That little bit of exercise

Read the post here.

Brian Mossop is currently the Community Editor at Wired, where he works across the brand, both magazine and website, to build and maintain strong social communities. Brian received a BS in Electrical Engineering from Lafayette College, and a PhD in Biomedical Engineering from Duke University in 2006. His postdoctoral work was in neuroscience at UCSF and Genentech.

Brian has written about science for Wired, Scientific American, Slate, Scientific American MIND, and elsewhere. He primarily cover topics on neuroscience, development, behavior change, and health.

Contact Brian at brian.mossop@gmail.com, on Twitter (@bmossop), or visit his personal website.

Tummy Time

My first short feature for Slate ran last week, covering the importance of tummy time for infants.

The Back To Sleep Campaign was instituted by the American Academy of Pediatrics in 1992 to battle the number of infants dying each year from SIDS. And it was hugely successful, cutting SIDS cases in the US in half since it started.

Infants are no longer spending time on their stomachs at night, and many are not getting enough belly playtime (called "tummy time") either. New research has correlated tummy time deficits to lags in pre-walking motor skill development, which in turn has been linked in large birth cohort studies to physical and cognitive ability later in life.

Four years after the Back to Sleep campaign launched, its inadvertent effects started trickling into the clinic. Most notably, some infants had disfiguring flat spots on the back soft crowns of their heads. It took a few years for researchers and doctors to realize that the change in sleeping position also affected prewalking motor skills (whether or not a baby had a misshaped head). Then in 2004, a research team led by Bradley Thach at the Washington University School of Medicine studied the difference in head movements between stomach and back sleepers. Thach showed that babies who spent nights on their bellies quickly developed the brain connections and muscle strength to turn their heads from side to side—one of the first motor-skill hurdles. Babies who consistently slept on their backs, on the other hand, were less likely to have sufficient head mobility at 3 to 5 months.

Whether we are talking about tummy time, breastfeeding, or watching Baby Einstein videos, it's important to understand that child development doesn't hinge on one thing. Rather, a multitude of genetic and environmental differences factor in to make us who we are. But I think it's important to get as much information to the public as possible about potential new links researchers uncover.

Photo via Flickr / samgranleese

Mastering Mania: The Link Between Creativity and Mental Illness in the Brain

A New York Times story grabbed my attention today, “Just Manic Enough: Seeking Perfect Entrepreneurs”. Telling the story of 21-year-old Seth Priebatsch – a guy who successfully secured a $750,000 investment from venture capitalists for what some may argue is just a crazy idea – the article showed how this certain young entrepreneur seemed to tread a very fine line between being a workaholic, self-confident entrepreneur, and full-blown clinical manic. With hypomania, people experience similar mood and behavior swings as those with clinical mania. But although the two conditions share common symptoms like increased vigor, persistently elevated moods, and reduced desire or need for sleep, hypomania does not seem to prevent people from experiencing a fully functioning life. In fact, some have argued the symptoms may be conducive to success. The NYT article highlighted several well-known, professionally-accomplished hypomaniacs, such as George S. Patton and Theodore Roosevelt, both of whom seemed able to keep the condition in check – arguably, just enough – to rise to the top of their respective professional circles.

Over the past few weeks, I’ve grown increasingly interested in the connection between creativity and mental illness. There have been numerous books and articles written on the ideas that famous writers and artists, many of whom ended up taking their own lives, suffered from bipolar disorder or other clinical mood problems.

So I started looking into the scientific literature around this idea, to see if researchers have been able to pinpoint specific brain circuits that prove the existence of this alleged gray-zone between creativity and mental illness. In other words: could the same brain structures fuel a raging fire of creativity in an individual on moment, yet cause disastrous mental illness at a later point in time?

[NOTE: In a very cursory search, I found an enormous amount of information. I plan to share the most interesting findings I come across over the next few weeks as short blog posts.]

A study published in May 2010 in the journal, PLoS ONE, by Örjan de Manzano and colleagues from the Stockholm Brain Institute at Karolinska Institutet, Stockholm, Sweden tapped into the creative mind of healthy individuals using both positron-emission tomography (PET) brain imaging and standard psychological tests.

The Berliner Intelligenz Struktur Test is a divergent thinking exercised often used to gauge creative prowess. The researchers would ask the participants to list every possible use for a brick that comes to mind within a given amount of time, or create as many novel drawings they can using just a few line segments. The ability to rattle off variations of an initial idea taps into the associative mind, and is not necessarily correlated to general knowledge or intelligence, at least in the standard definitions of the terms.

Örjan de Manzano and colleagues hypothesized that creativity may in fact be linked to defunct dopamine signaling in certain areas of the brain. After all, from previous studies, they already knew that people carrying the A1 allele of the dopamine-receptor gene DRD2 TAQ IA exhibited increased creativity, as seen by higher scores on the divergent thinking test, with absolutely no changes in generalized intelligence.

Using PET imaging, researchers can determine the functionality of D2 receptors by introducing a radiotracer that binds to these receptors. By measuring the D2 receptor binding potential of these tracers – a measure of how long the radiotracer stays attached to the receptor substrate – researchers can measure the strength of dopamine signaling in different areas of the brain.

In a very small group of healthy volunteers (this is probably the biggest criticism of the study), Örjan de Manzano and colleagues found that the level of D2 receptor binding potentials in the thalamus were negatively correlated (r = -0.64) to their score in the divergent thinking test, which means the more creative the people were (as determined by the divergent thinking test), the LESS dopamine activity they had in the thalamus. No such correlations were found in other areas of the brain, such as the striatum or the frontal cortex.

The thalamus is often considered a gate to the cortex, the area where much of the higher order processing of stimuli takes place.  The cortex is the region where we essentially discriminate one sound from another, or determine a circle is different than a square.   The authors think that less dopamine signaling in the thalamus leads to a less regulated flow of information to the cortex.  In other words, the creative brain isn't filtering out information at very low levels – it’s actually letting more and more through.  Increased chatter in the cortex may transiently put the brain in a different state, allowing the mind to rapidly switch between thoughts and ideas.

As the authors point out, the sudden burst of info would more than likely come at a cost to the cortex, however, and may materialize as a decrease in selective attention. A study has corroborated this theory, showing that people who score higher in divergent thinking tasks may be more creative, but are also more easily distracted.

Although preliminary, this study suggests a powerful link between creativity and reduced dopamine signaling in the thalamus. If true, creativity might be due to more information making it past the thalamic gatekeeper, and into the cortex, where different neural circuits – ones that may not usually talk to each other – begin to harmonize in creative synchrony.

This paper offers no direct evidence that a less active thalamic filter correlates to mental illness.  Still, the authors speculate how a more information moving through the thalamus might also be related to so-called positive symptoms in psychiatric disease.  Though most of the discussion on mental illness relies on hand-waving explanations, the authors still clearly articulate a few good points.  Hallucinations and delusions are thought to be due to an overactive cortex in one way or another, so the possible link is at the very least worth considering – perhaps in my next post.

photo via Flickr /yago1.com

de Manzano, ?., Cervenka, S., Karabanov, A., Farde, L., & Ullén, F. (2010). Thinking Outside a Less Intact Box: Thalamic Dopamine D2 Receptor Densities Are Negatively Related to Psychometric Creativity in Healthy Individuals PLoS ONE, 5 (5) DOI: 10.1371/journal.pone.0010670

Stress Hormones and Competition

I just finished my first post for Wired Playbook,  which talks about the hormonal changes that occur in the body during competition.  Whether the hormones levels increase or decrease may give some insight into the psychological readiness of a contender.

Armed with cotton swabs coated with pulverized Sweet Tarts candy, researchers took saliva samples minutes before two monkeys engaged in a staged competition for a pile of food. When dominant males won, there was a clear increase in the stress hormone right before the competition. In these cases, the dominant male was ready. He had sized up his opponent and knew, no doubt, that he’d prevail.

Conversely, when the dominant male lost, the hormone level decreased before the food game. Although these apes live in very well-defined social societies – and the dominant male had more than likely battled with this opponent before and won – something had psyched him out.

Read the full post here.

My Scientific American Story on the Father-Child Bond

Sorry, but this post is nothing but shameless self-promotion! My first short feature article was published in Scientific American today, which discusses the neurobiology of the father-child bond.  Give it a read!

Last May, I took a trip to San Diego for my brother-in-law’s graduation from college, and to meet his 4-month old son, Landon, for the first time. Throughout the weekend, I couldn’t suppress my inner science nerd, and often found myself probing my nephew’s foot reflexes. Pressured from my wife’s disapproving looks and the blank stares I received from her family as I explained why his toes curled this way or that, I dropped the shop-talk in favor of baby-talk.

Click here to read the rest.

Sex, Stress, and Neurogenesis

There’s an article in the latest issue of Wired by Jonah Lehrer explaining just how dangerous stress can be to our health.  It’s a fascinating read -- and instead of relying on my poor attempt to paraphrase -- I suggest checking out the article in its entirety.

The part of the story that struck a particular chord with me was Lehrer’s explanation of the experiments done by Elizabeth Gould, who studies how stress hormones affect the growth of new brain cells in adult brain, a process called neurogenesis.  Gould’s previous work, as noted by Lehrer, showed that when animals get stressed out, levels of glucocorticoids -- one type of stress hormone -- skyrocket in their brains.  With brain cells wading in a constant bath of these stress hormones, neurogenesis comes to a screeching halt.

The take-home message from Lehrer’s article: glucocorticoids are bad.  And indeed, they do make bad things happen in the brain.  Aside from the fact that stressed-out animals have less neurogenesis, if you take an animal and inject glucocorticoids directly, new brain cells also stop forming.  Lehrer’s suggests that if we find ways to prevent or otherwise interfere with stress hormones (through a vaccine or otherwise), we could mitigate the effect stress has on our emotional well-being and, ultimately, its complex interaction with disease.

I’ve been putting off (for several weeks now) writing a post on the most recent experiment to come out of Gould’s lab, published in mid-July in PLoS One.  Lehrer’s story finally lit the fire under me.

The term “stress” has a very deliberate negative connotation.  We need this term to bucket somewhat-hard-to-explain feelings, like experiencing “pressure” at work.  But the term is far more encompassing than that.  Stress, by definition, is a measure of how the body responds to a challenge.  Sometimes the challenge can be a threat -- a deadline at work or a difficult family situation -- and triggers the all-too-familiar anxiety we’ve come to expect.  This is the bad type of stress Lehrer discussed.  But the challenge can also be a something, well, good, that temporarily takes our body out of balance.  Consider what happens when you exercise.  Going out for a run will create a physiological burden as the heart beats faster and faster, trying to match blood flow to the demands of the muscles and lungs.  This physical exertion is also a type of stress, a good kind of stress, if you will.

The effects of the two types of stress on the brain are completely different: While the bad stress decreases neurogenesis, the good type of stress, on the other hand,  actively stimulates extra brain cell growth.  Although the brain responds in different ways, both good and bad stress increase the levels of glucocorticoids in the body.  Knowing glucocorticoids are dangerous to the brain, researchers still scratch their heads over how exercise could battle these stress hormones, and win.

But Elizabeth Gould has a new theory.

Exercise makes us feel good about ourselves.  We like the sense of accomplishment.  We celebrate the weight we’ve lost and our increased fitness.  Gould believes that this hedonistic value of exercise could somehow trump the nasty effects seen when glucocorticoid levels rise.  But exercise is such a complex action.  Sure, there’s a hedonistic component, but there’s also a hefty physiologic one.

To give her theory some teeth, Gould would have to prove that another stressor with hedonistic value also boosts neurogenesis.  So this time around, instead of exercise, Gould’s lab used a simpler, less physically-demanding, but equally powerful positive stressor: sex.

While not typically considered a stress by popular definition, sex fits the bill, as it’s been shown to increase glucocorticoid levels in the brain.

Gould’s results show that a single sexual encounter is enough to raise glucocorticoids and increase neurogenesis in the hippocampus of male mice.  After repeated sexual experiences, the glucocorticoid levels stabilize, but the brain continues to grow new neurons and the number of synapses increases.

While this study doesn’t answer all of the questions surrounding glucocorticoids, stress, and the brain, it shows the story is far more complicated than initially thought.  Chronic good stress continually increases neurogenesis, but it also seems to level off the stress hormones themselves.  Gould’s results support the notion that the hedonistic aspect of good stress may in fact be the active ingredient that keeps the dangerous effects of glucocorticoids at bay.

Leuner, B., Glasper, E., & Gould, E. (2010). Sexual Experience Promotes Adult Neurogenesis in the Hippocampus Despite an Initial Elevation in Stress Hormones PLoS ONE, 5 (7) DOI: 10.1371/journal.pone.0011597