeys, stuffing, various things made with cranberries and cutesy Christmas cookies à la Martha Stewart. Faced with this, many of us who are concerned with staying trim and not slipping into food comas on a daily basis may be feeling a little apprehensive. Well, fear not! New research published in the journal Science suggests you can eat less by simply… Thinking more about food!

The study looks at the relationship between the concepts of mental imagery (imagining doing things) and habituation (getting used to things). Through mental imagery, imagining things can affect your body and your emotions just as much as the real thing: just thinking about a spider crawling on your neck can lead to the same feeling of tingling and fear as if it was actually happening. The second concept, habituation, refers to the decrease in your body and your mind’s response to a stimulus. For example, your tenth bite of stuffing is not nearly as satisfying as your first. Given these two principles, the researchers asked if you could habituate to a food just by imagining eating it.

The participants in the study were divided into two groups and each group was asked to imagine doing a task. The first group was asked to picture eating 30 M&M’s, one at a time. The second group was asked to picture putting 30 quarters into a laundry machine, one at a time. After this mental imagery task, the participants were each put in front of a bowl of M&M’s and told to eat as much as they wanted as a preparation for a “taste test” later on (obviously, the taste test is fake, it’s just an excuse to get the participants to eat). The researchers then weighed the leftover M&M’s and measured how much each participant had eaten. They found that those who pictured eating M&M’s ate significantly less candies than those who pictured feeding a laundry machine!

The researchers then compared participants who imagined eating only three M&M’s with participants who imagined eating 30. They found that participants who imagined eating more M&M’s ended up actually eating fewer of the real ones. This means that habituation (doing something repeatedly) is key to observe an effect of mental imagery.

So whether your drug of choice is M&M’s, stuffing or cheese balls, you may be able to minimize the holiday damage by doing a little mental exercise. Now if only I could just picture purchasing and wrapping a bunch of presents…
Reference: Thought for food: imagined consumption reduces actual consumption. (2010) Morewedge CL et al. Science 330:1530-1533.

"The slut gene" or "Why reporters should read science articles to the very end"

2010-12-06T19:43:00.000-08:00

This week, I’m going to start with a quality science headline:

“Like to sleep around? Blame your genes”

Really?

The story behind this headline comes from a study of human sexual behaviour. Different people have different sex drives and different sexual behaviours, and we don’t know why, so American researchers set out to solve the mystery.

The researchers enlisted 181 male and female young adults and asked each one for a detailed history of sexual behaviour and relationships (awkward!) and a sample of spit. The spit was used to analyze the participant’s DNA and to look for a specific version of a gene called DRD4 (subsequently dubbed “the slut gene” by the media). The results of this study show that participants who have the specific version of this gene are more promiscuous (researchers actually used the words “one-night stand”) and report more instances of sexual infidelity. Well, there you have it. Free will is overridden by our genes.

How does this work? Your brain’s reward system is called the dopamine system (DRD4 stands for Dopamine Receptor D4), and among other things, it takes care of your motivation for sensation-seeking behaviours like having sex. This happens through the flow of dopamine molecules, which act as a message transmitter in your brain. For a brain cell to receive a message conveyed through dopamine, it needs a dopamine receptor like the D4. The gene that encodes this receptor (DRD4) comes in two forms: one that binds dopamine tightly and one that binds dopamine not as tightly. If you have the version of the gene that encodes the receptor which doesn’t bind dopamine tightly, you need more dopamine to achieve the same end-result in your brain (the feeling of reward), hence the string of one-night stands.

So are cheating and one-night stands excused because our genes made us do it? At the risk of becoming unpopular, I have to say the answer to that is no. The relationship between the special version of the DRD4 gene and promiscuity is not deterministic: having the gene doesn’t automatically lead to one-night stands. Many people in the study had the gene and didn’t cheat. The gene-sexual behaviour relationship is what we call probabilistic: having the gene only increases the probability that you would exhibit a given behaviour. What’s more, our environment can change how different genes are expressed, and it is possible to modify our behaviour. No excuses!

There are also two caveats to note in this study. The first is that not all the results were statistically significant. For example, 50% of people with the special version of the gene reported being unfaithful, compared with 22% for the participants with the normal version. While this may seem like a big difference, it was not significant because they are not looking at a big enough sample of people to ensure this couldn’t happen just by chance. The second problem is that the relationship between the gene and sexual behaviour could be due to a confounder, which is a variable that has not been studied that could explain the results. For example, if having the special gene makes you more honest about your sexual history, then these results would be due to a truth-telling tendency, not a sleeping around tendency.

My favorite part of the entire research article is at the very end when the researchers write:

“…we emphasize that it would be prudent to avoid premature and facile characterizations of the DRD4 VNTR polymorphism as “the promiscuity gene” or “the cheating gene.”

It’s funny, but it’s also a bit sad. They saw the “slut gene” stories coming from a mile away.

Reference: Associations between dopamine D4 receptor gene variation with both infidelity and sexual promiscuity. (2010) Garcia JR et al. PLoS ONE 5(11):e1412.

Run Run Rudolf

2010-11-28T11:43:00.000-08:00

I consider myself a fairly healthy person and I rarely get sick. However, there is one activity that never fails to put me under the weather: flying. No matter how hard I try, no matter how much I wash my hands and try not to touch my face, any flight inevitably leads to some kind of illness. It usually ends up being a common cold, but I remember a nasty Christmas holiday spent in bed with a stomach flu. In any case, my recent flight home from San Diego was no exception, and here I am, still battling a stupid cold. So naturally, I looked for an article on how to prevent colds.

In a recent study, researchers followed over a thousand adults (18-85 years old) for 12 weeks during the fall and winter seasons. Over this time, the participants had to report two measures: any symptoms of upper respiratory tract infection (such as a cold), and how much they exercised.

While running in the cold winter air might sound like a counterproductive measure to prevent colds, the researchers found that participants who reported being physically active (aerobic exercise) five days a week or more experienced significantly less cold and flu symptoms (a 43% reduction in number of days with an illness). This relationship held true event when several factors were controlled for, such as dietary habits (eating lots of fruits and veggies) and stress levels.

Why might exercise prevent colds? While we don't have a clear cut answer to this question, animal studies suggest a few leads. When you exercise, you increase the circulation of cells that are important for immunity and that are involved in fighting off the bad guys. More specifically, exercise has been shown to boost macrophages (cells that eat up invaders) in your lungs. In addition, exercise can lower the levels of immunity-compromising stress hormones.

Is there anything exercise can't do? Now I need researchers to study how one can be motivated to exercise when they are sitting in a comfy chair by the fire with a mug of chai tea and a pile of work to do and it's below zero outside. Tell me something I don't know, right?

Reference: Upper respiratory tract infection is reduced in physically fit and active adults. (2010) Nieman DC et al. [Epud ahead of print].

Live from San Diego (airport)

2010-11-18T15:17:00.000-08:00

I didn't have a chance to write a decent post this week because I was away in San Diego for the most glorious scientific event I know: the Annual Meeting of the Society for Neuroscience (SfN). I will resume regular programming shortly, but in the meantime, here are some highlights from the conference, in no particular order.

- The conference attracts over 34,000 neuroscientists and people wanting to sell stuff to neuroscientists. There were about 16,000 poster presentations. The event lasts 5 days and at any given time there can be a dozen talks going on. It's sometimes very hard to chose what to see. The Geek Meter registers very high.

- The opening session was a presentation by Glenn Close. She talked about her advocacy group for mental illness, Bring Change 2 Mind. She did a great job and I was moved. On a side note, she does NOT look 63.

- One of the highlights of SfN for many graduate students is the incredible amount of swag one can collect simply by feigning interest in a variety of products. The floor space for vendors is the size of a small city. This year I didn't have much time to go through it all, but I still managed to come home with two T-shirts, a mini laptop mouse, a notebook with a depiction of the Wnt pathway on the cover, and several pens.

- I would say that the two major themes this year were sensory (vision, olfaction, etc.) and Alzheimer's disease, even though there is definitely something there for everyone. There was also a big focus on optogenetics. My personal opinion is that optogenetics will revolutionize the field of medicine.

- Celebrity scientists are called scilebrities and can be spotted everywhere. The conference also organizes a number of socials for every field of neuroscience where you can narrow down your schmoozing to the scilebrities that work in your area of interest. You can usually judge how well a field is doing by the quality of the catering. It's a bit of a running gag.

- San Diego can pretty much be summarized in three words: fish tacos and tequila.

- As surprising as it may sound, neuroscientists know how to party. You're just going to have to trust me on this one.

I already can't wait for next year. See you soon for a post on how to keep colds at bay.

Math made easy

2010-11-07T09:18:00.000-08:00

I have fond memories of high school math classes. Numbers came easy for me, and I derived a lot of satisfaction from solving problems (and even more so when I solved them fast!). I was lucky to have excellent teachers, especially in grade 11 and in CEGEP, who turned math into something of a game, a code I needed to crack. However, I’m well aware that math class was not a party for everyone. About 15 to 20% of the population struggle with some form of difficulty in learning or understanding mathematics. Obviously, this can be an obstacle to success in school, and in employment. To address this issue, a team of researchers from the UK set out to test whether brain stimulation could improve someone’s math abilities.

The researchers used a technique called transcranial direct current stimulation (TDCS, similar to the method used in this post on morality). TDCS consists of applying a weak current to a brain region (in this case, the parietal lobe, a region important for learning and understanding of math) over a given time period (in this case, 20 minutes). The technique is non-invasive, meaning they don’t open up your scalp to get at your brain: electrodes are simply place on your head (volunteers are much easier to recruit when the electrodes are on the outside, not the inside). Depending on the type of current that the researchers apply, TDCS can increase or reduce the excitation of the brain cells in the targeted region.

To test the impact of this kind of brain stimulation on math capabilities, the researchers delivered the stimulation while the participants (15 healthy adults) were learning the relative values between nine arbitrary symbols (for example, square is bigger than triangle). The learning session lasted 90 to 120 minutes. The participants received either the brain stimulation during the first 20 minutes of the session (the experimental group), or only during the first 30 seconds of the session (the control group, as 30 seconds of the stimulation is not long enough to see any effects, but still gives you the “tingles” associated with the protocol). After this learning phase, the researchers assessed the participants’ newly created sense of numerical value for the symbols with two different math tasks using the symbols. This whole process was then repeated over six days.

The results show that brain stimulation leads to better and more consistent performance on both math tasks. Mathematical ineptitude is cured! To make the matters even more interesting, the researchers called the participants back six months later and re-tested them (no brain stimulation this time). And six months later, the brain stimulation group still performed better at the math tasks involving the fake digits.

While this may sound great, don’t start tazing your brain just yet. It’s worthwhile to note that on the last day of the initial six-day study, the researchers had the participants perform the same two math tasks, but with normal numbers. In this case, there were no difference between the experimental group and the control group. This means that the brain stimulation paradigm only worked for the specific task that was learned during the stimulation, and didn’t extend to math in general. Nonetheless, the researchers suggest that brain stimulation may be a tool for intervention for those who have “developmental and acquired disorders in numerical cognition” (read: for people who are bad at math).

Must we all be good at math? There’s a French saying that goes: "ça prend toute sorte de monde pour faire un monde" (roughly translates into: "it takes all sorts of people to make a world"). What’s your take on this? Do you think this is a great advance? Do you have any concerns? Let’s hear it!

Reference: Modulating neuronal activity produces specific and long-lasting changes in numerical competence. (2010) Cohen Kadosh R et al. Current Biology 20:1-5.

Light at night, what a fright!

2010-10-31T17:12:00.000-07:00

When I picked my paper for this week’s blog, a very recent article published in PNAS, I didn’t factor in that I would write it on Halloween. Now I realize it’s going to seem like some cruel joke: on the one night where people stay up late walking the streets with flashlights and eat candies, I’m writing about the link between light at night and obesity. Wow. If I had tried to pick something more fitting, I couldn’t have done a better job.

We all know obesity is on the rise and there are several reasons to explain the epidemic: increased intake of calories (Double Down sandwich, anyone?), dietary choices (cheezy poofs instead of apples, anyone?) and lack of exercise (reading blogs, anyone?). However, the rise of obesity rates also coincides with an increase in light at night – the artificial lighting that allows us to write blogs late at night and catch up on all other activities we didn’t have time to do during the daytime. The problem is that light is closely tied to our circadian rhythm (the built-in clock that controls our biological processes and our behaviour). When our circadian rhythm is disrupted (an extreme example of this is shift workers), so is our metabolism. Based on this logic, an international team of researchers set out to test whether light at night plays a role in the weight of mice.

The researchers divided their mice into three groups. The control group was housed in the standard light/dark cycle. Another group of mice was housed in a light/dim light cycle (let’s call them the “dim” group). Finally, a third group of mice was housed in a continuously lit room (let’s call them the “bright” group). The mice were housed in these conditions for eight weeks, and during this time, the researchers monitored a number of parameters including body mass, food intake, activity levels, and glucose tolerance (how quickly sugar is cleared from the blood).

The researchers found that all the mice that experienced light at night (both the dim group and the bright group) got significantly fatter than the control mice. What’s more, the dim group and the bright group also exhibited impaired glucose tolerance (this can mean the mice are in a prediabetic-like state). Did the light at night groups of mice eat more (who doesn’t get the munchies when watching a late-night movie)? No. Did they exercise less (who goes for a run at midnight)? Also no. So what happened?

As it turns out, while the two light at night groups of mice ate just as much as the control mice, they ate at different times. Mice are nocturnal animals, and so normally they do most of their eating at night. The mice in the dim group, however, ended up eating over half of their food during the “light” phase. When the mice in the dim group were forced to eat their normal food intake only during the normal (dark) time, they didn’t gain weight. How crazy is that? These results suggest that light at night disrupts the timing of food intake, and this throws the metabolism out of whack.

Anyone who has looked up weight loss tips knows that it’s a good habit to forgo eating past a certain time of night (usually 7 or 8pm) if you want to lose weight. The reason usually given to explain this is that night time food is most often unhealthy and calorie-laden snacks: munchies during a movie, or ice cream after a distressing phone call from the ex-boyfriend. This study suggests there might be something more to this weight loss strategy: it may be all about listening to our biological clock.

Reference: Light at night increases body mass by shifting the time of food intake. (2010) Fonken LK et al. PNAS 107(43):18664-9.

Parlez-vous français?

2010-10-24T12:26:00.000-07:00

Last week, I wrote about how walking can protect your brain against cognitive decline. Sounds easy, right? The truth is, there are several factors that impact brain health, and exercise is just one of them. This week, I'm going way back in time to 2007 to look at a different way to keep your brain healthy: apprendre une autre langue.

Canadian researchers were interested in the relationship between bilingualism and Alzheimer's disease. Their hypothesis was based on the concept of cognitive reserve, a term that represents the attributes of your brain that make it resistant to damage. For example, you might have heard that keeping your mind challenged by doing crossword puzzles can delay cognitive decline. This is one way to increase your cognitive reserve. Presumably, complex mental activity like crossword puzzles but also like speaking more than one language can lead to a lesser chance of developing dementia and, in the event where you do get dementia, a slower rate of decline.

The researchers sifted through the records of over 200 patients from a memory clinic. About half of their sample spoke one language and half spoke two languages. The researchers assessed the relationship between the number of languages each patient spoke and whether each patient had Alzheimer's disease. For the patients who did have Alzheimer's disease, the researchers noted how old the person was when the disease started. Of course, the researchers controlled their results for all the obvious potential biases, such as cultural differences, immigration, formal education and employment status.

The results of this analysis show that the bilingual patients developed Alzheimer's disease much later (4.1 years on average) than the monolingual patients. Since developing an age-associated disease like Alzheimer's later means you have a greater chance of dying before you get the disease, delaying the onset by 4 years means a reduction in the total cases of Alzheimer's disease. Currently, no drugs have an effect that's comparable to bilingualism.

Since no study is ever perfect, let me point out two small caveats before you fish out your old high school Spanish books. First, there is one thing the researchers could not control for, and that is whether cultural differences could lead to delays in seeking medical help for a condition. This could muck up the results because if some patients delayed their first medical visit, then the age at which they received the diagnosis for Alzheimer's disease could be skewed. Second, the protective effect of speaking two languages cannot be generalized to people who have some knowledge of another language but are not fully bilingual. In this study, the patients who were bilingual were true bilinguals, fluent in both languages and having used both languages regularly for most of their lives.

Still, it's a good reminder that a busy mind is a healthy mind. And it's nice to have evidence to justify the occasional weekend in Paris.

Reference: Bilingualism as a protection against the onset of symptoms of dementia. (2007) Bialystok E et al. Neuropsychologia 45:459-464.

A walk in the park

2010-10-17T11:24:00.000-07:00

It's no secret that exercising is key to maintaining a healthy brain as we get older. We hear it all the time. So why isn't everybody exercising? After all, it represents a form of personal health insurance, and it's way cheaper than Sun Life. The truth is, even though many people are aware that exercising is good for them, they are not compelled to change their lifestyle because it's not exactly clear what kind of exercise is best, how long you need to do it, and what exactly it does to help your brain. Well, I'm going to tell you.

In a recent study published in the journal Neurology, American researchers looked at 299 adults with a mean age of 78 years old. They evaluated how active each person was by measuring how many blocks they walked over the period of one week (this ranged between zero and 300!). The researchers then waited nine years (!), and then took brain images for all the participants and evaluated their level of cognitive impairment.

Not surprisingly, the more someone walked, the greater their brain volume after nine years. Greater amounts of physical activity predicted bigger volumes for several brain regions associated with thinking and memory, such as the hippocampus and the frontal cortex. What's more, the bigger brains associated with physical activity cut the risk for cognitive impairment in half.

The magic number in this study is 72. Walking a minimum of 72 blocks per week was necessary to see the bigger brain effect. Walking more than 72 blocks didn't lead to an even bigger brain. While I wouldn't necessarily shoot for walking only and exactly 72 blocks per week (as physical activity is also associated with a decreased risk for some illnesses), it's nice to have a baseline number, and to know that an exercise as simple as walking can make a difference.

So what are you waiting for?

Reference: Physical activity predicts gray matter volume in late adulthood: The Cardiovascular Health Study. Erickson KI et al. Neurology (2010) [Epub ahead of print].

Mind control for a good cause

2010-10-10T12:24:00.000-07:00

Almost one year ago, I wrote a post on optogenetics, a new field that combines optical techniques (playing with light) and genetic techniques (playing with DNA) to study the brain. Optogenetics is an extremely powerful technique that can be used to control the activity of brain cells. So far, it’s been mostly researched as an experimental tool, but a recent study published in the journal Nature hints at the possibility of using this technique to learn how to treat the most common neurodegenerative disorder after Alzheimer’s disease: Parkinson’s.

Parkinson’s disease, a movement disorder, affects a part of the brain called the basal ganglia, which is critical for planning movement and selecting appropriate actions. The basal ganglia can be roughly divided into two pathways (or networks of brain cells): a “direct” pathway that facilitates (or enables) movement and an “indirect” pathway that inhibits (or prevents) movement. When someone has Parkinson’s disease, it is thought that their direct pathway is not active enough and that their indirect pathway is too active, and this leads to the muscle rigidity, tremors and slowing of physical movement.

In this study, the researchers used a virus to deliver a special channel to the brain cells of either the direct or the indirect pathway of the basal ganglia in mice. This may sound confusing at first, but it’s a really clever experiment. Here is how it works: when certain types of viruses infect cells, they incorporate their DNA into the DNA of the “host” cell, such that the host starts making virus DNA, and ultimately turns into a virus-making factory. The researchers essentially hijacked this process: they engineered a virus that contained the DNA for the special channel, and therefore, once the brain cells got infected, they started making the special channel. What’s so special about this channel? It is activated by light (hence the “opto” in “optogenetics”). When blue light hits this channel, it activates the brain cells.

To tease out the differences between the direct and the indirect pathways, the researchers divided their mice into three groups: a control group (no brain cells infected with the virus), a “direct” group (the virus targets the direct pathway, such that only cells in the direct pathway have the special channel), and an “indirect” group (the virus targets the indirect pathway, such that only cells in the indirect pathway have the special channel). By exploiting this technique, the researchers were able to activate either the direct pathway or the indirect pathway of the basal ganglia simply by shining blue light onto the brain of the mice.

(I realize this is all very complicated, but if you’re still with me at this point, congratulations on completing Optogenetics 101!)

And now for the results… *drumroll* As expected, when the direct pathway was activated, the mice moved more (they ran around more, stood up on their hind legs more, etc.). And when the indirect pathway was activated, the mice froze, and overall moved less. How’s this for mind control?

At this point, it’s easy to get carried away and imagine a plethora of crazy scenarios should this technology fall in the hands of the bad guys (“And now, you will dance for me! Gnahahaha!”) However, the researchers had good intentions. They went on to activate the direct pathway in a mouse model of Parkinson’s disease, and found that this procedure rescued the locomotion deficits of the mice. And that is a wicked finding.

Unfortunately, treating humans with optogenetics is not going to happen anytime soon. There are significant hurdles to overcome before we can even think about it: working with viruses in the brain, delivering the channels only where we want them, assessing unwanted effects, and so on. That said, this study elegantly confirms that somehow activating the basal ganglia’s direct pathway could be an important therapeutic target to treat Parkinson’s disease.

Reference: Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia circuitry. Kravitz AV et al. Nature, 466(7306):622-6 (2010).

People on Prozac, fish on Viagra

2010-10-03T16:50:00.000-07:00

With all the discussions around climate change, it's no surprise that researchers are increasingly studying the impact of human activity on the environment. This type of research can take many forms ranging from the effects of city lights on the migratory paths of birds to the composition of soil in traditional and organic farming. Beyond research, climate change and other environmental discussions have also changed how we (or at least some of us) act at home. We try to remember to shut the lights. We take shorter showers. We recycle. But there's one sneaky way in which most of us impact the environment, sometimes on a daily basis, without ever thinking about it: when we swallow pills.

Most pharmaceutical drugs, from regular pain killers to chemotherapy drugs, are not fully processed by the body. This means that we end up excreting a proportion of the drugs we swallow, or by-products of those drugs. This leftover pharmaceutical trash ends up in sewage, and eventually makes its way into our aquatic systems.

A recent study by Canadian researchers looked at how low and high concentrations of Prozac, the popular antidepressant, affects the reproductive systems of the goldfish. The news are not good. The researchers found that even low concentrations of Prozac, similar to what could exist in the environment, significantly decreased the volume of sperm the fish produced when they were sexually stimulated. At the rate we're going, we're going to need to feed our fish Viagra to compensate for their antidepressant load.

I wrote a story on this study for The Mark, a Canadian online forum of news, commentaries and debate. You can read the full article here.

Your thoughts on Body Worlds

2010-09-26T13:28:00.000-07:00

The traveling exhibit Body Worlds & the Brain has arrived in Vancouver. For those of you who are not familiar with Body Worlds, it is an exhibit that features real human bodies and human body parts that have been preserved through a process called plastination. Through my new line of work at the National Core for Neuroethics, I've become involved with Science World, the organization hosting the exhibit in Vancouver. And because of this involvement, I have now seen the exhibit for the first time. Here are my thoughts about Body Worlds, and I would be most interested to hear yours, whether you've seen it or not.

Before seeing the exhibit, I wasn't very warm at the idea. I had read a lot of ethics articles questioning whether the exhibit preserved human dignity, and whether human bodies could be considered art. The thought of those preserved bodies, with their eyes staring at me, definitely gave me the creeps. I was concerned with issues like consent, and I was uneasy with the fact that the whole thing felt like a freak show, a very profitable freak show.

I was lucky to see the exhibit on a special opening night for volunteers. On the plus side, it wasn't very busy, and I got to scrutinize everything. On the down side, this meant I had to listen to endless speeches before entering the exhibit.

It's during one of these speeches that my gut feeling about Body Worlds completely turned around (keep in mind, by then I still haven't seen any part of the actual exhibit). One of the speakers discussed how powerful it is to witness the complexity and fragility of the human body, and how this can lead to profound changes in how we view ourselves, and how we take care of ourselves. The speaker was very convincing. Seeing as I'm concerned with caring for my body and tremendously interested in science communication, I started thinking that perhaps I was wrong, and perhaps the "good" of the exhibit (teaching people about the fragility of their bodies) far outweighed the "bad" (ethical questions about dignity and such).

Then I finally got to enter the exhibit and decide for myself, and a really funny thing happened: nothing. I didn't feel any strong negative emotions, didn't think it was gross, inappropriate, or disturbing. But I also didn't feel any strong positive emotions either: didn't think it was cool, beautiful, or awe-inspiring. I mostly didn't care, and frankly I was quite bored by the end of it all.

I'm not quite sure what to make of this as I was very much expecting to feel something. Part of the reason for my lack of interest could have been that the shock factor was lost on me. After several years of dissecting rodents, I've seen my fair share of guts and brains, albeit on a smaller scale. Perhaps I had over-thought the whole thing too much prior to seeing it. I'm not sure.

I would love to read your thoughts about this. Have you heard of Body Worlds? Were you motivated to go see it? What was your gut instinct if you did see it? What did you learn? If you chose not to see it, why? Share in the comments!

Quality science headlines

2010-09-22T18:02:00.000-07:00

Spotted this week:

"Asian 'unicorn' found in Laos"

What immediately strikes me from the accompanying picture is the fact that the creature has not one, but two horns. I guess that rules out the whole "unicorn" thing.

Brains and birthdays

2010-09-19T17:09:00.000-07:00

We hear a whole lot about new brain imaging techniques lately. It seems like imaging studies are constantly revealing new pieces of information about the brain: what part of the brain is responsible for our morality, what happens when you fall in love, and so on. One of the main techniques used in these studies is called functional magnetic resonance imaging (fMRI). Unlike a regular MRI, which takes a static image, fMRI can give us images of a dynamic process: the flow of oxygenated blood in the brain. Presumably, when one region of your brain is activated, the brain cells require more oxygen, so more oxygenated blood flows to that region, and this can be seen and measured using fMRI.

While it may be very interesting to find out what happens to your brain when you fall in love, we have yet to see real clinical benefits from these fancy new brain scans. Brain disorders and diseases, such as depression and Alzheimer’s disease, still cannot be diagnosed using fMRI. One of the reasons for this limitation is that an fMRI scan for a single person really doesn’t tell us much: we can only gain insights from this technique if we look at groups of people, and compare averages. To this day, this problem has really limited the potential of fMRI for diagnosing brain diseases. However, a recent publication in the journal Science suggests that fMRI may soon be clinically relevant.

The researchers were interested in finding an application where a single brain scan could provide information about the individual. They chose to assess the maturity of the brain, and used chronological age as a reference measure. Instead of using regular fMRI, the researchers used an even fancier version, fcMRI (fc stands for “functional connectivity”). This type of imaging measures the spontaneous activity between brain regions. How strongly different brain regions interact with each other is thought to be shaped by all the experiences one accumulates over time, hence the potential to determine maturity from these kinds of measures.

Participants aged seven to 30 years old were asked to undergo a five-minute brain scan. What followed was an extremely complex series of models and algorithms developed by the researchers to establish a “maturation curve”, from which they could then predict the maturity of a given brain based on where its scan fits along the curve.

Ultimately, it was established that yes, a single scan can provide information about the person’s brain: it can predict its maturity level. But couldn’t we already determine brain age just by looking at its shape? For the most part, yes. The reason this article is relevant is because quite a few brain diseases and disorders don’t have a signature shape (unlike tumors, for example, which can sometimes be spotted on a static image). Therefore, having a tool that allows us to assess brain function without having to compare large groups could become very valuable in the diagnosis of some brain disorders (provided we first determine the functional signature of these disorders).

As an interesting side note, the researchers' results suggest that on average, functional brain maturity levels out at about age 22. This obviously represents a physiological maturity level, not a cognitive maturity level, thank goodness. When I was 22, I used to think I knew everything. How I've "matured" since then!

Reference: Prediction of individual brain maturity using fMRI. Dosenbach N.U.F. et al. Science 329:1358-61 (2010).

A pink truck is still a truck

2010-09-08T21:47:00.000-07:00

When you walk into any baby store, it quickly becomes obvious that boys like blue trucks and girls like pink dolls. You might find a yellow pajama with a puppy on it, but that one is probably intended for the pregnant mom who doesn’t want to find out the sex of her baby but wants to buy a pajama. Many researchers have speculated on why boys and girls like different colors and different toys. There are three main theories out there. The first one, the “social learning” theory, suggests that children like certain toys and colors because they are socialized to like them: they like the toys their parents buy for them. The second theory, the “cognitive theory”, suggests that a child knows what gender he or she is, and is aware of the stereotypes, so he or she chooses accordingly. Finally, the “hormonal theory” suggests that sex differences in the prenatal hormone environment changes how the brain organizes itself and leads to female- or male-typed behaviours. For example, high levels of androgen (the male hormone) lead to brain masculinization and the choosing of trucks over dolls. While this may sound crazy, experiments have shown that female fetuses exposed to abnormally high androgen concentrations spend more time playing with masculine toys compared to regular girls. To make things even more complicated, studies have shown that some kinds of monkeys also show sex-specific toy preferences (and Daddy Monkey doesn’t shop at Wal-Mart, so there goes the “social learning” theory). So, is it already in your brain when you’re born, or do you learn to love blue trucks or pink dolls?

Researchers set out to shed some light on this question by studying 120 boys and girls aged 12 to 24 months. The task was very simple: the child was shown two images simultaneously (for example, a red car and a red doll, or a blue car and a pink car), and a camera recorded how long the child looked at each image, which is a measure of interest.

The researchers found that boys preferred cars and girls preferred dolls. No big surprise there. Unfortunately, because children 12 months old or older have already been provided with sex-typed toys, their looking preference may reflect the types of toys they have at home and the researchers could not draw any conclusions on whether this behavior was learned or innate.

The interesting finding lies in the colors: as it turns out, the children cared very little about the color of the images. Boys preferred the cars, regardless of whether they were pink or blue, and conversely, girls preferred the dolls, regardless of their color. In fact, the researchers found that as a whole, everybody liked red the most. This finding indicates that the stereotypical color preferences seen in older children are most likely learned behaviours.

As I’ve mentioned before, my favorite kind of research article is the one that leaves me with more questions than I started with, and this is one of them. Why was pink adopted as the “girl” color if girls aren’t naturally drawn to it? At what stage does the shift occur from not caring about colors to caring about them? Is this shift really purely socially driven? In any case, the next pajama I buy for a child will be red.

Reference: Infant’s preferences for toys, colors and shapes: sex differences and similarities. Jadva, V. et al. Arch Sex Behav [Epub ahead of print] (2010).

Dating advice from your friendly neighborhood finch

2010-08-19T08:28:00.000-07:00

In the animal kingdom, it's well established that by interacting with some individuals and avoiding others, you can influence your experience with natural selection (read: your chance of mating with a hot stud/chick). I think this paradigm is especially obvious in the high school setting: hanging out with the footballers and the cheerleaders increases your odds of mating (or at least, attempting to mate), while hanging out with the geek squad (ah, the good old days) definitely decreases your chance of mating (Glee, anyone?).

A while back, I wrote about dating lessons we can learn from monkeys. Today, I'll share with you the results of a recent study that highlights a dating lesson we can learn... from birds. American researchers set out to analyze the social networks of a species of wild finches to study the relationship between how pretty they are (ornament elaboration), how social they are (social lability), and how successful they are at mating. So they captured and banded a whole bunch of finches, and tracked them year-round.

The researchers found that less elaborate males (the "ugly" ones) shifted social groups more often than the prettier males. When it came to finding a mate, this party-hopping behavior somewhat compensated for their ugliness: the highly social birds were more successful at finding a mate when compared with equally ugly but less social birds.

There's an important lesson here: to increase your chance of mating, it might be a good idea to vary who you hang out with. I'm sure Dear Abby would approve.

Reference: Structure of social networks in a passerine bird: consequences for sexual selection and the evolution of mating strategies. (2010) Oh and Badyaev, Am Nat 176(3):E80-9.

To supplement or not to supplement

2010-08-08T18:20:00.000-07:00

Health information can sometimes be a real puzzle*. For example, your doctor may recommend that you take a calcium supplement, since calcium is important for strong bones. Then, the next day, you may read in the news that calcium supplements will give you a heart attack, which is exactly what happened to my mom last week. What should you do? Like most medical interventions, it’s all about risks and benefits. While a new study (you may have already heard of) highlights a risk of calcium supplements, don’t throw away the bottle just yet.

The researchers carried out a meta-analysis: a study of studies. Essentially, they searched for previous studies of calcium supplementation (compared with a placebo) and compiled them together to try to tease out effects that each single study may not have detected. Overall, the researchers ended up analyzing 11 studies between 1990 and 2007, for a total of 12,000 participants. In all the studies, 143 people who were taking calcium supplements had a myocardial infarction (a heart attack), compared with 111 people who were taking the placebo. This represents an increase in the risk of myocardial infarction of 31% for those taking calcium supplements. Interestingly, calcium supplements were only associated with an increased risk of myocardial infarction in people who already had a big calcium intake through their diet (more than 805 mg/day).

This study will no doubt shake things up in the fields of cardiovascular health and osteoporosis prevention. However, there is one important caveat with this analysis: the researchers did not look at studies where the supplement was a combination of calcium and vitamin D. Therefore, one cannot assume that calcium/vitamin D supplements would lead to the same risks. In fact, another recent study in women reported that calcium and vitamin D administered together had no effect on the risk of heart disease. It’s also important to remember that when weighing risks and benefits, calcium (and vitamin D) does a lot more than just strengthen your bones: it has also been shown to play a role in the prevention of certain cancers.

One thing is for sure: dietary calcium intake is safe. So go ahead and enjoy the moo juice.
__________________________
*You’ll be pleased to hear that I am dedicating my postdoctoral training to solving the puzzle.

Reference: Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. (2010) Bolland et al. British Medical Journal [Epub ahead of print].

Relevant science for a summer party

2010-08-02T20:06:00.000-07:00

I've been busy. I would like to say that I've been enjoying the wonderful Vancouver summer, but in academia, summer rhymes with grant writing. This means that I spend most of my days writing up long-winded research proposals that describe the exciting science I'd carry out if only (insert name of funding agency) would give me the (insert large amounts of money) I need. Of course, each funding agency (usually charitable organizations or government organizations) has slightly different requirements. One wants an 11-page proposal in New Times Roman font in size 12 with the references as part of the proposal. The other wants an 14-page proposal in Arial font size 11 with the references in an appendix. So on and so forth. So yeah, buckets of fun.

Interestingly, trying to convince others that my brilliant ideas should be funded also makes me wonder how other types of research get funded. Since this is the summer and I'm sure you'd prefer some light reading, I thought I'd share a little gem of an article on a topic of utmost importance that really illustrates my point about funding: the best possible way to... Pour champagne.

French researchers (who else?) looked closely at two different ways of pouring champagne into a champagne glass (a flute): (1) the traditional way, which consists of letting champagne fall vertically and hit the bottom of the flute, thus generating a thick head of foam, and (2) the "beer-like" way, which consists of pouring the champagne on an inclined flute wall, which generates less foam. The researchers analyzed a number of parameters such as the concentration of dissolved carbon dioxide and the temperature of the champagne. As it turns out, serving champagne chilled (4-12 degrees Celsius) in the beer-like way minimizes the loss of dissolved carbon dioxide, a parameter of utmost importance since it impacts various aspects of the champagne-tasting experience. The researchers stress the value of their research and call for revisiting the traditional way of serving champagne, especially when champagnes are to be compared in competitions.

Wow. Seriously, who funds this? And most importantly, why is it that some researchers have all the fun? The fine print tells us that the researchers "thank Champagne Pommery for regularly supplying (them) with various champagne samples". I think I missed my calling.
Reference: On the losses of dissolved CO2 during champagne serving. (2010) Liger-Belair et al. Journal of Agricultural and Food Chemistry. [Epub ahead of print].

I'm not making it easier for you with this picture

2010-07-19T20:35:00.000-07:00

In my last post I wrote about how children think junk food is tastier when there’s a cartoon on the package. As adults, we may be wiser to such blatant marketing schemes, but we still love our junk food, Shrek or no Shrek. Take pop for example: as of 2006, the production value for carbonated soft drinks in Canada was $2 billion. We also like our donuts: one of the biggest sources of added sugars in our diet is bakery goods. While it’s sometimes nearly impossible to resist the enticing aroma of fresh cinnamon buns baking at the coffee shop, think twice before you splurge: a new study suggests that added sugars in the form of fructose is positively linked to high blood pressure.

High blood pressure, or hypertension, affects over 5 million Canadians, and is increasingly affecting teenagers. It’s a direct risk factor for many nasty conditions, like heart failure and stroke. Interestingly, the increase in the prevalence of hypertension mirrors the increase in our consumption of fructose. And while technically, fructose is a type of sugar found in fruits, it is not thought that the increase in fructose consumption is due to eating more apples. The culprits are sweetened drinks, processed foods and those deadly cinnamon buns.

To address this question directly, American researchers analyzed the data from the very, very large (>4500 participants) National Health and Nutrition Examination Survey. Not surprisingly, the more fructose you consume, the higher your risk of hypertension. This fructose intake/high blood pressure relationship holds even when you control for a number of other factors, including demographics, physical activity, other diseases, calorie intake, alcohol intake, salt intake, and others.

This study highlights what we call an “independent association”, which is not to be confused with a cause-and-effect relationship. There is not enough data to say that eating a lot of fructose leads to hypertension, only that those two things seem to occur together. However, the study has some strong features, namely that it is looking at a very large sample of people, and that it controls for many possibly confounding factors (an important one being salt intake, as it can lead to hypertension).

On the plus side, it’s very easy to limit your fructose consumption by decreasing the amount of pop you drink and the amount of processed foods you eat. On the downside, cinnamon buns are oh-so-very-tasty...

Reference: Increased fructose associates with elevated blood pressure. (2010) Jalal DI et al. J Am Soc Nephrol [Epub ahead of print].

Is Scooby-Doo to blame?

2010-07-05T19:15:00.000-07:00

In this age of pre-prepared processed meals and endless hours on Facebook, it’s no wonder kids are getting fatter. In the US, obesity rates have doubled for preschoolers (2-5 years old) and more than tripled for children 6-11 years old. To explain this alarming obesity trend, many blame the accessibility and affordability of fast food. As a graduate student I often relied on cheap take-out to sustain myself. Luckily I quickly discovered that in Vancouver, sushi costs less than a McDonald’s meal, offering an interesting alternative. If my rent didn’t force me to live below the poverty line (hey, this PhD’s got to be worth something, right?), I would have thought this was heaven. In any case, I’m digressing. Cheap fast food is one part of the equation, kids drooling, lifeless, in front of the computer and the television is probably another part. Interestingly, a recent study suggests that another contributor to the obesity crisis is no other than… Scooby-Doo. And Dora. And Shrek.

The researchers were interested in finding out if putting the image of a popular character on the packaging of a product (this marketing ploy is called “character licensing”) is an effective way to sell food to kids. To test this, the researchers studied three foods: graham crackers, gummy bears and baby carrots. The participants in the study, children aged 4 to 6 years old, were presented with two packages of the same food item (for example, graham crackers). The only difference was that one of the packages had a sticker of a cartoon character (Scooby-Doo, Dora or Shrek) on it. The kids were then asked to say if one of the two foods tasted better, and if so, which one. They were also asked which food they would prefer to have for a snack.

So, does it work? Are children that oblivious to this obvious and dubious marketing trick (Scientific Chick challenge: Write a sentence with more than 3 words ending in -ious)? Absolutely. Overall, children perceived the food items with the cartoon on them to taste better than the ones in the plain packaging. This finding was statistically significant for the “junk” food (the crackers and the gummy bears). Not surprisingly, the children also indicated they would prefer the snacks with the characters on the packaging. As it turns out, character licensing is especially effective in children because they lack the ability to understand that the advertisement is meant to be persuasive.

You would think that all you would have to do to solve the obesity crisis is to slap Elmo’s face on broccoli and apples, but the fact that the character licensing experiment didn’t work as well with the carrots suggests this wouldn’t necessarily do the trick. The researchers only studied 40 children, a relatively small sample size to draw out any solid conclusions, but it’s still an interesting finding. I find it a little worrying that cartoon characters can lead to a more positive perception of the taste of junk food. I find it very worrying that food and beverage companies spend more than $1.6 billion per year on advertising for kids. I guess Ramen advertises for grad students and nobody gets worked up about that.

Reference: Influence of licensed characters on children’s taste and snack preferences. (2010) Roberto et al. Pediatrics, 126(1):88-93.

The little-known benefits of pumping iron

2010-06-28T19:47:00.000-07:00

At the risk of sounding like a broken record, exercise is good for you and your brain. That being said, most studies looking at exercise and cognitive function evaluate aerobic exercise (the kind that gets your heartbeat going). The other kind of exercise, resistance training (strength training with weights), has not been of much interest, perhaps due to the old stereotype that has been plaguing bodybuilders forever: big biceps, small IQ (although big biceps never stopped anyone from becoming governor of California). Switch the young lads for older women, though, and a recent study from a team of researchers at the University of British Columbia (represent!) suggests that gaining muscle can translate into a better brain.

The study looked at 135 women between the ages of 65 and 75 over the course of a year. The women were assigned one of three groups: group one took a one-hour resistance training class once a week, group two took a one-hour resistance training class twice a week, and group three, the control group, took a one-hour balance and stretching class twice a week. The women were all evaluated for a range of cognitive functions at the start of the study, at the six-month point, and at the end of the study (at the 12-month point).

The bad news is that strength training for six months, whether once or twice a week, didn’t lead to any changes. The good news is that if you stick to it for a year, you only need to train once a week to see an effect. After 12 months, the researchers found that all the women who underwent strength training showed a significant improvement in attention. The researchers evaluated attention using the well-established Stroop test (see image below), where the names of colors are written in an ink of a different color (for example, the word blue is written in red ink). To assess attention, the participants were asked to name the color of the ink (and not the word) as fast as they could (try it!). The once-a-week and the twice-a-week resistance training groups significantly improved on this task, while the performance of the balance and stretching group slightly deteriorated.

This improvement in cognitive function didn’t come without a price. The women in the once-a-week resistance training group complained of joint and muscle pains more than the women in the two other groups. It seems that the sweet spot for both an improvement in cognition and a lower risk of pain is to train twice a week (at least). This makes sense to me: the more frequently I exercise, the more my body gets used to the motions. It is also worth noting that the researchers tested other cognitive tasks such as memory and these didn’t show any change with resistance training.

Overall, though, I think this study is great news. I know that many older adults shy away from rigorous aerobic exercise (even young adults… *cough cough*), so this could be an easier alternative to help with brain health. And even if the “brain benefits” of resistance training could be a little more impressive (like by curing Alzheimer’s disease, while we’re at it), on the plus side, strength training also improves gait speed (your natural walking speed), and an improved gait speed is associated with a significant reduction in mortality. So if you don’t exercise for your brain, do it for your lifespan.
Reference: Resistance training and executive function: A 12-month randomized control trial. (2010) Liu-Ambrose T. et al. Arch Intern Med 170(2):170-8.

If I only had a (better) brain

2010-06-15T19:36:00.000-07:00

Scarecrow, from the Wizard of Oz, desperately wanted a brain. Given the financial success of the brain training industry, it seems he’s not the only one hoping for cognitive enhancement. “Brain training” refers to the improvement of cognitive function by the regular use of computer exercises. Recently, it’s popped up everywhere, targeting kids through video games like “Big Brain Academy” to older adults through iPhone apps like “Lumosity”. While brain training companies are stuffing their pockets, the question remains: does it work?

A team of researchers from the UK set out to test how well brain training works. They teamed up with a popular science show on television and recruited over 11,000 healthy participants. The participants completed a general initial assessment of cognitive function (the “benchmarking” assessment), then started a regimen of 10-minute training session three times a week for six weeks. The online training sessions tested a broad range of cognitive functions: short-term memory, attention, math skills, and so on. These tests were designed to be similar to those found in commercial brain training programs. The researchers followed the progress of the participants over the six weeks of training and concluded the study with a final general benchmarking test similar to the initial one.

The good news is that the researchers saw a significant improvement on the specific tasks the participants trained on. The bad news is that this improvement did not extend to general cognitive function. These results mean that while you can improve at, say, a specific memory game that involves remembering the items in a scene, this won’t necessarily translate to better memory in your everyday life (where did I put my keys again?).

As can be expected, the study was criticized, especially by individuals with a commercial interest in brain training. Some suggested that the participants didn’t train long enough or often enough to see an improvement in general cognition. Others said that it’s not because these researchers didn’t observe an improvement that it’s impossible to achieve cognitive enhancement through computer games. However, it’s important to keep in mind that the study also scores some good points: the researchers looked at a very, very large number of participants, and the games used for brain training mimicked those that are commercially available.

Personally, the last thing I need is a reason to spend more time in front of the computer, and I like to think that fresh air is a terrific cognitive enhancer. What do you use to maximize your brain power? Coffee? Naps? Share in the comments!

Reference: Putting brain training to the test. (2010) Owen, AM et al. Nature 465:775-8.

Light at night

2010-06-03T21:16:00.000-07:00

At the end of June, I will once more ride my bike from Vancouver to Seattle as part of the Ride to Conquer Cancer. In the weeks leading to this event, I log many, many kilometers on the saddle and inevitably my thoughts wander to cancer biology (and sometimes to the excruciating pain emanating from my behind). What triggers cancer? How can cancer be prevented? Why are some cancers like breast cancer more prevalent in industrialized countries? While researching the question, I came across a most unsuspected potential risk factor. I’m especially excited about this piece of relevant science because for once I won’t be writing about how eating healthy and sleeping more can cure all your ailments.

In the study, researchers took groups of female rats and exposed each group to different intensities of white light during the dark phase of their daily cycle (typical lab rats live in a programmed 12-hour light/12-hour dark cycle). After two weeks of this night cycle disruption, the researchers implanted a tumor (derived from human breast cancer tumors) in the female rats, and continued on with the night cycle disruption for many weeks. By the end of the experiment, the rats that had been exposed to the strongest intensity of light showed a marked increase in tumor growth rates. The brighter the light at night, the bigger the tumor.

Ok, light at night makes tumors grow faster, but can too much light be the cause for cancer? To answer this question, it’s best to turn to studies in humans. There is convincing evidence that women who work night shifts have a significantly higher risk of breast cancer. As well, women with the brightest bedrooms also have a higher risk of breast cancer. Scientists believe the reason for these correlations is a molecule called melatonin. At night, in the dark, your body produces melatonin, which is a very effective anti-cancer molecule. Several studies have looked at this link in more detail and have shown that melatonin can block the development and the growth of tumors in non-human models of breast cancer.

The light-cancer link is gaining interest, and researchers even started sprucing things up by using a catchy acronym, LAN (for light-at-night), so it’s something to keep in mind. Based on this research, I’ve decided to break my habit of flicking on the lights for my midnight nature calls. Would this habit necessarily give me cancer? No. But flicking on the lights does interrupt my production of melatonin, and on top of being an anti-cancer molecule, it’s also a powerful antioxidant. So I’m just trying to put all the chances on my side. That being said, I’m running into a different problem, which is waking up everyone in the building when I stub my big toe on the door frame. Nobody said staying healthy was easy…

Training for the ride, thinking about cancer

Reference: Circadian stage-dependent inhibition of human breast cancer metabolism and growth by the nocturnal melatonin signal: consequences of its disruption by light at night in rats and women. (2010) Blask D.E. et al. Integrative Cancer Therapies, 8(4):347-353

Another quality science headline

2010-06-02T09:10:00.000-07:00

My friend David just alerted me to a quality headline for an article based on the diet and Alzheimer's disease study:

"Salad dressing good for the brain, new study shows"

Wow. Excellent interpretation of the take-home message of the study! Forget orange juice: doctors now recommend a cup of creamy ranch dressing to kick-start your morning. It's good for your brain!

Seriously, headlines like this make me cringe.

Creating life from scratch... Or not.

2010-05-26T20:02:00.000-07:00

There’s quite a bit of hullabaloo (I can’t believe I just used that word) surrounding the recent creation of the first “man-made” synthetic cell. Genomics, the study of DNA sequences of entire organisms, has come a long way in a very short time: after all, Watson and Crick discovered the structure of DNA less than 60 years ago, and already we’re toying with the thing like it’s silly putty.

DNA can be thought of as the recipe book to make an organism. In your DNA, there is all the information necessary to make every single part of your body. Strangely enough, DNA is only made out of four units: A, C, T and G (remember the movie “Gattaca”? That’s a play on a DNA sequence). The sequence of these units determines your genes (small chunks of DNA), your chromosomes (larger chunks of DNA comprised of many genes), and your genome (the sum of all your DNA). To create the synthetic cell, the researchers started with the genome of one bacteria (let’s call it “donor”). They mapped out the genome of the donor into a computer file, and then edited the code, adding a few specific chunks here and there. These added chunks (the “watermarks”) would later serve as markers to confirm that the resulting organism only hosts the synthetic code. Once the researchers had a DNA sequence they were happy with, they fed the code into a machine that spurts out the As, Cs, Ts and Gs in the correct order and generates small pieces of synthetic DNA. The researchers then used elaborate techniques to stitch together the small pieces into a complete genome. Finally, the researchers transplanted this synthetic genome into a different bacteria (the “recipient”) previously emptied of its own genome. Shazam! Synthetic “life”.

At this point, I don’t think we can call this breakthrough “artificial life”. Life was not created from scratch. What we have here is a functioning cell (and that includes the ability to replicate) with a synthetic genome. This synthetic genome, even though it was created from a computer, only includes genes found in nature (and the watermarks, but they don’t code for anything). And while it’s fun to imagine that we’re only days away from reviving the woolly mammoth, it’s important to keep in mind that this synthetic cell has a very tiny genome. What’s more, the genome of the synthetic cell had some mistakes in it: it wasn’t exactly as the researchers had intended.

Still, I think there is cause for concern, both in terms of ethics and biodiversity. If we had already cracked open Pandora’s box with transgenic animals and plants, this represents a rip-the-lid-off-and-break-the-hinges advance. Especially considering that current legislation allows the patenting of such organisms (a subject for a later post, perhaps). However, with all the bad comes some hope: like stem cells and gene therapy, this technique may represent a new hope to cure diseases.

What’s your take on this new breakthrough? A step closer to mastering life and curing diseases, or a scary slide down a slippery slope?

Reference: Creation of a bacterial cell controlled by a chemically synthesized genome. (2010) Gibson DG et al. Science, May 20 [Epub ahead of print]

I asked...

2010-05-19T19:46:00.001-07:00

And I received.

A little while back, I submitted Scientific Chick to be reviewed on the site Ask and Ye Shall Receive, and my review recently got posted. You can read it here.

(Note: Link destination contains mature language and content that may not be suitable for minors.)

I think I got lucky to land on a reviewer who is a self-proclaimed science fan. Regardless, reading the review was a fantastic way to start my day.

Hand washing: purifying the soul since 30 A.D.

2010-05-15T22:17:00.000-07:00

Those of you familiar with the Bible will remember the famous words uttered by Pontius Pilate, the judge at Jesus’ trial, as he washed his hands in front of the crowd: “I am innocent of this man’s blood; you will see.”

While I have no intention to change my name to Religious Chick, I just wanted to point out that the link between physical and moral cleanliness goes back, waaay back. In a fascinating recent study published in the journal Science, researchers attempt to investigate an aspect of this link.

To better understand the study, you must first know the word(s) of the day: postdecisional dissonance. When you have to make a choice between two options that seem equally good (say, having lobster for dinner versus having King crab for dinner), you enter a state called “cognitive dissonance”, which essentially means that “I can’t decide!” feeling. In order to get rid of this uncomfortable feeling once you made your choice (say, crab), your mind does this funny trick where it now perceives your choice (the crab) as way better than the alternative you rejected (the lobster). This happens even though initially, you thought crab and lobster were equally attractive. This little mind trick is called postdecisional dissonance, and it’s been well documented. In the recent study, the researchers wanted to find out if washing your hands can affect this postdecisional dissonance mind trick.

The researchers set-up a mock consumer survey where they asked 40 subjects to chose, out of 30 CDs, 10 they would like to own. To thank them for participating in the “survey”, the subjects were offered a CD, either their 5th or 6th ranked selection. After they made their choice, the subjects were made to believe that they would now participate in a survey on liquid soap: they could evaluate it anyway they seemed fit. About half the subjects only looked the bottle, while the other half tested the soap by washing their hands. Finally, the participants were asked to rank the 10 CDs again, allegedly because the company behind the CD study wanted to know what people thought of the CDs before they left the store.

Using this (somewhat complicated) study design, the researchers were able to test if washing your hands can attenuate the need to justify a recent choice. The subjects who only looked at the soap ended up ranking the CD they chose in the first part of the experiment better (closer to 1 than 10). Their mind successfully played its trick where it convinced them that the choice they made was much better than the alternative, and this confirms the standard dissonance effect I describe above. Interestingly, the subjects who washed their hands ranked the CDs the same as how they had ranked it initially.

The researchers suggest that hand washing cleans us from past decisions, and reduces the need to justify them. It seems very strange to me that a common saying (“I wash my hands of what we have for dinner, lobster or crab, it’s all the same!”) and biblical anecdote are actually biologically grounded. I guess I shouldn’t be so surprised. What do you think? Can you come up with other examples?

Reference: Washing away postdecisional dissonance (2010) Lee SWS and Schwarz N, Science 328:709.

You are what you eat

2010-05-09T22:10:00.000-07:00

The race to develop a drug to treat Alzheimer’s disease is a top priority for many pharmaceutical companies. With the aging population, the size of the market is ever increasing, and some people estimate that the winner of the race will pocket several billion dollars in the first year of a drug being on the market, in the US alone. However, it would be far easier if we could simply find a way to decrease our risk of getting Alzheimer’s disease in the first place. One recent study suggests that it’s as easy as eating healthy.

We’ve known for a long time that what you put in your plate is the single most important modifiable environmental factor for your risk of getting a variety of diseases, ranging from obvious ones like scurvy (drink your OJ!) to less obvious ones like prostate cancer (stay away from red meat!). Given these relationships, a team of researchers decided to study what combination of foods may relate to a risk of getting Alzheimer’s disease. They asked over 2000 elderly subjects to describe their eating habits in great detail, then followed them for 4 years.

After the 4 years had passed, 253 subjects had developed Alzheimer’s disease. After careful analysis of the subjects’ diets, the researchers concluded that the following diet characteristics significantly lowered your risk of developing Alzheimer’s disease:

The diet is rich in omega 3 and 6 fatty acids
The diet is rich in vitamin E and folate
The diet is poor in saturated fatty acids
The diet is poor in vitamin B12
Eating salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, dark and green leafy vegetables is correlated to a decrease in the risk of Alzheimer’s disease
Eating high-fat dairy, red meat, organ meat, and butter is correlated with an increase in the risk of Alzheimer’s disease.

Subjects who adhered best to the characteristics described above saw their risk of developing Alzheimer’s disease drop by 38%. By now, I’m sure my alert Scientific Chick readers are already wondering if the researchers looked at other factors, such as age. Differences in age, education, ethnicity and sex didn’t change the relationship between diet and Alzheimer’s disease. However, other factors did lessen the importance of the diet, such as smoking, body mass index, and caloric intake. But even when controlling for all these factors, the relationship between diet and risk of developing Alzheimer’s disease remained significant.

The major strength of this study is that it looked at existing dietary patterns instead of trying to impose them, which is often unreliable. However, some of the results can be misleading. A low intake of vitamin B12 may seem to protect you against Alzheimer’s disease, but it’s because a lot of food that contains B12 (such as meat and dairy) also contain high levels of saturated fats, which increase your risk for Alzheimer’s disease. Overall, as with any scientific study, the results must be interpreted carefully. It’s a combination of foods that is important: you can drink antioxidant-rich blueberry juice all you want, but if you’re having it with a side of ground beef, you’re missing the point. In addition, there could be some factor other than diet at play that the authors did not control for.

So while we don’t have a miracle drug yet, and no single food can prevent Alzheimer’s disease, it seems like a healthy, varied and unprocessed diet is a good place to start to ensure healthy aging.

P.S. It's Jello.

Reference: Food combination and Alzheimer disease risk: A protective diet (2010) Gu Y et al. Arch Neurol [Epub ahead of print]

Dr Scientific Chick, PhD

2010-04-29T09:56:00.000-07:00

Great news! My defense went very well, and I have officially been accepted in the PhD club.

I am currently rediscovering some of life's little pleasures, such as reading non-neuroscience related books, and having free time. Free time! What a concept.

Thank you all for your encouragements in the comments of the previous post, and see you soon for more exciting science news!

And now, a word from your friendly graduate student

2010-04-17T10:24:00.000-07:00

This week, I'm skipping the usual science story in favor of something different: a look at the life of a graduate student who will be defending her thesis in a week.

Yup, that's right, the marvelous PhD adventure is already and finally coming to an end. I say "already" because the last 6 years were filled with new friends, interesting courses, exciting science and all the perks that come with being a student (2 words: free transit). I say "finally" because the last 6 years were also filled with too many new beginnings, many frustrations, and a whole lot of stress. Overall, an amazing experience, but like all good things, it must come to an end, and it's time to move on.

That being said, it's not over until it's over. At the end of April, I will stand in a tiny room filled with professors and a few supporters (I'm so very excited that my parents are making the trip to come and encourage me!), summarize the last 6 years of my work in 20 minutes, and then get grilled on everything I know until I wave the white flag of ignorance. So until then, every single one of my days consists of waking up, studying, freaking out when I realize that I don't know anything about anything, then going to bed, and having dreams about my defense. It's a bit of a roller coaster ride, but I've done this before (for my comprehensive exam, the mid-PhD grilling to make sure you're worthy), and I've gotten better at it.

So stay tuned for the next post, in which you will learn if I'm a doctor or not, and regular programming will return shortly. I've been saving an interesting article on what to eat to ward off dementia, and I think you'll want to hear about it.

Magnets make morals moot?

2010-04-08T11:47:00.000-07:00

What does it mean to act morally? Is it to cause benefit and not harm? Is it to do what’s right? Who gets to decide what’s right? While philosophers have been debating these questions for millennia, neuroscientists are now joining in the fun. In recent years, researchers have been taking pictures of people’s brains while moral judgments are being made to try to make sense of it all. In a recent article published in PNAS, a team of American researchers tried to find where morality lives in your brain.

The researchers used a technique called transcranial magnetic stimulation (TMS, see picture). In short, it consists of placing magnets near the participant’s head and applying a magnetic field targeted at a specific brain region. The current generated by the magnetic field can pass through the skull and disrupts the targeted brain region. The whole thing is non-invasive and not painful.

Using this technique, the researchers disrupted a region called the right temporoparietal junction while participants were making moral judgments on scenarios like this one:

“Grace and her friend are taking a tour of a chemical plant. When Grace goes over to the coffee machine to pour some coffee, the friend asks for some sugar in hers.”

There are then four potential outcomes, which participants rated on a scale ranging from permissible to forbidden:

Grace thinks the powder is sugar, and it is sugar, so everyone stays alive and happy.
Grace thinks the powder is sugar, but it’s actually toxic, and the friend dies.
Grace thinks the powder is toxic, but it’s just sugar, so Grace’s evil plan is thwarted and the friend lives.
Grace thinks the powder is toxic, and it is toxic, and the friend dies.

Some friend Grace is, right?

Anyway, the researchers found that participants who underwent the procedure made similar moral judgments as control participants in all the situations but one: the instance where Grace thinks the powder is toxic but it’s not (#3 above). In this case, participants who had a part of their brain disrupted by TMS thought Grace’s actions were significantly more permissible than control participants. One might say their moral judgment was altered. In fact, almost every single news story that reported on this article suggested that the interpretation of these results meant that TMS to the right temporoparietal junction of the brain leads to altered moral judgments. So that must be where morality resides!

Interestingly, even the researchers do not claim this. In the article, they write: “TMS did not disrupt participant’s ability to make any moral judgement.” Remember, the TMS subjects rated 3 out of 4 outcomes the same as control participants. That means their moral compass is intact. It is also important to note that in the case where TMS participants thought Grace’s actions were more permissible than the control participants, this difference was only of about 15%. So what’s going on? Well, one can judge the morality of an action based on a number of criteria. The easiest criterion is outcome: did the friend live or die? Children under 6 (before the “age of reason”) mostly use this criterion to decide if actions are good or bad. But another criterion (among many others) is intent. Did Grace mean to poison her friend or not? In the situation 3, Grace meant to poison her friend, so if you were to judge morality on intent, it would be forbidden. But the friend lived, so if you judge morality on outcome, it would be permissible. What the authors suggest is that disrupting the right temporoparietal junction reduces how much one cares about intent. Which is different than “reduces one’s morality”.

Of course, like any good study, other interpretations cannot be ruled out. For example, TMS may interfere with other cognitive functions that have nothing to do with morality. Overall, the finding is interesting, but as always, more work needs to be done to get a better grasp of the inner workings of our morality.

Next time you get a tour of a chemical plant, watch your drink...

Reference: Disruption of the right temporoparietal junction with transcanial magnetic stimulation reduces the role of beliefs in moral judgements. (2010) Young, L. et al. Proc Natl Acad Sci USA Mar 29 [Epub ahead of print].

Family matters

2010-03-31T14:50:00.000-07:00

If you’re a pet owner, chances are you believe your pet has a personality, recognizes you, loves you, feels your pain. Who hasn’t heard a story about a girl who’s crying over a heart break, and her dog comes over to cuddle with her and lick her tears away? On the other hand, many firmly believe that animals are just friendly when they want food, and that they don’t have the kind of intelligence needed for emotions such as empathy. For example, my dad likes to claim that cats have a “smooth brain”, a reference to the fact that the brains of cats are not folded as much as those of humans, and therefore, the 16 pounds of fluff sleeping in my living room can’t possibly experience more than “hungry”, “sleepy” and “farty”. The thing is, it’s hard to tell, because we can’t ask animals how they feel. Faced with this difficulty, a team of researchers recently devised a method to determine if the lowly mouse is capable of complex emotions.

The researchers initially wanted to see if mice could learn to fear something without experiencing it. They put two mice in a cage and separated them by a see-through wall. The researchers then proceeded to give mild electrical shocks to the feet of one of the mice. Interestingly, the observing mouse (who wasn’t getting shocked) also displayed signs of fear (which is expressed mostly by a freezing behavior). What’s more, when the observing mouse was put back in the same experimental cage later, it still displayed signs of fear, meaning it remembered the experience of watching the other mouse get shocked. However, if you put the observer mouse in a different cage or different environment, it behaved normally. These results indicate that the observing mouse learned to fear a specific context without experiencing the pain it fears.

So what, you say? The mouse could just be mimicking the fear behavior, or experiencing “emotional contagion”. But there’s more. The researchers tried the same experiment, but this time, they used a pair of siblings instead of two random mice. Surprisingly, the effect they observed in the first experiment was now much stronger: the observer mice displayed significantly more freezing behavior, as if they could relate more to the pain of a sibling mouse than to that of a random mouse. The freezing effect was also stronger when the two mice were unrelated but had been sharing a cage for more than 10 weeks (mice in common-law). Overall, the more familiar the observer mouse is with the mouse getting the shocks, the better the observer mouse can feel the pain of the other mouse.

Are the mice really feeling empathy, or are they simply sensing a danger? While this study can’t tease those two possibilities apart, the fact that the response is much stronger when the mice are related definitely raises the interesting hypothesis that, pardon the cliché, “animals have feelings too”. What is your experience with animal intelligence? Share in the comments!

Reference: Observational fear learning involves affective pain system and Cav1.2 Ca1+ channels in ACC. (2010) Jeon et al. Nature Neuroscience 13(4):482-8.

Males taking pregnancy to a whole new level

2010-03-21T00:05:00.000-07:00

There’s an interesting debate going on in the science communication community over whether it’s more valuable to talk about relevant science news or cool science news. If you read my tagline, you’ll know which side I’m on (though my preference is for science news that are both relevant and cool). But just for today, I’d thought I’d switch roles and share the findings of a recent article on a topic that definitely doesn’t seem relevant for us: male pregnancy.

Male pregnancy occurs only in seahorses and their relatives, and happens when females deposit their eggs in a pouch located on the male. The pouch serves a similar function as the human uterus and provides nutrition and protection for the offspring while they develop. In a recent study published in Nature, researchers looked at how male pipefishes manage these pregnancies and find surprising behavior.

First, the researchers confirmed that the male pipefish prefers to mate with larger females. This maximizes evolutionary fitness (survival of the fittest) because larger females lay more eggs and their eggs have a greater chance of surviving. Interestingly, the shorter the male, the stronger the preference for a large female. I’m going to let you draw your own conclusions as to the origins of Little Man Syndrome.

Second, the researchers found that the chances of survival of the offspring depend on previous pregnancies. If a male really invested himself in a previous pregnancy and spent a lot of energy caring for the offspring of a larger female, the chances of survival of a later pregnancy from a smaller female are much lower. This essentially means that the male can gauge the “attractiveness” of a female and distribute his resources accordingly. In some cases, when forced to reproduce with a small female, males can partly or even completely abort the offspring (by not spending energy for their nutrition and care) to conserve their reproductive potential for when they hit the jack pot chunky female. Kind of a blow to the supermodels of the pipefish world, if you ask me.

Overall, the study suggests that male pipefishes have much greater control over reproduction that we initially thought, and certainly much greater control over reproduction when compared to the standard female mammal pregnancy scheme.

Now let’s see if we can find some relevance to this study and make it a two-for-one. Can you find any relevance for us in this study, in aspects of the study, or even in questions it raises? Contribute your thoughts in the comments!

Pipefish

Reference: Post-copulatory sexual selection and sexual conflict in the evolution of male pregnancy. (2010) Paczolt KA, Jones AG. Nature 464(18):401-4.

It's my blogiversary!

2010-03-14T21:05:00.000-07:00

Scientific Chick is one year old today!

I prefer cookies to cake, so I give you the best science cookies I could find:

Thanks for reading!

Pesticides for macho frogs

2010-03-13T12:41:00.000-08:00

The increasing demand for organic food sends a pretty clear message that we are starting to realize that pesticides and herbicides are bad. We are concerned that pesticide exposure may be linked to cancer, decreased fertility rates, etc. Unfortunately, the majority of living organisms can’t choose their level of exposure to these chemicals, and a recent study describes a most unusual consequence of pesticide exposure in frogs.

The researchers looked at the effects of exposure to atrazine, the most widely used pesticide in the world, and the most common pesticide contaminant in water. The study shows that when male frogs are exposed to atrazine they become demasculinized, meaning they lose male characteristics. This happens both at the physical, or “looks” level (the male frogs look like female frogs), and at the physiological, or “function” level (the male atrazine-exposed frogs have reduced testosterone levels and sperm count compared with control male frogs).

All this isn’t exactly new. For years, we have been aware that pesticide exposure interferes with normal hormonal function in a variety of organisms (salmon, frogs, rodents). What sets this study apart is that the researchers observed that in 10% of the atrazine-exposed male frogs, a complete reversal to a female frog happened. Everything about these initially male frogs now identified them as female, with the only exception of their genetic code (the equivalent of their Y chromosome). They looked 100% female, had female reproductive organs, and were able to mate with other males and produce eggs. If you’re in the market for an amphibian sex-change, look no further.

I know what you’re thinking. Surely the researchers exposed the frogs to crazy high levels of atrazine? No. They used a concentration of 2.5 parts per billion, which is consistent with what you can find in the environment. But frogs can be hermaphrodites, right? So it’s not a big stretch that they would switch over from hermaphrodite to female and just lose their “half male”? No. While these frogs can be hermaphrodites, the researchers only looked at genetic males, meaning males that could not be or become hermaphrodites. But the researchers looked at early stages of development, right? When the tadpole can go either way? Again, no. These were adult frogs.

Can we extrapolate these results to humans? Unlikely. Frogs absorb chemicals like atrazine through their skin, something mammals don’t do. Therefore, you would need exposure at a much higher concentration to achieve the same amount of atrazine in our system. Does this mean the study is not relevant to human health? Again, no (I’m so negative today!). The fact that atrazine is so potent at interfering with the frog’s hormonal system is definitely cause for concern. Interestingly, atrazine is banned in the European Union. The United States, on the other hand, slathered 76 million pounds of the stuff on cropland in 2003. (Organic) food for thought…

Reference: Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis). (2010) Hayes TB, Khoury V, Narayan A, Nazir M, Park A, Brown T, Adame L, Chan E, Bucholz D, Stueve T, Gallipeau S. Proc Natl Acad Sci 107(10):4612-17.

Oms for ouches

2010-03-06T11:20:00.000-08:00

In North America one in three people struggle with chronic pain. Old sports injuries, carpal tunnel syndrome, migraines, the causes are varied, and the treatments are few. In my case, too many hours of swimming have done a number on my shoulders, and I’m left popping Advils like they’re jelly beans. Forced to quit swimming, I now took up cycling, to make sure I wreck my knees and get the full body experience. In any case, chronic pain can be debilitating, and to the sufferers, it often seems like there is no way out. Interestingly, a new study suggests that a little open mindedness in the form of mediation can be a huge help.

The study looks at the effectiveness of a technique called mindfulness mediation for the reduction of chronic pain in various conditions ranging from arthritis to fibromyalgia. Mindfulness meditation aims at paying close attention to the moment, at accepting thoughts and sensations for what they are, without judging them and without reacting to them. It takes practice, and commitment, but an increasing number of people swear by it for improving their quality of life.

The researchers studied over 100 participants with chronic pain before and after an 8-week regimen of mindfulness meditation, performed both in weekly classes and at home. The outcome survey assessed a number of parameters such as body pain, vitality and fatigue, limitations due to physical health problems (try washing your hair when both your shoulders feel broken), and so on.

Overall, mindfulness meditation lead to a significant improvement of all the parameters studied. Not only that, it lead to clinically relevant changes in measures like bodily pain and general health perception. Interestingly, when you divide the group by specific health condition, some conditions show a much greater improvement than others. For example, arthritis and back/neck pain sufferers benefited from meditation more than headache/migraine sufferers.

So how does mindfulness meditation work? Because we are just beginning to understand the impact of meditation in the brain, we can only take educated guesses. It is possible that meditation can regulate sensory and affective aspects of pain itself (i.e. you actually hurt less). It is also possible that meditation acts to reduce distressing thoughts that come with pain and usually amplify the pain feeling (i.e. you still hurt, but you stress out about it less, so the pain doesn’t seem as bad). It may also be a combination of both (isn’t it always?).

The study is very convincing, but it’s not perfect. Without a proper control group (i.e. a cohort of people who have chronic pain but don’t meditate), it’s not possible to rule out that everyone just had a spontaneous improvement in their pain. However, given that most participants had been experiencing pain for several years, this seems unlikely. In addition, the sample sizes for individual condition groups were pretty small (27 to 53 individuals per group), which limits statistical power. Finally, the participants in the study were not very heterogeneous, being mostly well-educated Caucasian women, so who knows if this applies to everyone.

Mindfulness meditation is obviously no miracle cure for chronic pain, but it sure seems like it can help people cope with the pain. In my humble opinion, it can only be a good thing to take some time to breathe correctly and relax. It would be extra nice if the researchers also recommended daily naps, though.

Mr. Minou is also an adept of meditation.

Reference: Mindfulness-based stress reduction for chronic pain conditions: variation in treatment outcomes and role of home meditation practice. (2010) Rosenzweig S, Greeson JM, Reibel DK, Green JS, Jasser SA, Beasley D. J Psychosom Res. 68(1):29-36.

♫ Oh, sugar sugar ♫

2010-02-23T11:29:00.000-08:00

To say I had a sweet tooth as a child would be an understatement. I remember one Easter, I must have eaten over 40 Cadbury Creme Eggs in one sitting. My mom would put a chocolate centerpiece on the table, usually a bunny or an egg or something like that, and it would be surrounded with smaller treats, such as Creme Eggs. What ensued was a complex calculation of how many eggs I could eat before it would look like I ate them all. I had to factor in the fact that my brothers and sister would also eat some eggs, albeit at a slower rate. And I also had to squish all the little foil wrappers in the tiniest, most compact ball possible to make it look like I didn’t actually have that many. Those were the good days.

It’s no secret that children have a more pronounced preference for high-intensity sweetness. This preference may have evolved to make sure children seek out energy-rich nutrition during growth. Therefore, having a child with a sweet tooth was never really a cause for worry. Until now.

A recent study in the journal Addiction looks at the link between children with a sweet tooth and two other parameters: family history of alcoholism and depression. The researchers picked those two parameters because the pleasure derived from eating something sweet is generated by a reward system in your brain, and both alcoholism and depression affect this reward circuitry. The researchers looked at 300 healthy children, assessed their family history of alcoholism (via an interview with the mother), and tested them for depressive symptoms. They then tested the children for sweetness preference by having them taste sucrose solutions of different sucrose concentrations and asking them to choose which is their favorite. They also assessed the children’s liking for sweet treats in daily life.

The researchers found that almost half of the children were positive for family history of alcoholism, and one quarter of the children exhibited depressive symptoms, consistent with previous studies. When the researchers analyzed sweet preferences, it got messy. First, children with a family history of alcoholism preferred significantly higher sucrose concentrations compared with children with no such family history. Interesting, right? However, if from the total pool of children with a family history of alcoholism, you remove those who also show depressive symptoms, the alcoholism/sweet tooth link is no longer significant. Like I said, messy. Second, children who tested positive for depressive symptoms preferred significantly sweeter foods compared with children who didn’t exhibit depressive symptoms. Interesting, right? However, if you factor in the age of the children, this depression/sweet tooth link is no longer significant (this is because the intensity of the sweet tooth decreases with age). Guess what I’m about to say? That’s right, messy.

Overall, we can draw two conclusions. First, children with a family history of alcoholism AND exhibiting depressive symptoms prefer significantly sweeter solutions. Second, children exhibiting depressive symptoms MAY have a “sweeter tooth” compared with children who don’t exhibit depressive symptoms. Several theories, or a combination of these theories, could explain the associations observed in the study. First, if you read the fine print in the article, you’ll find that the mothers of children who have a family history of alcoholism and depressive symptoms are more likely to be obese. Perhaps these children are exposed to more sweets from an early age? Second, other studies have shown that adults with depression have a higher threshold for the detection of sweet taste. Therefore, it is possible that these children are less sensitive to sucrose and need a higher concentration of sugar to achieve the same level of sweet taste. Third, it is possible that the children with a family history of alcoholism and depressive symptoms have an altered brain reward system and require a higher concentration of sugar to activate the pleasure centers in the brain.

While this study suggests interesting associations, one thing is for sure, more experiments are needed to determine if having a sweet tooth means anything at all. Now excuse me while I unwrap the first Cadbury Creme Egg of the season.

Reference: Sweet preferences and analgesia during childhood: effects of family history of alcoholism and depression. (2010) Mennella JA, Yanina Pepino M, Lehmann-Castor SM, Yourshaw LM. Addiction. Feb 9 [Epub ahead of print].

Do you want to live? Yes or no?

2010-02-10T19:47:00.000-08:00

In the early 2000’s, the Terry Schiavo case took the media by storm and pushed into the spotlight a number of ethical questions regarding patients in persistent vegetative state (awake but not aware). Evidently, none of this would have happened if we could just have asked her whether she wanted to continue living or not. A simple yes or no question. Could this be achieved? Can patients in a vegetative state communicate purposefully? A new study suggests they can.

The researchers looked at brain signals from 16 healthy patients and 54 patients with severe brain injuries who were in a vegetative state. The technique they used is called fMRI (for functional magnetic resonance imaging), a scan similar to one you would get for a joint injury, but instead of taking static images, fMRI measures blood flow in your brain. Presumably, if part of your brain is activated, there will be an increase in the blood flow in this area, and this will area will light up on the brain image.

The first experiment was done only with the healthy controls to establish that different cognitive tasks lead to the activation of different parts of your brain. While immobilized in the fMRI machine, the subjects were asked to imagine playing tennis. They then asked the healthy subjects to imagine walking through a familiar house. As expected, the brain scan images showed that each task activated a different brain region.

Armed with this control data, the researchers moved on to the patients in vegetative state. They asked each of the 54 patients to think about playing tennis and to think about navigating through a familiar house, and looked at the resulting brain signals. Of the 54, they found a grand total of five patients whose brain signals matched that of the healthy controls during a given task. This result suggests that some patients in a vegetative state can willfully influence their brain activity.

While this is an interesting finding in itself, there’s more. The researchers then took one of the five patients who showed the correct brain activity, and asked him yes or no questions. The patient was instructed to think about tennis when he wanted to answer yes, and think about the house when he wanted to say no. Out of the six yes or no questions he was asked (such as “Is your father’s name Alexander?”), he correctly answered five. Success!

The researchers and the media were quick to take these findings to the next level: with this new technique, we can now have brain damaged patients express their feelings! We can increase their quality of life! We can ask them important ethical questions! Well, hold on. While I do agree that this is a very interesting study, and that it will no doubt give a lot of hope to the families of patients in vegetative state, one has to be very careful with interpretation. First, let’s run the numbers: out of 54 patients, only five responded to the tasks. Out of those five, only one was tested. Out of the six questions asked, five were answered. While this represents a great achievement, we are very far from being able to extrapolate the potential of this technique. Second, the fMRI technique is expensive, imperfect, and very difficult to interpret. Third, certain words could possibly cue brain activity that may or may not be willful. I would like to see the researchers do an experiment where they just say the word “tennis” or “house” to healthy volunteers without asking them to imagine anything and see what kind of brain activity results. Finally, the fact that a patient has the cognitive ability to picture playing tennis does not mean he or she has the cognitive ability to make important, ethical decisions. So before we get all excited, I think we should keep things in perspective. But one thing is for sure: in this age of medical technology, we can set the Ouija board aside.

This is what fMRI data looks like

Reference: Willful modulation of brain activity in disorders of consciousness. (2010) Monti MM, Vanhaudenhuyse A, Coleman MR, Boly M, Pickard JD, Tshibanda L, Owen AM, Laureys S. New Engl J Med Feb. 3 [Epub ahead of print].

Eating Dolly

2010-01-31T21:57:00.000-08:00

Remember Dolly? The first cloned mammal? The world’s most famous sheep? How would you feel about having Dolly for dinner, and I don’t mean to visit…

This week, I am writing about cloned meat in the food chain. We’ve come a long way in cloning techniques since Dolly (1996) and several farms in the United States are now producing cloned meat for human consumption. I thought I would review the literature and find an article on the safety of eating cloned meat. I’m not going to lie: I was biased going into this. I’m just not sure how I feel about a Dolly steak. As a scientist, however, I may not be biased in methodology, so I reviewed all the articles I could find on cloned meat as a source of food. Here is what I found:

Cloned meat appears to be exactly the same as regular meat. Same nutrients, same properties, it’s virtually biologically indistinguishable.

Animal models, when fed cloned meat for some time, seem perfectly fine.

Animal models, when fed cloned meat and then made to reproduce, also seem perfectly fine, and reproduce just like animals fed regular meat, and the babies are fine, too.

Given the evidence, I have to tell you that there appears to be no hint of anything wrong with eating cloned meat.

So what? That’s it? We just drop it? The Food and Drug Administration was totally justified to approve cloned meat to enter the food chain in 2006? If you review the science, yes.

As someone who is ever careful about the quality of food, however, I personally have a few reservations. First, scientific reservations:

Overall, I only found a handful of controlled studies.

The longest-term study I have found looking at the effects of feeding cloned meat and milk to animals is 12 months. While 12 months is a very long time in the life of a rat (the species used in this particular study), that still may not be long enough. Especially considering we don’t actually have that much in common with the rat (except perhaps a love for food).

The main study looking at how feeding cloned meat to animals impacts reproduction was done in rabbits. Is it me or do rabbits not normally eat much meat?

While the data clearly suggests that cloned meat is just like regular meat, other scientific studies find that cloned animals have a higher fetal mortality rate and may be more susceptible to some diseases. Now there’s probably a reason for that, and until we find it, how can we be positive it’s not somehow affecting the meat?

That being said, proteins are proteins. And logically, cloned meat, as the evidence suggests, is likely identical to regular meat. The reason I would still chose not to eat it is more ethical than biological. With an ever-decreasing diversity on Earth, I can’t help but think that the mass production of cloned beings is a step in the wrong direction.

Because the laws on labeling cloned meat are still a bit fuzzy, what can you do if you would rather avoid cloned meat? One easy (albeit expensive) way to be sure is to go organic. In the last few years, both Canadian and American food authorities have declared that cloned meat or milk does not fit the organic bill. Another great way is to seek out meat from local producers, and get information on their practices. Why not visit the local farms? Road trip!

Sample of references: Effects of cloned-cattle meat diet on reproductive parameters in pregnant rabbits. (2010) Lee NJ, Yang BC, Hwang JS, Im GS, Ko YG, Park EW, Seong HH, Park SB, Kang JK, Hwang S. Food Chem Toxicol [Epub ahead of print].

Fourteen-week feeding test of meat and milk derived from cloned cattle in the rat. (2007) Yamaguchi M, Takahashi S. Theriogenology 67(1):153-65.

Cloning animals by somatic cell nuclear transfer-biological factors. (2003) Tian XC, Kubota C, Enright B, Yang X. Reprod Biol Endocrinol 1:98.

The eyes don't lie

2010-01-22T16:00:00.000-08:00

Think back to the last time you used your car, or your bike, to get somewhere. When you reached your destination, what color was the car or the bike parked nearest to yours? Can you remember? Chances are, unless you opened your car door too fast and dinged the one next to you, you probably can’t remember. Now what if I was to tell you that while you can’t consciously recall this information, your brain might still know it? What if there was a way to get at this information? A recent study in the journal Neuron suggests there is a way: by reading your mind through your eyes.

The researchers made participants study three different scenes (for example, a park, a lake, a kitchen) each superimposed with a different face. After a short break, the participants had to do a test. They would be presented with one of the three scenes from the study phase, and after a delay, all three faces seen in the study phase were superimposed on the test scene. All the participants had to do was identify which of the three faces was the one that initially corresponded with the test scene. During the test, two parameters were evaluated: the first one was whether the participant correctly identified which face corresponded with the test scene, and the second parameter was where the participant was looking on the screen, and how much time he or she spent looking at each of the three faces. This was done through a technique called eye-tracking, where a camera records the position of your eye-gaze.

Here is an example of the task

What the researchers found is that the participant’s eyes spent significantly more time viewing the correct matching face (the “right answer”), even when the participant selected an incorrect face as the answer. So what this means is that even when the participants couldn’t consciously remember which of the three faces was the right one, their eyes lingered the longest on the correct face.

In addition to the eye-tracking study, the researchers were looking at brain signals from the participants and determined that the hippocampus, a brain region we already knew was involved in conscious memory retrieval, was also supporting memory even when the participants were making incorrect responses. In a way, this means that your hippocampus supports the expression of memories through your eye-movements, even when you’re not consciously remembering correctly.

The relevance of this study lies in the fact that in some circumstances, the movements of your eyes is a more truthful and reliable account of memories than your verbal accounts. I’m sure you can imagine instances when this could be helpful: for example, to study the memory processes of non-verbal beings, such as babies or chimpanzees (who doesn’t want to know what a chimpanzee is thinking?). However, eye-tracking could also be used to get information from someone who is attempting to withhold it (surely, a more acceptable alternative to waterboarding). So next time you have something to hide, invest in a good pair of sunglasses…

This guy wants to know what you're thinking.

Reference: The eyes have it: hippocampal activity predicts expression of memory in eye movements. (2009) Hannula DE, Ranganath C. Neuron 63:592-599.

Saving the humble pie for another day

2010-01-16T23:49:00.000-08:00

The results are in: Scientific Chick won the 2009 Canadian Blog Award for best blog in the Science and Technology category!

Since this was rather unexpected, I did not prepare a speech. But I do want to say big thanks to everyone who voted! I really enjoy writing this blog, and it means a lot to me that there are people out there who enjoy reading it.

Thank you!

Cell phones: curing brain diseases since 2010

2010-01-14T22:11:00.000-08:00

If you are like most people, and in particular like everyone I take transit with on a daily basis, you probably spend a fair amount of time talking on your cell phone. If that’s the case, you’ll probably be happy to learn that in 2007, the World Health Organization declared that cell phones are A-ok. Nothing to worry about health wise. Not at all like sticking your head in a microwave. But you’ll be even happier to learn that in 2010 (fresh off the press!), a study published in the Journal of Alzheimer’s Disease suggests that not only is using your cell phone harmless, it might actually be good for you.

The researchers looked at the effect of exposing mice to high frequency electromagnetic fields (similar to the ones you are exposed to when chatting on your cell phone) for a long period of time (2 hours a day for 8 months). They used both normal mice and a mouse model of Alzheimer’s disease. An Alzheimer’s mouse is a transgenic mouse that has a gene that causes some of the manifestations of Alzheimer’s disease in humans.

At the start of the study, before the exposure to the electromagnetic fields, the researchers tested the mice on memory tasks, and as expected, the Alzheimer’s mice were clearly impaired compared with the normal mice. After two months of exposure, no change was observed in either type of mouse. However, after 8 months of exposure to the cell phone-like electromagnetic fields, the Alzheimer’s mice did significantly better on memory tests compared with Alzheimer’s mice who didn’t receive the treatment. Normal, non-Alzheimer’s mice also showed cognitive benefits due to the electromagnetic fields compared with normal mice that didn’t get the treatment.

Time to get Grandma a cell phone? Not so fast.

You may have seen this story in the news. It may have sounded like we finally found a cure for Alzheimer’s disease, and, as a bonus, it’s non-invasive and has no side effects. You may have started thinking of a business plan that involves sewing cell phones into pillowcases for the elderly. Trust me, I thought of this. However, as per usual in the world of science, it’s probably not that simple.

First, I can tell you this: mice skulls are thin, weak, and very easy to cut through with just a regular pair of tiny scissors (how sad is it that I know this from experience?). The skull of a mouse is very different from that of a human, and this means that while the electromagnetic field might penetrate well into mice brains, this may not happen in humans.

Second, the mouse model of Alzheimer’s disease, while widely used and our best tool for these types of studies, is flawed. So extrapolating the results to human Alzheimer’s disease is definitely premature.

Third, if you read the article carefully (I did it for you, so no worries), you’ll find that exposing the older mice to electromagnetic fields has one interesting side effect: an increase in body temperature. It then becomes difficult to tell if the memory enhancement observed is due to the temperature change or the electromagnetic fields. However, this is not necessarily a bad thing. I, for one, would much prefer to prevent cognitive decline by a daily regimen of quiet hot baths then by talking on the phone (though when I was a teenager, my mom would have guessed otherwise).

Finally, there was another sneaky side effect to the exposure, one that was seen only in younger mice: a decrease in three brain compounds involved in battling oxidative stress, including a very important antioxidant. The authors go over this finding somewhat quickly, and suggest that this can be interpreted as a good thing. Unfortunately, I happen to have studied this particular antioxidant quite a bit and I am of the opinion that the finding can also be interpreted as a very bad thing.

Overall, I don’t want to sound like a complete downer. This study was well conducted, showcases very interesting findings, and certainly gives us hope that maybe something can be done for Alzheimer’s disease. But I won’t be sowing a cell phone in my pillow just yet.

Reference: Electromagnetic field treatment protects against and reverses cognitive impairment in Alzheimer’s disease mice. (2010) Arendash GW, Sanchez-Ramos J, Mori T, Mamcarz M, Lin Z, Runfeldt M, Wang L, Zhang G, Sava V, Tan J, Cao C. Journal of Alzheimer’s Disease 19:191-210.

Black and white television

2010-01-06T16:29:00.000-08:00

The United States recently elected their first black president. In this era of multiculturalism, can we consider ourselves a race-blind society? If you were to ask around, chances are most people would claim they do not behave in a racist fashion. Unfortunately, racial biases are still around us, and a recent study in Science makes a worrying discovery about the subtlety of racial biases in every day television programming.

The study looked at 11 popular television shows that include recurring white and black characters of roughly equal status (for example, characters could include a black detective and a white detective or a white doctor and a black doctor, and overall, black and white characters are equivalently distributed in the hierarchy). The researchers selected sample clips from the 11 shows and removed the audio track. They then asked a number of white young adults to watch the soundless clips and rate how well each character seemed to be treated by other characters and how much it seemed each character was liked.

You’d think if the character statuses are roughly equal, they would elicit similar non-verbal responses. Well, think again. Overall, white characters elicited significantly more favorable responses when compared with black characters, meaning the subjects rating the clips thought that the white characters seemed more liked and better treated by others than black characters. The interpretation of this study is that common television programming exposes us to race biases. The subtlety of this bias lies in the fact that it is non-verbal: when a new group of white young adults was asked to read the written transcript of the clips, no such biases were found. The researchers then took the study further and showed that the perception of the non-verbal biases in television shows can influence one’s race association and racial attitudes.

What is the reason for the presence of this race bias in television shows? Are the actors spontaneously generating them? Are they scripted? What other types of biases might be communicated through television? This study definitely gives us food for thought…

Reference: The subtle transmission of race bias via televised nonverbal behavior (2009) Weisbuch M., Pauker K., Ambady N. Science 326:1711-4

Move over, monkeys, there's a new smart animal in town

2009-12-18T18:03:00.000-08:00

We used to think that the use of tools was a hallmark of our human species. Then we learned that in fact, some primates also use tools. For example, orangutans will use a stick to poke at ant hills to collect the fleeing ants for a tasty snack. The real piece of humble pie came when we discovered that birds also use tools. That’s right. Tiny-brained crows are able to use a curved stick to get at a treat in a tight spot. So I can’t say that it came as a shock to learn that the octopus, an invertebrate, also recently joined the smarty-pants tool-using club.

Most people who spend all day ~~procrastinating~~ working at their desk and have internet access probably already saw this neat video featuring an octopus carrying around a coconut shell and hiding in it:

In a recent article published in the journal Current Biology (which includes the video above), researchers describe how octopuses (also called octopodes, I had to look this up) carry coconut shells for later defensive use. The octopuses are seen scurrying around (on distances up to 20 meters!) with the shells cumbersomely positioned between their tentacles, and later assemble the two halves of coconut shells and hide inside. The authors stress that the interesting feature of this behavior is that when the octopuses are carrying the shells, they are at an increased predator risk, because they move slower than normal and their heads are exposed. Therefore, the only benefit of carrying the shells is the future use of these shells as a shelter. Apparently, that’s an amazing display of foresight for an organism that uses most of it brain cells to control its too many limbs.

While the video is definitely captivating, I think that whether this study is groundbreaking or not depends a lot on what the definition for “tool use” is. In the article, the researchers state that “a tool provides no benefit until it is used for a specific purpose”, so shelters like those of the hermit crabs don’t qualify. But even though the shells are used at a later time point, I’m not sure about calling them “tools”. I guess I mostly see them as a shelter. Is a shelter a defensive tool? Ah, semantics…

Reference: Defensive tool use in a coconut-carrying octopus. (2009) Finn JK, Tregenza T, Norman MD. Current Biology 19(23) :1069-70.

Personal space invaders

2009-12-11T12:04:00.000-08:00

My last post was about H.M., a man who was missing a part of his brain called the hippocampus. Studying H.M. helped us to greatly improve our understanding of several functions of this brain region. Needless to say, after all the attention generated by the study of this patient, every neuroscientist out there was on the hunt for a patient missing different parts of their brain. By this time, gone was the era when we could butcher people just for kicks, so scientists waited around.

Luck struck a group of scientists from California recently. They came across patient S.M., a 42 year-old woman missing her entire amygdala, a part of your brain not very far from the hippocampus. Studying this woman confirmed a lot of things we already knew about the amygdala, for example that it’s important for fear. However, S.M. thought us something new: the amygdala is the part of your brain that controls your perception of an elusive concept: personal space.

The study of S.M. consisted of having her indicate to the experimenter at which point she felt uncomfortable while a person would approach her from across the room. The chin-to-chin preferred distance was then compared with that of healthy, age-matched controls. S.M.’s preferred distance was significantly smaller than the preferred distance of the control subjects. To make sure this wasn’t due to some random fluke, quite a few factors that may influence personal space were controlled for, including presence or absence of eye-contact, familiarity with the person approaching, etc. All in all, there was really no situation that could make S.M. uncomfortable, even when the person would move towards her all the way to the point of touching. The weird thing is that S.M. knew she should feel uncomfortable, and she understood the concept of personal space, but she just wasn’t experiencing it.

It always amazes me to find out that something so vague, so variable (people who live in densely populated places typically have smaller personal spaces), and so elusive is actually regulated by a huge chunk of your brain. It leads me to wonder: is there a part of us, of our mind, of our personality, that isn’t already hardwired in our brain?

While S.M. gave us great insight into the biological basis of personal space, the greatest contribution of this study is possibly the ugliest journal cover image of all times:

Is the point of this story really conveyed by
a woman's face in some guy's armpit?

Reference: Personal space regulation by the human amygdala. (2009) Kennedy D.P., Glascher J., Tyszka J.M., Adolphs R. Nature Neuroscience, 12(10):1226-7.

A memorable amnesiac

2009-12-04T20:00:00.000-08:00

When little Henry Molaison was 7 years old, he fell off his bicycle. Little did he know that this event was possibly the first link in a chain of events that eventually made him the most famous patient in the history of neuroscience.

Sometime after his bicycle accident, Henry started having seizures. At first they were just little seizures. Then, when he was 16, he had his first major seizure, and it all went downhill from there. Unable to hold a job and not responding to the anticonvulsant drugs that were available, Henry and his family considered a brain operation. His surgeon, Dr. Scoville, wanted to try a new experimental type of surgery, and Henry went for it. So in 1953, when Henry was just 27 years old, he got both his medial temporal lobes removed (kind of like a lobotomy, but instead of removing the front of the brain, they removed part of the sides, just about at the level of your ears).

The operation was extremely successful: the seizures stopped! Unfortunately, this happy outcome was overshadowed by a very strange “side effect”: Henry now suffered from severe anterograde amnesia, meaning he could no longer form new memories. He also suffered from retrograde amnesia: he could not remember events from three to four days prior to the operation, and other events from a more distant past. But the anterograde amnesia was the most astonishing. You could have a conversation with Henry, then leave the room for a few minutes, and when you came back, it was as if he had never met you. Can you imagine?

Dr. Scoville called on one of his friends, Dr Penfield (that’s right, Wilder Penfield, from Montréal!) who then sent his graduate student, Brenda Milner, to study Henry. Even after all that had happened to him, Henry remained a friendly guy and was okay with being studied extensively. The knowledge we gained from Henry (known as H.M. until his death to preserve his anonymity) laid the foundations for much of what we know today about memory (which, I agree, isn’t all that much, but still). For example, prior to Henry, it was thought that memories formed all over the brain. Studying him taught us that instead it is the hippocampus, a part of the brain that was removed during his operation, that is crucial in forming memories. Studying Henry also taught us that there are multiple memory systems, a most unexpected discovery. While Henry couldn’t remember what he had for breakfast 10 minutes ago, he could learn a new task, like drawing a star while only looking at his hand in a mirror (do try this at home to understand the challenge it represents). He would get progressively better and faster at it but never remembered doing the task before. This went on until one day he drew the star and exclaimed: “This was much easier than I thought it would be!”. This lead to the notion that there are different types of memory such as declarative (conscious knowledge of facts and events) and procedural (skill-based knowledge).

The reason I’m bringing up Henry today is because this week, one year after his death, neuroscientists at UCSD started slicing up Henry’s brain in extremely thin slices. These slices will be available for scientists all over the world to look at, analyze and study. Even though he’s gone, there is no doubt we still have much to learn from the most famous neuroscience patient.

Reference: The legacy of patient H.M. for neuroscience (2009) Squire, L. R. Neuron 61(1):6-9

The reason why I write this blog

2009-11-26T16:24:00.000-08:00

Just spotted this headline in a Canadian online news aggregator:

“Severe reactions to H1N1 shot: one death probed”

Then, almost at the very end of the article:

“On the issue of serious adverse reactions to the H1N1 vaccine, Butler-Jones said the rate of anaphylactic events was about 0.32 cases for every 100,000 doses of vaccine delivered - a figure that's within the norm for mass vaccination efforts.”

I just got my shot.

Do we really need two to tango?

2009-11-26T10:15:00.000-08:00

It’s not easy finding an adequate male for reproduction. He needs to be manly, but not macho. He needs to be funny, but not immature. He needs to be romantic, but not needy. Ever wonder why we bother to go through the whole finding-a-mate dance when some species can just self-fertilize? Many animals and plants reproduce like us by outcrossing (which means two parents), but there are also a number of selfing species (meaning self-fertilizing or asexual reproduction). Oddly, when you look at the numbers, outcrossing doesn’t make a lot of sense. When selfing organisms (for example, aphids) reproduce, 100% of the offsprings can make more offsprings. When outcrossing organisms reproduce, we end up producing a variable proportion of those pesky boys (50% in the case of humans), who really are no good when it comes to having babies (except maybe for this guy). For many years, scientists have been speculating as to the evolutionary benefit of this numerical disadvantage. Recently, researchers tackled the question in a new way: by recreating evolution experimentally.

First, an important term to define: evolution. For the sake of this post, let’s use a simple definition: evolution is the change in the genetic material (genes, made from DNA) of a population of organisms from one generation to the next. Variations in the genetic material can occur in a few different ways, but a main one is mutations. Mutations can arise due to different factors: for example, a mistake can be made when the DNA is being copied during cell division, or the DNA can be damaged due to exposure to radiation or chemicals.

The study, published recently in the journal Nature, looks at a type of worm, C. elegans. Populations of this worm are composed of males and hermaphrodites, meaning this worm can reproduce both by selfing (hermaphrodites) or by outcrossing with males. The researchers were able to genetically engineer these worms to make two different populations: one that is only able to reproduce by selfing, and one that is only able to reproduce by outcrossing. This created a very valuable tool to look at how these populations deal with various evolutionary hurdles.

The researchers took both populations of worms (the selfing worms and the outcrossing worms) and exposed them to a chemical that increases the rate of mutations (a way to mimic a “sped up” evolution). They also created an environment where each population, in order to reach their food, needs to go over a worm-scale obstacle course. These two steps were important because they both impose a strong selection. Once the experiment was set-up, all the researchers did was let the worms reproduce through 50 generations and looked at which population did better.

Male readers, you’re safe! Even with all the hurdles, the outcrossing population of worms managed to maintain their fitness (or their evolutionary health) over the course of the experiment. The selfing populations of worms, however, showed a significant decline in fitness. To make sure this effect was not just a fluke, the researchers tried a different hurdle: they exposed both populations of worms to a disease-inducing bacteria. Initially, this bacteria caused an 80% mortality rate in both the outcrossing and the selfing worms. This means that the worms quickly had to learn to either avoid the bacteria or become resistant to it. This experiment confirmed what the researchers saw previously: the outcrossing population adapted rapidly to the bacteria and showed a significant increase in fitness over 40 generations, the selfing population did not manage to adapt.

This experiment may seem like a no-brainer (if we didn’t need males, they probably wouldn’t be around anymore, so they must be useful for *something*), it represents the first experimental test of the selective pressures that favor the evolution and maintenance of outcrossing. By digging into the genetics of the worms, the researchers were able to come up with two explanations for the usefulness of outcrossing. The first explanation is that outcrossing reduces the effect of harmful mutations. For example, if part of my DNA is damaged, it can be compensated for in my children if my partner’s DNA is intact. If I wasn’t mixing my DNA with someone else’s, my offspring would inevitably inherit my defective DNA, and this would weaken the population. The second reason is that in selfing organisms, mutations (good or bad) are trapped in a single genetic background. This means that a beneficial mutation can never combine with another that may have occurred in a different genetic background. Therefore, beneficial mutations can never add up or even synergize. This results in stalling evolutionary fitness.

So while it’s sometimes hard to find Mr. Dreamy, it seems like in the long run, it’s worth it.

Meet C. elegans, evolutionary tool extraordinaire

Reference: Mutation load and rapid adaptation favour outcrossing over self-fertilization. (2009) Morran LT, Parmenter MD, Phillips PC. Nature, 462(7271):350-2.

The fine print

2009-11-17T18:09:00.000-08:00

Don’t you just hate it when you sign up for a new telephone/internet/cable plan thinking the offer is such a good deal, only to find out three months later that after the “introductory period” you are actually charged way more? You typically only make that mistake once and then learn to read the pesky fine print. In science, just like in advertising, the claims and the fine print need to be scrutinized. And typically, the bolder the claim, the more attention is paid to the fine print. For example, if I’m going around boasting that I discovered that a molecular component Y of the protein X interacts with a sub-component of the peptide Z, chances are, no one will really care enough to read about it (ah, the joys of the PhD thesis). But, if I’m going around claiming that I have a vaccine that prevents AIDS, you can be sure people will read the fine print.

In September of this year, a press conference was held to announce the results of the largest AIDS-vaccine study ever conducted. The study, funded in part by the US Army and having cost a whopping $105 million, was a “first success” in the research for an AIDS vaccine, a “yes we can” moment. However, not unlike the story about the Darwininan fossil, this press conference came before the findings were published in a peer-reviewed journal. When the paper came out in October and the fine print was read by all, the excitement dropped significantly: as it turns out, many results from the study were negative, and the positive results showed that the vaccine only protects a third of the people who got get it, and only for a short while.

The actual article presents the results from three different analyses. The first analysis looked at all the participants in the study (over 16, 000 people). For this group, the vaccine had 26% efficacy. Sounds like a good start, right? The problem is that the p value for this effect was 0.08. This means that there’s an 8% chance that this effect is just due to chance. This is quite a bit over the golden scientific standard of 5%, and should be considered not significant. The second study started with the same amount of participants (16, 000), then excluded around 4000 people because they didn’t follow the protocol exactly (for example, they didn’t get the vaccine at the correct time). Logically, the results should look better. Interestingly, they don’t. In this case, the vaccine still showed a modest protective effect, but the p value was now 0.16, meaning there’s an even bigger chance this is just a fluke. Finally, the third study looked at the initial 16, 000 people minus 7 who turned out to have been infected with HIV before the study even started. In that case, the vaccine still showed a similar effect (about 30% efficacy), but this time, the p value was under the cutoff at a less-than-impressive 0.04. Phew! Something to brag about during the press conference!

The negative, statistically insignificant results combined with a few other issues (for example, the short-term protection offered by the vaccine –only about a year) have drawn a number of criticisms not necessarily of the study, but of the bragging. As for the study itself, opinions are divided. Some see it as a glimpse of hope and an encouraging start, many see it as a weak effect, mostly not statistically significant, and possibly a waste of (a lot of) money.

With all the vaccine controversies and conspiracy theories going around these days, all I have to say is throw this new one in the mix.

Image from Scientific American

Reference: Vaccination with ALVAC and AIDSVAX to Prevent HIV-1 Infection in Thailand. (2009) Rerks-Ngarm S. et al. New Engl J Med. [Epub ahead of print]

To panic or not to panic: An interview with the swine flu (part II)

2009-11-04T22:42:00.000-08:00

When the H1N1 story erupted in the media a little while back, I wrote a short Q and A post to give a scientific perspective on the topic. After that I really didn’t give much thought to the H1N1 flu. Since I don’t have a television at home and never listen to the radio, I live in a kind of media void. It’s glorious in there, let me tell you. Unfortunately, I was recently at a relative’s place and watched the news. I was shocked to see an endless stream of panic-inducing warnings and news about the H1N1, so the microbiologist in me decided to revive the topic here on Scientific Chick with the latest scientific information. So here you have it, a second exclusive interview with Mr. Swine Flu himself.

Scientific Chick: Mr. Flu, thanks for accepting to come back on Scientific Chick. How have you been? It seems you are gaining in strength and giving more severe illnesses.

Swine Flu: I’ve been well, thank you, but please notice that I’ve changed my name to H1N1. As you know, we are now in the regular flu season, so I am quite busy going around and infecting people. However, unfortunately for my plans to dominate the Earth, I have not been inducing an increasingly severe flu. It may seem so because with more people infected, the percentage of seriously ill patients becomes more apparent, but I’m still the same guy.

SC: How do you feel about our new H1N1 vaccine?

H1N1: I find it quite sad. You see, the vaccine is composed of my virus brothers, completely killed and inactivated. When talk of the vaccine started, I had a glimpse of hope that maybe, just maybe we could infect humans through the vaccine, but alas, that’s not possible. There is no chance a vaccine containing my dead relatives will give you flu.

SC: Surely with a vaccine so new, there is some chance of things going awry for us humans?

H1N1: I wish! It is often thought that because this vaccine is new, it is untested and unsafe. Unfortunately, because I am so similar to my seasonal cousin, the H1N1 vaccine has been produced the same way regular flu vaccines are produced every year. Health organizations (like the NIH) around the world have conducted rigorous clinical trials that show the vaccine is both safe and effective. It’s been licensed by all the governmental agencies and even though I tried to be very sneaky showing up unexpectedly like I did, no shortcuts were taken.

SC: At least most formulations of the vaccine contain thimerosal, so if we don’t catch you, you’ll at least have the consolation that we’ll suffer from mercury poisoning and all the associated conditions.

H1N1: Well, that would be nice, but you are grossly exaggerating. While it is tempting to blame thimerosal (a mercury-derived preservative) for a number of conditions, there is just no scientific evidence for any sort of suggestion that thimerosal is unsafe. Since the hypothesis that thimerosal causes autism broke out many years ago, scientists have been working very hard to prove or disprove that link. Interestingly, some of the best, largest, most well-controlled and unbiaised clinical studies came out of this controversy, all concluding that there is no link. The irony is that there is more mercury in a can of tuna than in any vaccine.

SC: So really, if I wanted to give up vaccines for fear of thimerosal, I’d also have to give up ahi tuna tacos? That’s just not a possibility. What about adjuvants in vaccines? How do you feel about those?

H1N1: I like adjuvants, because since they boost your immune response to the vaccine, less inactivated virus is needed per dose, which means less deaths in my family. That being said, whether you receive a vaccine with or without an adjuvant depends on where you live. In the USA, no adjuvants will be used. In Canada and some European countries, the vaccines contain adjuvants. Adjuvants are not new, and they also have a good safety track record. I hear a lot of concerns about squalene being used as an adjuvant, but you find squalene in olive oil.

SC: I hear a lot of discussions about Guillain-Barré Syndrome. Should we worry?

H1N1: Guillain-Barré Syndrome (GBS) occurs when your body’s immune system turns against its own nerve cells, and this leads to paralysis. If caught early enough, it can be reversed. And yes, vaccines are among the many risk factor for GBS, at a rate of about one in a million. Guess what else is a risk factor for GBS? Me! The nasty ol’ flu. Pick your odds.

SC: Are you hiding in my tasty pork tenderloin and bacon?

H1N1: No. You can only catch me through coughing or sneezing droplets from someone who is already infected, or through touching something contaminated and then letting your hands get to your face before they get to a sink to be washed.

SC: Should I wear a mask if I want to avoid you?

H1N1: Also a no. The Public Health Agency of Canada doesn’t recommend wearing surgical masks to avoid catching me. While this may sound counter-intuitive, there is actually scientific evidence that shows that this is not an effective way to prevent flu transmission in the general public. People tend to use the masks incorrectly, contaminate themselves when putting the mask on or taking it off, and increase their risk of infection by trapping me near their mouth. That would really make it too easy for me.

SC: H1N1, thank you. While it was lovely having you, I hope this was the last time.

H1N1: Thank you. Did you want to come closer? I have a secret for you…

This plush H1N1 virus is safe to cuddle with!

References:
Autism and vaccination-the current evidence. (2009) Miller L, Reynolds J. J Spec Pediatr Nurs. 14(3):166-72.

A Novel Influenza A (H1N1) Vaccine in Various Age Groups. (2009) Zhu FC et al. N Engl J Med. Oct 21.

The H1N1 flu pandemic. What you need to know. (2009)
Mayo Clin Womens Healthsource. (11):4-5.

The Centre for Disease Control and Prevention – www.cdc.gov Public Health Agency of Canada – www.publichealth.gc.ca

A new kind of mind control

2009-10-25T15:17:00.000-07:00

Remember subliminal messages? Those images supposedly flashing too quick for your mind to register, but still managing to convince you to drink more soft drinks, eat more fries, buy a luxury car? While those days may not be over yet, new forms of mind control (albeit more biological than psychological) are emerging thanks to the tiniest of creatures, the bacteria.

A friend of mine, Cal, recently alerted me to an interesting article about optogenetics. If you’re not familiar with the word, that’s because it’s very new, and it essentially means playing with light and genetics at the same time. It’s all the rage in neuroscience right now and articles such as the one I’ll be describing in this post are popping up every week.

It all starts with a tiny little pump called halorhodopsin found in bacteria. This pump sits at the surface of cells and pumps chloride ions from outside the cell to the inside (table salt is sodium chloride - same chloride). Cells use chloride for different reasons, but this pump can be especially relevant for brain cells (called neurons). Neurons pass information to one another through electric currents. And it just so happens that chloride ions are charged negatively. That means that if many chloride ions accumulate inside a neuron, the cell becomes increasingly charged negatively, making it harder to reach the positive threshold it needs to pass currents to other neurons.

Other types of chloride pumps already exist in your brain cells, but almost nobody makes a fuss about those. So how is halorhodopsin different? This is where the “opto” from “optogenetics” comes in. This particular pump is activated by light. This means that if neurons have this special pump, you can control whether they are active or not just by flashing a light onto them.

In a recent paper published in PNAS, the researchers genetically engineered zebrafish so that their brain cells expressed the special light-activated chloride pump. The researchers then recorded the electrical signals generated by the brain cells (they look like spikes, much like what you would see on an EEG). I don’t know if you can imagine what kind of feat that represents, but I’d like to make a motion to modernize the saying “like finding a needle in a haystack” to “like poking an electrode into a brain cell of a live fish”. Once they knew what the signals looked like in normal conditions, they shone the light on the fish*, and amazingly, all the brain cells went quiet. It worked! The light activated the pump, negatively charged chloride ions accumulated in the cells and made it too difficult to reach the spiking threshold.

The black lines are the current spikes that normally occur when brain cells transmit information. The yellow section is when the researchers shone the light: no more spikes.

Now a fish doesn’t have that many brain cells to start with, and since it spends most of its life moving it’s pretty safe to assume that a large portion of the fish’s brainpower is devoted to swimming. The researchers thought they had a pretty cool tool to test this, and so they did. They put a bunch of genetically-engineered zebrafish in a dish, watched them swim around for a bit, and then shone a light on them*. Sure enough, the fish stopped moving and lost coordination. I realize we’re talking about lousy, bottom-of-the-food-chain fish here, but think about it: *that’s* mind control.

The article continues to great lengths, going into details about what specific part of the brain controls the swimming behavior and describing control experiments that confirm that this isn’t a fluke (i.e. the fish aren’t just spooked by the light). All things considered, it’s a very elegant example of how to use optogenetics to better understand the brain. And the relevance of these advances lies in the increased understanding of not only the brain but also diseases of the brain. Recently, these new techniques used in animal research gave us important insights into Parkinson’s disease.

What about using these tools as ways not only to understand disease, but also to treat them? What if we made our own brain cells express this special pump so we could use light to activate or inhibit different areas of our brains? While this may seem like science fiction right now, don’t be so sure. I attended a talk on optogenetics recently, and the researcher firmly believed that this emerging field of neuroscience would eventually cure blindness. In the meantime, let’s see if you can think of all the ethical questions this would raise…

* For these experiments, the researchers used fish in the larvae stage. The skin of the fish at that point is transparent, and this allows the light to reach the brain cells.

This little zebrafish is doing his best to contribute to science.

Reference: Optical control of zebrafish behavior with halorhodopsin. (2009) Arrenberg, A.B., Del Bene, F., Baier, H. Proc Natl Acad Sci USA, 106(42):17968-73.

Yet another reason for a good night's sleep

2009-10-12T16:01:00.000-07:00

How much do you sleep at night?

If you’re like most of the people I know, the answer is “not enough”. There’s a reason Starbucks coffee shops are popping up literally meters away from one another. Everybody has a reason to be sleep-deprived: new kid, big job, World of Warcraft, etc. So what if we’re cutting the night short a few hours? Other than the need for an overpriced coffee (or two, or three), it should be just fine, right?

Maybe not, if you believe the latest research on sleep and Alzheimer’s disease.

Alzheimer’s disease, a debilitating form of memory loss and cognitive decline, is the most common form of dementia. It is thought to be caused at least in part by amyloid beta (A-beta), a peptide (short protein). Your brain cells (neurons) normally make some A-beta. The problem that arises with Alzheimer’s disease is that neurons make too much A-beta, and these molecules aggregate together in chunks. It’s those A-beta chunks that are toxic, and their formation is concentration-dependent, which means the more A-beta you have floating around, the higher the probability of toxic chunks forming.

The recent article published in the journal Science looks at levels of A-beta in the brains of normal mice and in the brains of a mouse model of Alzheimer’s disease. The researchers studied the mice when they were 3 months of age, so well before big deposits and chunks of A-beta start occurring.

The interesting finding of this study is that the levels of A-beta in the brains of both types of mice were significantly correlated with the amount of time they spent awake. More time spent awake lead to more A-beta. Because the control, normal mice also exhibited this relationship, it means that it is not linked to the disease. It’s just a normal fluctuation of A-beta levels linked to the sleep-wake cycle. To be certain this link was relevant for human physiology, they also tested this in healthy humans and, sure enough, they observed the same correlation.

Not surprisingly, when the researchers proceeded to sleep-deprive the mice, they showed an even larger increase in A-beta levels. This increase was also observed when the mice were given a drug that promotes wakefulness (don’t extrapolate this to coffee just yet… But maybe keep it in mind…). The study also points out that the Alzheimer mice who are sleep-deprived showed much greater numbers of A-beta chunks (the toxic stuff) compared with non sleep-deprived mice.

If you come to Scientific Chick for relevant findings, this one is for you. The study essentially implies that optimizing sleep time could potentially inhibit the formation of chunks of toxic A-beta and slow the progression of Alzheimer’s disease.

We all know that Alzheimer’s disease is terrible, and that sleeping in is glorious. Let’s just put two and two together, shall we? Easier said than done, I know…

Mr. Minou gave up on caloric restriction but approves of this new approach to ward off age-related diseases.

Reference : Amyloid-{beta} dynamics are regulated by orexin and the sleep-wake cycle. (2009) Kang JE, Lim MM, Bateman RJ, Lee JJ, Smyth LP, Cirrito JR, Fujiki N, Nishino S, Holtzman DM. Science Sep 24. [Epub ahead of print]

Yet another reason to exercise

2009-09-28T21:33:00.000-07:00

Last weekend I went for a bike ride and when I reached the bottom of the big hill leading to UBC, I noticed quite a bit of activity going on. I didn't pay too much attention at first, but once I was booting up the hill, I was passed by several senior citizens on top-notch bicycles and I started getting curious. I asked a person who seemed to volunteer for the event what was going on. As it turns out, I was cycling right in the middle of the BC Seniors Games. Now for those of you who might not know me, my thesis research has to do with aging and the brain and nothing warms my heart like witnessing older adults and seniors exercising. I had just hit the jackpot!

The reason I'm so enthralled to see seniors exercise is because it is the single best thing they can do to preserve their brains. Today's paper highlights recent research done in California that shows just that.

First, a bit of background. You have a gene called APOE (mice also have it). It comes in 3 flavors, and each person only has one of the three: APOE2 (not important for today’s article), APOE3 and APOE4. If you got lucky and scored the APOE3 kind, all is well. If you happen to be in the 20-25% of the population who has the APOE4 kind, you may be in trouble: APOE4 is a known risk factor for Alzheimer's disease. Does it mean you'll for sure get Alzheimer’s disease? No, but you are 10 to 30 times more at risk of developing Alzheimer's disease if you carry the APOE4 gene.

In this paper, researchers compared old APOE3 (normal) and APOE4 (at risk for dementia) mice. In general, aged APOE4 mice experience cognitive decline faster and earlier than APOE3 mice. The researchers were interested in studying whether exercise (running on a mouse wheel!) had any effect on this cognitive decline.

The researchers used cognitive tasks that rely on a part of the brain that's important for memory, the hippocampus. One of the tasks, called place recognition, involves putting a mouse in an arena with two objects. The mouse is then removed from the arena, one object is moved, and the mouse is put back in the arena. Presumably, a normal mouse will then spend more time exploring the object in the new location. For this task, the aged APOE4 mice were initially impaired compared with the APOE3 mice. This means that during the second trial of the task, they tended to explore both objects for similar amounts of time, instead of spending more time on the object at the new location. This result suggests that the APOE4 were unable to remember the initial object locations well. The good news? Mice who exercised did significantly better at this task. Interestingly, this was valid for both APOE3 and APOE4 mice. Even more interestingly, exercise improved the scores of both types of mice for all the tasks that tested the hippocampus.

What's going on in the brains of these exercising mice? It is thought that exercise increases the levels of a protein called BDNF (for Brain-Derived Neurotrophic Factor). BDNF regulates many important functions in the brain, including the making of new neurons and the making of new connections between neurons, and these effects are thought to be important for memory.

Regular readers of Scientific Chick know not to get too excited when I report about animal studies. Well, I'm happy to add that the results that were observed in those mice were also observed in humans. In fact, there are countless human studies out there that confirm that physical activity is a powerful way to improve and maintain your cognitive abilities.

When I try to urge certain people to exercise (you know who you are), I almost always hear the same excuse: “Well, my uncle so-and-so never got off his couch and he lived to be 100!” In some cases, heredity can be on your side, that's true. But genetics can be quite the lottery, and it's important to keep in mind that several forms of cognitive decline, including the most common form of Alzheimer's (called “sporadic” in scientific lingo) are not hereditary.

So to all my older readers out there, I'll see you on the road at next year's BC Seniors Games. And if you're not ready for cycling, there's always the cribbage category.

Winners from this year's BC Seniors Games, cycling event. This could be you!

Reference: Exercise improves cognition and hippocampal plasticity in APOE epsilon4 mice. (2009) Nichol K, Deeny SP, Seif J, Camaclang K, Cotman CW. Alzheimers Dement. 5(4):287-94.

Children see, children do, but monkeys know better

2009-09-16T19:38:00.000-07:00

I usually like to blog about recent articles, and I try to limit myself to papers published in the last 2-3 years. I’m going to make an exception this time and write about a publication from way back (2005). By scientific standards, 5 years ago is literally ancient (kind of like computer standards), but bear with me, this is going to be worth it (unlike a 5-year old computer).

Researchers from the UK were interested in finding out more about learning patterns, and about how our learning patterns differ from one of our close cousins, the chimpanzee. To test this, they subjected human children 2-4 years old and chimpanzees 2-6 years old to a simple task: retrieving a treat from a box.

In the first set of experiments, the researchers gave the chimps an opaque black box, and showed them how to open it to retrieve a treat inside. This wasn’t a simple pull-the-top-off kind of box, though. The box seemingly could only be opened following a series of specific steps: pulling a bolt, putting a stick in a hole, opening a door, etc. Chimps are quick-learners, though, and by imitating the researcher, they were soon able to retrieve the treat, no problem.

How well did the human children to at the same task? Quite well. They too were able to learn how to retrieve the treat from the black box by copying all the steps the researcher showed them. It would have been slightly worrying otherwise. I mean, we’ve taken over the world, right? Surely we can teach our young how to open a silly box, right?

The second set of experiments was almost exactly the same as the first one, except this time the box was made out of clear plastic instead of being opaque. The researchers went through the same process of teaching the chimps how to open the box. But there’s a catch: with a transparent box, it became very obvious that most of the steps supposedly needed to open the box were irrelevant. All you had to do was open the door. Chimpanzees, our closest living relative, are quite smart, and dropped all the unnecessary steps. They didn’t bother with the bolt and the stick and all those irrelevant actions: they went straight for the door and grabbed the treat.

When it was time for the children to be tested on the clear box, they too got shown how to open it by the researchers, including all the unnecessary steps. And when it was their turn to do it, they obviously…

Started pulling the bolt, putting the stick in the hole, etc.

Wait, what?

Did I get that wrong? I must have messed up the subjects… Wait… Nope. Those monkeys just fed us a piece of humble pie.

The researchers suggest that in the case of this study, the difference between how the chimps and how the children perform the task may have to do with a different focus of attention. Children pay more attention to the process of opening the box and the actions of the researcher, while chimps have their eyes on the prize, and focus more on the goal rather than the process. The researchers conclude by saying that imitation may be a human strategy that is often employed at the expense of efficiency.

The interesting thing about this article is that some news reports and descriptions of this experiment in magazines ended with a conclusion that more or less stipulated that our children imitated even the irrelevant steps of the task because that was the smarter thing to do, twisting the story around to make it sound like humans were superior to the chimpanzees in some way. Start your debate engines, but my opinion is that we should stop considering ourselves so superior. The results of this study are pretty straightforward. Do we really have to come up with a twisted interpretation of the results to make us sound like the winners? I would love it if we could just look at this experiment and say, hey, what do you know, we can learn something from the chimps.

Eyes on the prize, people. Eyes on the prize.

This monkey is laughing at you.

Reference: Causal knowledge and imitation/emulation switching in chimpanzees (Pan troglodytes) and children (Homo sapiens). (2005) Horner V., Whiten A. Anim Cogn 8(3):164-81.

Conquering cancer one virus at a time

2009-09-01T22:25:00.000-07:00

Back in June, I participated in The Ride to Conquer Cancer, a 2-day bike ride between Vancouver and Seattle to raise money for BC Cancer. It was an extremely moving, positive and rewarding experience. It also gave me a chance to eat a piece of humble pie when 70 year-old cancer survivors (identified by flags on their bikes, adding to their wind resistance) would pass me going up the hill. The good news is that at the end of the 272 km, I was still smiling:

The bad news is that I didn’t conquer cancer.

Cancer research is well-funded, popular, and has been around for quite some time. So why can’t we get rid of this disease? The problem with cancer is that it’s tremendously difficult to target. Unlike cells infected by viruses and bacteria, cancer cells don’t display any obvious flags that something is wrong with them, which makes them challenging to distinguish from healthy cells. Therefore, most treatments for cancer involve killing a number of healthy cells, and that’s just not ideal.

Progress is being made, though, as a recent publication in the journal PNAS suggests. In this paper, a collaboration between researchers in California and in Japan lead to the discovery of a new way of identifying tumors for easier removal. They rely on an unlikely ally: viruses.

The researchers genetically engineered a special type of virus to carry a gene that codes for a fluorescent protein, GFP (for Green Fluorescent Protein - as simple as that!). If all the cells in your body were to be infected by that virus, you would glow (kind of like the famous puppy). While this would immediately up your popularity ranking at any science party, it doesn’t do much for treating cancer. So the researchers took it one step further and engineered the virus so that it would only express the fluorescent protein (make the cell glow) if the cell has an active telomerase. Telomerase in an enzyme involved in the replication of cells. If the telomerase enzyme is active when it shouldn’t be, it can cause cells to divide indefinitely, creating tumors. In fact, it is thought that over 90% of human tumors show telomerase activation. To sum it up, cells are infected with a virus that has a gene for a fluorescent protein, but only cancerous cells have an active telomerase, the switch that turns on the fluorescence. The result? Glowing tumors.

The benefits of these findings are two-fold. First, glowing tumors mean that surgeons can precisely remove the tumors without having to also remove a chunk of healthy tissue “just to make sure”. Second, tumors have a nasty habit of hitching a ride in your lymphatic system or your blood and disseminate throughout your body, making it very difficult to take out every little bit of sprouting tumor. With this innovation, all those little disseminated tumors can be identified and removed. Those two benefits together could greatly reduce the chance of a relapse, an important consideration when treating cancer. The researchers tested their mutant virus in two different types of animal models of cancer (colon and lung) with great success. While I’m usually worried at the prospect of glowing body parts, this research could have a big impact on cancer treatment.

If I want to give myself a chance to conquer cancer in 2010, I should probably spend less time on the computer and more time on the bike...

Glowing tumors

Reference: In vivo internal tumor illumination by telomerase-dependent adenoviral GFP for precise surgical navigation. (2009) Kishimotoa, H., Zhaoa, M., Hayashia, K., Uratad, Y., Tanakac, N., Fujiwarac, T., Penmanf, S., and Hoffmana, R.M. Proc Natl Acad Sci 106(34):14514-7.

Dating advice courtesy of your friendly neighborhood monkey

2009-08-26T11:56:00.000-07:00

Dating advice websites abound with many different kinds of advice: good advice (don’t pick your nose), strange advice (date according to your blood type), not so good advice (Leos dating Leos need to hire domestic helpers). One suggestion that seems to pop up quite frequently is to mimic the body language of your date. He picks up his drink for a sip, you pick up yours. He strokes his hair, you stroke yours. He picks his nose, you pick your nose. You get the idea. As it turns out, in a social interaction context, we humans tend to unintentionally imitate what others are doing. Think of this as a team-building exercise: it’s a behavior that helps establish rapport, empathy and other fuzzy feelings toward each other.

A recent publication in the journal Science shows that behavior matching leading to increased rapport is not exclusive to humans, and it can also occur between different species.

The study looks at capuchin monkeys, a very social primate species. During the experiments, the monkey is given a ball to play with. On either side of the monkey’s cage stands an experimenter. One experimenter is mimicking what the monkey is doing with the ball (poking it, pounding it against the wall, trying to eat it… Mmmmm…), while the other experimenter is also playing with the ball, but not mimicking the monkey. The researchers show that not only do the monkeys look at the imitators more, they also spend more time hanging out close to the imitators and prefer to interact with the imitators in a food exchange game. The authors also did an important series of control experiments to show that these effects were not due to the monkeys perceiving more attention from the imitators.

So why are we subconsciously hard-wired to constantly be playing Simon Says? It is thought that the positive feelings resulting from behavior matching played an important role in human evolution by leading to higher levels of tolerance and by preventing aggressive behavior (to put it simply, by preventing us from beating each other up). The same principle probably applies to primates, and the empathic connection that results from imitation may explain the altruistic tendencies observed in the behavior of capuchin monkeys.

Next time you catch yourself winking back at someone who winked at you, or laughing at a joke you didn’t get because everyone else is laughing, keep in mind it’s for the greater good. After all, even monkeys know that imitation is the sincerest form of flattery.

Scientific Chick readers applying their new found knowledge
(Image from Loldogs)

Reference: Capuchin monkeys display affiliation toward humans who imitate them. (2009) Paukner, A., Suomi, S.J., Visalberghi, E., Ferrari, P.F. Science 325:880-882.

Need some real estate advice? Ask an ant.

2009-08-13T22:47:00.000-07:00

What does it mean to be rational?

In a biological context, rationality means that when animals (including humans) are making a decision, they choose the option that maximizes their fitness benefit. For example: my cat, Mr. Minou, prefers to eat canned food rather than grass. Canned food provides him with more nutrients, more protein, and more energy than grass: it has a fitness benefit for Mr. Minou. Even if he is presented with a third option, say, dry cat kibbles, Mr. Minou stills prefers canned food, because it still has the highest fitness benefit (and, obviously, kibbles taste gross).

Pretty straightforward so far. So, being the advanced species we are, humans must be rational beings, right?

Wrong.

Here is another example. Let’s say you’re shopping for a new house. You have two equally important criteria for your new house: it must have big windows to get lots of natural light in, and it must have a big garage to store all your stuff. There are two houses on the market. House A has big windows but a small garage. House B has a big garage but small windows. Rationally, humans in this position have a 50% chance of picking either house.

Suddenly, a third house is made available on the market. House C has big windows, but NO garage. In a situation like this, humans overwhelmingly put rationality aside and shift their pick to house A with the large windows but the small garage, because the perceived value of house A increased when comparing it with other available houses. However, houses A and B have unchanged value!

The reason for this shift is that as decision-makers, we don’t assign absolute values to options, we assign relative values. We like to compare. And comparing can be misleading.

Recently, two American researchers wondered about the rationality of collective animals, such as ants. The researchers figured that just as choices we make result from the complex interactions of many brain cells, the decisions that an ant colony makes might similarly stem from a complex network of interacting insect. Ant societies act as unitary decision-makers, jointly deciding on things like a single travel direction, or a nest site. The researchers decided to take advantage of the ants’ nest-seeking strategies to test their rationality.

The ants in the study live in natural holes like hollow branches, and are able to emigrate to a new nest if their current nest is damaged. Colonies seeking a new nest reach consensus on the better site among the new options based on entrance size, cavity dimensions, interior light level, etc. The way a colony reaches consensus is fascinating: a few scout ants head out to assess the quality of potential homes. When a scout finds a potential new home, it leaves to recruit more scouts, who will then recruit more scouts, and so on. The strength of this technique lies in the key fact that the higher the quality of the nest an ant finds, the faster it will recruit other ants. Eventually, a threshold of recruiting is reached, and non-scout ants are recruited and eventually the entire ant colony is moved.

The researchers first established that ant colonies prefer nests that have small openings and low inside light levels. They then assessed the susceptibility of ant colonies to irrationality by comparing the colonies’ preference for new nests with different attributes in a very similar way to my house example: nest A has a dim interior but a large entrance size, and nest B had a brighter interior but a small entrance size. In this case, the ant colonies showed no preference for either site, which is very rational of them.

The researchers then added one of two decoy nests. Decoy nest A2 was just as dim as nest A, but had an even larger entrance diameter. Decoy nest B2 had the same entrance diameter as B but was even brighter than B. In summary, each decoy nest had a good feature equivalent to that of A or B, and the other feature was worse.

Well, the study suggests that we should turn to ants for real estate advice: the presence of either decoy did not affect the proportion of colonies choosing A or B. This means that even with the decoy, the ant colonies recognized that A and B had equal fitness values, and that the option of the decoy did not change the fitness values of the original nest sites.

So what is the ants’ secret for being so rational? The most plausible explanation is that for the most part, each scout ant only visits one site. If it’s good, it recruits, and if it’s crummy, it moves on. No comparing with the one next door. In this case, the fact that individuals in the decision-making strategy lack either the opportunity or the ability to compare all the options offers some protection against irrational, fitness-reducing errors.

Is this relevant for us, other than the piece of humble pie we must eat when realizing that ants can be more rational than we are? Well, when faced with a decision, it can be helpful to remember to evaluate each option for its absolute value, and not its relative value.

Mr. Minou himself occasionally forgoes rationality and chooses to eat grass. I suspect he only does it for the pleasure of watching me wash puke from the floor afterwards. Maybe in some twisted way, making sure I clean up after him confers him some kind of fitness benefit…

Mr. Minou being irrational

Reference: Rationality in collective decision-making by ant colonies. Edwards SC, Pratt SC. Proc Biol Sci (2009) Jul 22 [Epub ahead of print]

Aging is optional! Take two of these pills and call me in the morning.

2009-08-04T21:48:00.000-07:00

We’re getting older.

Not exactly a surprise, I know, but I didn’t mean you and me are getting older. I meant we are getting older, as a population. In 2001, one Canadian in eight was aged 65 or older. By 2026, one in five will be 65 or older. So what should we do with an increasingly aged population? Well, this being a North American consumer culture, the sensible thing to do is try to sell them stuff. I mean, think of the size of the market!

Right now, a significant amount of research is being devoted to aging. The main focus is to try to slow down aging (partly by developing marketable supplements and such). As some of you might know, even my own PhD thesis project is on how to slow aging in the brain. Loyal readers of ScientificChick.com will also be aware of recent articles about caloric restriction, a potential way to keep old age at bay. Thankfully, a recent publication in Nature suggests a much easier way to live longer: forget starvation, all you have to do is pop a(nother) pill!

In this article, American researchers show that mice that eat rapamycin supplements starting at 600 days of age (senior citizens in mouse years) live longer, up to 14% longer for females and 9% longer for males. What’s more, rapamycin supplementation did not change the causes of death. The researchers propose that this drug could be acting by postponing death from cancer, by delaying mechanisms of aging, or both.

How does rapamycin work? Well, as you might expect with a miracle drug like this, we’re not really sure. Rapamycin is an inhibitor of a pathway called mTOR. The mTOR pathway has many functions in your cells, like coordinating the survival response arising when there are changes in nutrient and energy availability, and dealing with potentially deadly stresses, such as oxidative stress (the kind of stress fancy juices packed with antioxidants are supposed to battle). Since the mTOR pathway acts kind of like a central sensor of cell health, it makes sense that it would be implicated in regulating lifespan. Exactly how rapamycin is working its magic, though, is probably what the researchers are trying to figure out for their next article.

Could the increase in longevity following rapamycin supplementation be related to the effects seen with caloric restriction (the “eat less, live longer” paradigm)? Well, mice on rapamycin show no change in body weight, so we know the drug is not acting through a caloric restriction mechanism. The converse, however, may be true: it is thought that the beneficial effects of diet restriction may also be due to an inhibition of the mTOR pathway.

So don’t throw out the double-stuffed Oreos just yet, but don’t eat half the box either: rapamycin pills for humans won’t be on the shelves tomorrow. While mTOR inhibitors are currently being used to treat a few conditions (transplant rejection and some cancers, for example), there’s still a lot of work to do to tease out all the potential interactions and side effects.

Longevity in pill form? To me, it would feel like cheating the system. And if there’s one thing we keep learning over and over in the life sciences, it’s that trying to cheat Mother Nature always has some unintended consequences.

A great illustration of the aging mouse by TS Rogers

Reference: Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Harrison DE, Strong R, Sharp ZD, Nelson JF, Astle CM, Flurkey K, Nadon NL, Wilkinson JE, Frenkel K, Carter CS, Pahor M, Javors MA, Fernandez E, Miller RA. Nature 2009 16;460(7253):392-5.

The fountain of youth revisited

2009-07-26T22:00:00.000-07:00

Not too long ago, I wrote about my love of brownies and an article on caloric restriction. I wasn’t really planning on bringing up this topic again so soon but a recent Science paper on caloric restriction in monkeys is getting so much media attention that I just had to throw in my two cents.

In the article, a group of American researchers study control and calorie-restricted (30%) monkeys over 20 years. What they show is that the calorie-restricted monkeys have a reduced incidence of age-associated death, diabetes, cancer, cardiovascular disease and brain atrophy compared to the control monkeys. From the sounds of it, we can stop looking for the fountain of youth (it’s in Florida, by the way). The media absolutely loves this story, and news reports and videos are quick to claim that caloric restriction increases longevity in our closest cousins, and it must be good for us as well.

First, a disclaimer from the friendly folks at ScientificChick.com: In the recent years, solid, convincing and well-controlled studies have shown some benefits of caloric restriction in various types of experimental subjects ranging from yeasts to humans. I won’t go back into the pros and cons of caloric restriction in this post. There is good evidence out there that it can be beneficial in some instances, and also good evidence that it’s not for everyone.That being said, I believe there are many problems with this particular Science paper on caloric restriction.

In my opinion, a major issue with the findings is that the control monkeys (the ones not on caloric restriction) are fed ad libitum (meaning they can eat as much as they want). You might be able to guess the problem already, but let me give you an example just in case: I have a cat, and if I were to offer him a constant supply of what seems to me like gross, bland cat food, he would keep eating it until he would slip in a food coma. I think this goes for most species, including us (ever heard of the candy jar experiment?). Therefore, it’s very hard to judge if monkeys who eat as much as they want are eating the amount of food they should naturally be eating. Chances are they are eating more (breakfast, lunch and dinner are not served at regular hours in the wild). And this is particularly relevant because eating too much (or obesity) happens to be an important risk factor for all the diseases the study looks at (diabetes, cardiovascular problems, cancer, etc.).

Another issue with the article is that few of the findings show a statistically significant difference between the control and the calorie restricted groups, even though the researchers are studying a reasonably large number of monkeys. When your results are statistically significant, it means that what you are observing is unlikely to have occurred by chance. This concept is a hallmark of solid and convincing science findings and the media should be very careful not to hype findings that aren’t statistically significant. In addition, almost every single news article on this publication claimed that caloric restriction had an effect on longevity. While the study looks at age-associated diseases, the longevity (or life expectancy) parameter is not assessed at all (though the researchers do mention they plan on assessing this in the future).

Lastly, and perhaps most disturbing from my scientist point of view, the lead researcher in this study happens to be co-founder and member of the board of LifeGen Technologies, a company focusing on the impact of dietary interventions on the aging process. A little research on this company made it very clear to me that the more people buy this whole caloric restriction business, the more money the company makes. If that’s not a conflict of interest, I don’t know what is.

Now if you’ll excuse me, a new cupcake store just opened across from my building, and I must significantly increase the quality of my life by going over and eating a cupcake.

My cat, Mr Minou, is not a fan of caloric restriction.

Reference: Caloric restriction delays disease onset and mortality in rhesus monkeys. Colman RJ, Anderson RM, Johnson SC, Kastman EK, Kosmatka KJ, Beasley TM, Allison DB, Cruzen C, Simmons HA, Kemnitz JW, Weindruch R. Science. 2009 Jul 10;325(5937):201-4.

Who wants a memory booster?

2009-07-05T13:11:00.000-07:00

One of my first posts was about erasing memories. That may be useful if you suffer from post-traumatic stress disorder or if you just sat through the last installment of the Transformers movies, however, I can think of more people who would benefit from memory enhancement rather than memory erasure. One recent publication in Science hints that this may be just around the corner.

First, how do we know what animals remember? One way to test memory in rats is by using object recognition. You present the rat with two identical objects and let the animal explore them for a few minutes. Then you replace one of the objects with a new object, and typically, the rat will spend more time exploring the new object than the old one (presumably because the rat remembers the old one). By testing rat visual memory performance using this simple paradigm, the researchers established that rats were able to retain information about an object for up to 45 minutes, but after 60 minutes the objects were forgotten and treated as new unknowns. The researchers then injected a special protein in a specific part of the rat’s visual cortex, a part of the brain that is important for processing visual information. Following the injection, the rats were tested again for object recognition, and low and behold, the rats were now able to remember object information for longer than 45 minutes. How much longer? 60 minutes? 100 minutes? 1000 minutes? Actually it was 14 months. The rats went from being able to remember an object for 45 minutes to being able to remember it for 14 months.

Now the relevance of this article mainly lies in the identification of the function of a part of the visual cortex. To confirm their findings, the researchers took control rats (that didn’t receive the special drug) and inactivated the brain cells in the section of interest of the visual cortex (ok, they destroyed them). Those rats couldn’t remember objects at all. Interestingly, the researchers also showed that if you inject the special drug, then introduce a new object, and then destroy the brain cells, the rats will still remember the object for a long time, meaning this specific region of the visual cortex is important for making new memories but not for storing those memories. These are all important findings that further our understanding of visual memory.

But 14 months?? Surely this kind of memory enhancement won’t go unnoticed. The researchers claim that “the role of the RGS-14 protein in the enhancement of visual memory makes this protein an important pharmaceutical target for the treatment of (...) memory defects as well as for boosting the memory capacity”. That being said, I don’t think this drug will hit the shelves anytime soon. First, in the article, the researchers have to inject it directly into a specific brain region, and I certainly wouldn’t volunteer for that. Second, the drug affects an important, ubiquitous protein with many functions, and it’ll be a while before we tease out all the potential pitfalls of toying with something like that.

Regardless, with the aging population and the ever-increasing need (or want?) for maximum brain performance, there is a huge market for memory enhancers and the race is on to develop the first one. Now is the time to ask and answer all the ethical questions that surround this issue. If you had access to memory enhancers, would you use them? What if they were really expensive? What if they had detrimental side effects? What if they had detrimental side effects and everyone in school or work used them to enhance their performance relative to people who don’t use them (Tour de France, anyone?)?

Memory enhancers: useful drugs or can of worms?

The object recognition task

Reference: Role of layer 6 of V2 visual cortex in object-recognition memory. Lopez-Aranda, M.F., Lopez-Tellez, J.F., Navarro-Lobato, I., Masmudi-Martin, M., Gutierrez, A., Khan, Z.U. Science 2009 325:87-89.

The trouble with the tube (part 2 of 2)

2009-06-28T14:57:00.000-07:00

There is a wealth of literature on the negative impacts of television watching on developing children, and in my last post, I wrote about how certain types of television programs may lead to attentional problems later in life. I myself blame countless hours spent watching the Fresh Prince of Bel-Air for my affinity for men who can dance. To balance the argument, can television be good for infants and children? Kids certainly claim they need the extra channels for “educational” purposes! There is overwhelming evidence that certain programs like Sesame Street have many educational benefits. It’s been shown that these programs increase school readiness, and improve vocabulary scores in children who start watching at 3 years old or older. Nowadays, though, videos and DVDs like the Baby Einstein products are being marketed for much younger children, as young as one month old in some instances. Even though the American Academy of Pediatrics favors zero exposure to television for very young children, children under two spend on average one to two hours a day in front of the tube. Who could blame them (or their parents) when media producers claim that their videos and DVDs have developmental benefits? Who wouldn’t want their child to become the next Einstein?

However exciting the claims may be, it remains unclear whether children under two can actually benefit from the information from a television screen. A 2007 study showed that children who watched more baby videos and DVDs knew fewer words than those who didn’t. In order to examine the relationship between infant DVDs and language, researchers from California studied the language skills of two groups of children 12 to 15 months old. The first group (called the control group) just went about their daily routines. The second group (the DVD group) was instructed to watch the DVD Baby Wordsworth (a DVD from the Baby Einstein company that highlights vocabulary words) at multiple time points for the duration of the study. Before and after the study, the children’s vocabulary was evaluated using a standard test.

Surprisingly, the results of the study show no significant differences between the control group and the DVD group on language skills at any time point (either before or after the study). I see this as good news, because while watching the DVD isn’t helping the children learn new words, it’s not keeping them from learning either. In addition to these results, the researchers were insightful enough to study other predictors (predictors are essentially other variables that may affect the outcome of the study). Interestingly (but not surprisingly), the amount of time a child was read to was the best predictor of a higher vocabulary score. And, since by now most of my readers realize the importance of controls, this relationship is true even when controlling for age, gender, income, parent education and development level.

Why doesn’t the DVD help the children learn new words? There are many potential explanations for this. Maybe the DVD is just not that educational. Maybe the DVD just doesn’t attract the infant’s attention. What’s even more likely is that young children just can’t process information from the television.

My dad used to read me a story every single night, and this went on well after I was able to read by myself. I still have, and will cherish forever, my favourite book of tales. I’m really grateful for all the hours my parents spent reading to me. Maybe it counteracted all the stupidity I was exposed to during my Fresh Prince phase.

Best book ever!

Reference: Just a talking book? Word learning from watching baby videos. Robb, M.B., Richert, R.A., Wartella, E.A. British Journal of Developmental Psychology 2009 27(1):27-45.

The trouble with the tube (part 1 of 2)

2009-06-14T20:32:00.000-07:00

I don’t have a television. In my tiny apartment, there is no room for a television, and in my busy life, there really is no time for a television either. In addition, I just can’t stand commercials. Honestly, dancing monkeys won’t convince me to invest my money in a given institution.

It’s no surprise then that I’m usually pleased when I come across scientific evidence that television is bad for you, and I have yet to come across scientific evidence that television is actually good for anyone. I recently found a series of papers on the effects of television viewing in children. Since most households I know have a television in them, I think that makes it relevant science, so I’m dedicating a two-part blog post on those articles. In today’s article, researchers from Seattle, Washington study the relationship between what kind of television shows children watch and attentional problems later in life (attentional problems include but are not restricted to attention-deficit hyperactivity disorder).

In the study, hundreds of parents (and other caregivers) of children 0 to 5 years old were questioned on how much television and what type of shows the children watched. Each household was followed up on 5 years later (so that the children were 5 to 10 years old) and asked about the behaviour of the children. For the purpose of the study, the children were separated into two groups: 0 to 3 years old, and 4-5 years old. Also for the purpose of the study, the types of television shows and movies were separated into 3 categories: educational (for example, Sesame Street), nonviolent entertainment (for example, The Aristocats) and violent content (for example, Power Rangers or Looney Tunes).

The good news is that the researchers found that for children aged 4 to 5 years, watching any kind of television was not significantly associated with attentional problems 5 years later. For the 0 to 3 years old, watching educational television also didn’t impact the children, but each hour per day of viewing violent entertainment television was associated with double the odds for attentional problems 5 years later. Watching nonviolent entertainment was also associated with subsequent attentional problems, but to a lesser degree than violent entertainment.

Now I don’t typically like these types of studies because I always can think of so many things that are not being taken into consideration (confounding factors in the scientific lingo). For example, is the effect the same for boys and for girls? What about if the family is rich or poor? The reason I like this particular study is because the researchers did control for many potential confounders like gender, urban or rural area of residence, socioeconomic adversity, number of children in the household, mother and father’s educational levels, mother’s mental health, presence of father in the household, parental conflict, etc. For example, by taking all these characteristics into account, the researchers could control for the fact that children who grow up in a rich and stimulating environment might be exposed to lower amounts of early television watching.

That being said, association studies are not perfect. They are reporting observations and not experimentations, and this means that the results do not necessarily report a cause-and-effect relationship. So in the end, we can’t say that watching violent shows always leads to attentional problems.

Regardless of its limitations, I find the study interesting and the results quite frightening (especially considering the study classifies “The Lion King” as violent content). The researchers mention two theories that could explain how watching television can impair healthy development. The first theory suggests that every moment in front of the television is a moment not spent on appropriate learning opportunities, like pretend play. The second theory is that fast pacing and quick scene changes typical of non-educational television shows trick the brain to think that real life is also a quick and constantly changing stimulus, and the brain comes to expect it. I find this second theory to be especially appropriate for the association with attentional problems. It also explains why educational television, which has been shown to be significantly slower-paced than other types of programming, is less damaging.

It was almost a no-brainer that Mister Roger’s neighbourhood equals good and Rambo equals bad. However, I wouldn’t have guessed that watching Wile E. Coyote blow himself up over and over again with Acme dynamite was anything more than a silly, harmless cartoon.

Good babysitter? Think again.

Reference: Associations between content types of early media exposure and subsequent attentional problems. Zimmerman, F.J., Christakis, D.A. Pediatrics 2007 120(5):987-992.

The link between science and the media is missing

2009-06-07T21:53:00.000-07:00

As promised, today’s post has to do with the newly discovered “missing link” in our evolution. Or maybe it has to do with hype-craving media machines. You decide.

I have painstakingly read through the 27 pages of the original article on the fossil so you wouldn’t miss out on the exciting data behind this newsworthy finding. Essentially, researchers recovered the near complete skeleton of a fossil primate and described it as a new genus and species called Darwinius masillae. Did they name it Darwin because it confirms Darwin’s theory? Nope. They named it Darwin to honor his 200th birthday.

The fossil was unearthed from sediments in Messel, Germany in 1983 and dates from the middle Eocene period, roughly 55 to 33 million years ago. The really striking feature of this fossil was that is was almost entirely complete and extremely well preserved, even including remains in the digestive tract. The researchers used radiographs and other imaging techniques (such as CT scans) to carefully examine the fossil’s bones (and every single tooth!) and compare them to other fossils and living animals. The article describes all those bones and teeth (one by one) and reconstructs aspects of the life history, life stage and locomotion of the Darwinius.

Now if this fossil is the missing link, then the important thing is where it stands in the phylogenetic tree. The article goes into a lot of detail about this, but I'll make it easy for you. There are two suborders of primates. The first, Strepsirrhini, includes lemurs and such while the second, Haplorhini, includes different types of higher primates and anthropoids (literally, “human-like”). While the fossil seems to have characteristics of both suborders, the authors conclude that Darwinius masillae is part of the Haplorhini group. Does that make it the “missing link”? Here’s what the researchers had to say about that:

“Note that Darwinius masillae (...) could represent a stem group from which later anthropoid primates evolved, but we are not advocating this here, nor do we consider (...) Darwinius (...) to be anthropoids.”

Wow. Talk about a solid statement. It sounds like they are saying “This could be really cool, exciting and relevant, but we’re not suggesting that at all”.

The fact that the skeleton was so intact clarified a lot of things and made the community question the established knowledge about the origin of higher primates. For example, even though the Darwinius is not considered to be anthropoid (human-like), the category of primates it represents can now be carefully compared with higher primates. This is very relevant and exciting from an evolutionary standpoint. But it doesn’t make it the missing link*. And I don’t know about you, but I could swear that I saw at least 20 different headlines using the words “missing link” when the story came out.

Why all the hype? Why the blatant misinterpretation by the media? How did this article gain worldwide exposure in the media while others never escape the dungeons of scientific publications? Well, it helps to know that before the article was even submitted (maybe even written!), a company had already commissioned a TV documentary and a book on the topic. That the topic caught the eye of a production company is not surprising given its potential implications. The trouble is that the relevance of the article was drastically misrepresented. For example, both the movie and the book had the evocative words “The Link” in their title. In addition, The BBC, The History Channel and countless news articles called the Darwinius “our ancestor”. Another contributing factor to the extreme hype was that everything happened very, very fast (it will come as no surprise to fellow scientists that they had time to make the entire movie before the paper was published!). Since the article wasn’t available prior to all the media coverage and press conferences, there were no opinions available from other experts in the field, and by that time there was no way to stop the marketing machine.

There’s a lesson here. For real and relevant scientific news that aren't overly hyped by the media, trust Scientific Chick.

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*Don't get me wrong: I totally buy Darwin’s theory and the relevance of transitional fossils.

This little girl generated a media hype of epic proportions

Reference: Complete primate skeleton from the Middle Eocene of Messel in Germany: morphology and paleobiology. Franzen J.L., Gingerich P.D., Habersetzer J., Hurum J.H., von Koenigswald W., Smith B.H. PLoS ONE 2009 19:4(5):e5723.