The trouble with the tube (part 2 of 2)

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)

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

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.

--------------------------------
*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.

A case for smelly boys

Last week, I had the opportunity to attend the conference of the Canadian Association for Neuroscience. It was a fantastic meeting, and in addition to interesting talks from great scientists, there were excellent opportunities to snag free food, which is a surefire way to keep grad students interested. Many talks gave me ideas for this blog, but I settled on an article from Dr Sam Weiss from the University of Calgary. Dr Weiss gave the keynote talk on adult stem cells and his research on new brain cells struck me as relevant in many ways.

Not so long ago, the scientific community believed that you were born with a given amount of brain cells (called neurons). During development, some would die (the whole “use it or lose it” paradigm), and then you’d have more or less a stable number of neurons until you got old, at which point your neurons would start dying again. Essentially, it would be a one-way street: you could never get more neurons, just fewer. Well, lucky for us, it turns out that’s not the case. Neurogenesis, the birth of new neurons, happens throughout your lifetime in two specific regions of your brain: the hippocampus, an important region for memory, and the olfactory bulb, an important part of the brain for the sense of smell. The jury is still out on the significance of neurogenesis and how those neurons are integrated in your existing networks, but there’s a lot of research going on on neurogenesis because, well, it gives us hope that our brains aren’t doomed from age 30 on.

The article from Dr Weiss’ lab looks at how neurogenesis might be relevant for a natural behaviour of both female mice and female humans: how to pick a quality mating partner (a daunting task!). The researchers started by exposing female mice to odors from male mice, and then used a special chemical that dyes newly dividing cells to quantify neurogenesis in the brains of the female mice. After exposing the females to male odors for 2 days, the researchers saw no change in the numbers of new cells in the females’ brains. But after 7 days of exposure, there was a significant increase in proliferating cells in both the hippocampus and the olfactory bulb (I want to say that there’s a message here that guys should be persistent, but I’m not one to extrapolate results like that). Could this observation have been a fluke? It’s unlikely, given the large number of controls in the study. For example, the researchers show that this effect was not present when they simply exposed the females to new odors, it was not present when they exposed the females to odors from castrated males, and it was not present when they used a drug that blocks the females’ sense of smell. So far, I’m convinced.

Now male mice exist in a hierarchy, a kind of pecking order (some would argue just like male humans). Some males are more dominant, others are subordinate. To see if the brains of female mice react differently to dominant or subordinate males, the researchers exposed the female mice to a mix of dominant and subordinate male odors for 2 days (remember, 2 days doesn’t lead to an increase in neurogenesis). This initial phase of the experiment was important to establish memories of these odors. The females were subsequently exposed to either a dominant male odor or a subordinate male odor for 7 days. What the researchers observed then is that females exposed to dominant male odors show a marked increase in new neurons compared to females exposed to subordinate male odors. A biological explanation for the success of the 10-billion-dollars-a-year perfume industry, perhaps?

The last experiment is the most relevant for animal behaviour. Just like the previous experiment, female mice were exposed to a mix of dominant and subordinate male odors for 2 days to establish memories (again, no increased neurogenesis in this time frame). The females were then exposed to either one of the types of male odors for 7 days. The females were later put in a box with 3 compartments side by side (see figure below). The female was in the middle compartment, a subordinate male was on one side and a dominant male on the other. The mice could smell each other but not touch. The purpose of the experiment was to see which of the males would be more interesting to the female (which male she’d choose as a mating partner). Almost without fail, the females previously exposed to a dominant male (those females with increased neurogenesis) preferred the dominant male, while the ones previously exposed to a subordinate male (no increase in neurogenesis) had no preference. But here’s the really neat part: when the researchers used a drug that blocked neurogenesis during the “acquaintance” period with either a subordinate or a dominant male, the females no longer consistently chose the dominant males in the last part of the experiment, regardless of what they had been exposed to previously.

What does this mean? Well, the researchers conclude that male mice have odor signatures and female mice can identify and remember these signatures to carefully select prospective mating partners. Male odors stimulate an increase in new neurons in the female mice’s brains and these new neurons play an important role in selecting the best possible mate. This research is exciting because it means that not only do we make new neurons as adults, but those neurons may actually play a biologically relevant role in our brains. The other reason this research is exciting is because it is looking at an important specie-specific behavior. When studying the brain, many researchers using animal models like to use “humanized” tests and mazes to make the results easy to extrapolate to humans. When an old mouse can’t remember a given spot in a maze, it makes for a good story to suggest that this is akin to an old person not remembering their way home. In this study, I think it’s great that they are studying a phenomenon that we know happens in humans (neurogenesis), but using a real mouse behaviour context to really assess the significance of what they are observing in the greater scope of brain function.

And now, a shameless teaser for my next post: Heard all the hype surrounding the newly discovered “missing link” fossil? Stay tuned for the report of the research paper…

Reference: Male pheromone-stimulated neurogenesis in the adult female brain: possible role in mating behavior. Mak G.K., Enwere E.K., Gregg C., Pakarainen T., Poutanen M., Huhtaniemi I., Weiss S. Nature Neuroscience 2007 10:1003-10.

Experiment diagram from: Alpha males win again. DiRocco D.P., Xia Z. Nature Neuroscience 2007 10:938-40.

A bird named Sue

I sometimes wish I was a computer science blogger instead of a life sciences blogger. That would mean, or at least should mean, that I know a lot about computers. Unfortunately I’m not a computer science blogger, and I don’t know anything about computers, and that is why I must apologize for the delay leading to this post. Last Friday my computer died on me, dead as could be. I was working on it, got up for a drink (water, as I’m still free from coffee addiction), and when I got back, my trusty laptop had committed suicide (genetic disposition, no doubt). This event caused considerable grief and made me realize that while I am not addicted to coffee, I sure am addicted to using a computer. That being said, I’m back in ComputerLand, and to make up for the delay I am posting about a really, really cool study.

The research paper for today (published May 2009 in Nature) looks at zebra finches, a type of songbird. The song of zebra finches is like a cultural trait: individual finches have small variations in their song and geographically separated finch groups have local song dialects. Overall, though, the song from the zebra finch in the wild (called the “wildtype song”) can be recognized and described. Songbirds learn to sing during their development by being exposed to adult singing males (females lack a singing ability, but at Zebra Finch Idol, they do the judging). This begs the question: What if baby zebra finches aren’t exposed to singing males? To investigate this question, the group of researchers from New York took zebra finch eggs and raised them individually in sound-proof rooms.

Now a Pop Quiz for my readers, for 20 brownie points:
What happens when baby zebra finches aren’t exposed to adult singing males?

A) They never sing.
B) They sing normally.
C) They sing poorly.
D) They spontaneously break out in “A boy named Sue”.

Think about it: if the song is encoded in their genetic code, then it shouldn’t matter whether they are exposed to it or not, and the answer would be B. If the song isn’t encoded in their genetics and they only learn to sing by imitating adult birds, then the answer would be A. D was a red herring, and the correct answer is actually C. The isolated zebra finches sang, but the sound didn’t really resemble the wildtype song.

Good science is all about asking the right questions. Instead of stopping there and analyzing what went wrong, the researchers thought of a really creative way to address the results. They took a second batch of zebra finch eggs (the second generation), and raised them again individually in a sound proof roof, but this time each baby was raised with one adult bird (a singing tutor) from the first generation (the ones who sang poorly). I’ll spare you the quiz this time: the birds from the second generation learned to sing just like their tutors, poorly. However, their song was slightly different. The rhythm and other characteristics of the second generation song were a little closer to the wildtype song. And so the researchers continued: a third generation of birds was raised, this time with second generation tutors. And believe it or not, each generation sang a little more like the wildtype birds and by generation 4, the song was very similar to the original wildtype song.

The conclusion from the article is that song culture is partly encoded in the genetic profile of a population and partly encoded in the environmental variables. Song culture is also a “multigenerational” phenomenon, because it takes a few generations to emerge. It is a bit disappointing that this study doesn’t also look at the mechanisms of what’s happening. For example, song development is known to be associated with something called neurogenesis, which essentially means the birth of new brain cells. Could it be that over a few generations, there is an orderly progression of connections between the new cells? Are the brain cells and associations between brain cells getting reorganized with each new generation? The researchers do promise to look into it, so I’ll stay tuned and keep you posted.

This is what a zebra finch looks like. Pretty cute, huh?

Reference: De novo establishment of wild-type song culture in the zebra finch. Feher O., Wang H., Saar S., Mitra P.P., Tchernichovski O. Nature 2009 May 3 EPub ahead of print.

To panic or not to panic? An interview with the swine flu.

Due to the current international media hype on the swine flu, I’ve decided to stray from my usual modus operandi (for those of you just tuning in, my modus operandi is to write about a recent and relevant research article (not a news article!) in the life sciences). Instead of a research article, today I cornered the swine flu and grilled him like it was his PhD thesis defense.

Scientific Chick: What kind of name is swine flu?
Swine Flu: It’s a bit funny that I was called swine flu to start with, since I infected humans months before recently taking a liking to pigs in Alberta, Canada. The reason I was called swine flu is because part of my genetic code comes from a flu that usually infects pigs. However, other parts of my genetic sequence come from the avian flu, and some are from the human flu. I guess calling me “human flu” would have been even more panic-inducing. Anyway, I’m not called swine flu anymore, because pork producers thought it would be bad publicity, even though you can’t catch me by eating pork. My new name is the type A H1N1 virus, but I doubt that will stick with the media.

SC: Tell us a little bit about yourself.
SF: Well, I’m a virus. That means I’m tiny (about 100 times smaller than your average bacteria), and I’m essentially a collection of RNA segments (which is similar to DNA) and proteins (my machinery to infect you!) encased in an envelope. My H1N1 name comes from the types of proteins on my surface, hemagglutinin (H) and neuraminidase (N). I can only reproduce (for viruses like me, we say replicate) in living cells. When you catch me, I bind to your cells and weasel my way inside. Once inside your cells, my envelope degrades, and my machinery hijacks yours to start making mini-me’s. Once your cell has made a bunch of new viruses, the cell breaks open and releases all the new viruses so they can go and infect more of your cells. Sneaky, huh?

SC: What makes you special?
SF: Robert Webster, An American flu virologist, recently dubbed me as a “real super-mixed-up virus”. My genetics are so new and confusing that you don’t have any immunity to me. That’s all part of my plan for world domination.

SC: How fast do you spread?
SF: How dare you ask me questions about my reproductive habits? I’m not telling. To find out, you’ll have to analyze my basic reproductive number (R0), which is a variable that describes the number of new infections caused by one infected person.

SC: Will you kill me?
SF: Well, you are annoying me with all your questions, but right now I’d have to say no. It’s still unsure whether I will cause severe disease in many people. According to flu researchers, I apparently don’t seem to be anything different than seasonal flu.

SC: Then why did you kill all those Mexicans?
SF: I thought you’d ask. You should hear all the theories about this! Some think the Mexicans are more susceptible because of basic hygiene and medical care. Others suggest that air pollution aggravates my symptoms. Some think it’s because of genetic predispositions. But virologists think you shouldn’t jump to conclusions like that. The reality is, compared with Mexico, the number of the people I infected in the USA or in a country other than Mexico is still too small to pick up significant mortality rates, so it’s very hard to compare.

SC: Can we prevent you from infecting us?
SF: So far, regular flu-prevention measures apply. Wash your hands, stay away from the coughing sickly-looking person at the office, eat healthy and exercise, and take a deep breath. Should you go out and deplete your local drugstore of its surgical masks stock “just in case”? No, unless you’re a nurse working in the flu ward (and if that’s the case, I’d hope that your masks are provided). Those masks have only been shown to work if infected people wear them (that’s why you see them a lot in Mexico), and are not useful in preventing infection at this stage.

As for vaccines, I happen to know that you’re working hard on developing one. You’re going to have a problem, though. Growing viruses to make vaccines is a slow process, and the world’s influenza vaccine production capacity is limited to about 400 million doses a year. If you want to start making vaccines against me, you’re going to have to sacrifice the making of the regular flu vaccine. A bit of a gamble, isn’t it? Especially considering my seasonal flu brothers are pretty lethal (last year, they killed about half a million people). Good luck figuring that one out.

SC: Can we treat you?
SF: I wish I could say I’m indestructible, but I’m no teenager anymore. I’m treatable with two widely-known and used anti-influenza drugs, oseltamivir (Tamiflu) and zanamivir (Relenza), and countries are stocking up.

SC: You’ve been sequenced. What do you say to that?
SF: You think you’re so smart, and that because you know all the letters in my genetic code, you know everything about me. You fool! You still don’t know how virulent I am, and what my mutation pattern is.

SC: How did you evade our fancy pandemic prevention plans?
SF: I went unnoticed. I was clever and popped up at the end of the regular seasonal flu season, so no one paid attention to me for a while. By the time the World Health Organization and the Center for Disease Control realized what was going on, it was too late to nip me in the bud. Mouahahaha.

SC: Should I panic?
SF: One thing is for sure, it seems like the media wants you to panic. Should you give in to the hysteria? Well, it’s good to keep in mind that so far, I’m just like a regular flu. A friend of mine said it best: it’s good to be aware, but there’s no need to be alarmed.

An excellent graph from a site I like called GraphJam

References
As swine flu circles globe, scientists grapple with basic questions. Cohen J. and Enserink M. Science 2009 324:572-573.
Swine flu goes glocal. Butler D. Nature 2009 458:1082-1083.

The secret to eternal youth? Say goodbye to brownies.

You’ve heard of Atkins. You’re familiar with Weight Watchers. You probably know about the South Beach Diet. Well, there’s a new diet in town, and it’s called the “Longevity Diet”. It’s inspired by a relatively new hot topic in the life sciences called caloric restriction. As the name implies, it essentially means eating less, and it's hailed not so much as a weight loss strategy as an anti-aging solution. While I’m usually excited about new simple ways of changing daily habits to live a healthy life, this one I’m not sold on yet. You may remember that I like cheese. You may also remember that I like brownies. So obviously, I’m not too excited to hear that eating less is extra healthy. Especially since most caloric restrictions studies suggest you have to cut back anywhere from 30% to 60% of what you eat to see an effect.

So far, most of the really convincing data on caloric restriction slowing down the aging process have been carried out in model organisms that fit in your pocket: rats, mice, worms, all the way down to the tiny yeast. I personally would be reluctant to extrapolate those findings to humans. Surely worms don’t have the same kind of relationship with brownies that I do. However, one recent study looks at caloric restriction in healthy humans, and it’s hard not to take notice.

Researchers from Germany took 50 normal-to-overweight elderly subjects (sorry, Mom, in this case, “elderly” means 60ish, but the important thing is to be young at heart!) and divided them into groups. One group was told to not change their eating habits, and one group was put on 30% caloric restriction for 3 months. Before the study and after the 3 months, everyone’s memory was tested using simple tests like remembering a list of words. Well, I’m very sorry to say, but after 3 months, the group who ate less did significantly better at the memory tests. Sad but true.

During the study, the volunteers were monitored for many different biological indicators (such as cholesterol, insulin, inflammation, and cellular stress), in hopes of identifying the mechanisms responsible for the effects of caloric restriction. The one mechanism that really stood out and that showed a solid correlation with the memory improvements is insulin: the group on caloric restriction had lower insulin levels. Insulin is a hormone responsible for taking the sugar out of your blood and storing it in your liver and muscles to use when energy is needed, but it also plays an important role in keeping your brain healthy. When you have less insulin circulating in your body, you become more sensitive to it, and this sharpens and improves how your body (including your brain!) reacts to insulin. This may be why the group who ate less performed better on the memory tests.

So, throw out the cheesecake? I’m going to wait a little before I draw any solid conclusions, as there is still a very ongoing debate over caloric restriction. One side is claiming significant benefits like longevity, healthy aging and protection against age-associated diseases (think Alzheimer’s). The other side is critical of the methods and models used, as well as the contradictory results, and points to the downsides of caloric restriction, especially during the reproductive years. Not eating enough can also lead to the breakdown of muscles (and remember, your heart is a muscle), which is very important to consider if you have an active lifestyle. Interestingly, in this study, the authors show that the caloric restriction group lost a significant amount of weight, but did not lose body fat. Healthy? I think the jury is still out, but hopefully more well-controlled human studies will shed some light on this potentially exciting and easy way to fend off the effects of the ticking clock.

Learn to make these, shorten your healthy life expectancy?

Reference: Caloric restriction improves memory in elderly humans. Witte AV, Fobker M, Gellner R, Knecht S, Flöel A. Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1255-60.