Posts Tagged ‘ anxiety ’

5 Ways to Fight the Blues…with Science!

So you’re stuck in that mid-week slump…the weekend lies on the other side of a scorching desert of work, and you have no canteen because you gave up water for Lent (in this metaphor, “water” refers to alcohol…just to be clear).


But fear not! Neuroscience knows how to cheer you up! Nope, this isn’t another post about sex or drugs…though those are coming soon. This one’s about five things science says you can do right now – with your mind – to chase your cranky mood away.

1.Take a look around
Research shows that people who focus on the world around them, instead of on their own thoughts, are much more likely to resist a relapse into depression. This is easy to do – just find something interesting (or beautiful) to look at, and think about that for a few seconds…you’ll be surprised how quickly your worries fade.

2. Do some mental math
Scientists say doing a little simple arithmetic – adding up the digits of your phone number, for example – reroutes mental resources from worry to logic. Don’t worry; your emotions will still be there when you’re done…but they’re less likely to hog the spotlight if you don’t give them center stage.

3. Get out and about
Lots of studies show that physical activity raises levels of endorphins – the body’s own “feel-good” chemicals – and helps improve your mood throughout the day. You don’t have to run a marathon; even a quick walk around the block will get your blood pumping and help clear your mind.

4. Find some excitement
Some very interesting studies have found that courage – a willingness to face some of your fears – feeds on itself; in other words, the more adventurous your behavior is, the fewer things your brain considers threatening. In a way, it’s a “fake it ’til ya make it” situation…but instead of trying to be someone you’re not, you’re becoming more comfortable with the person you are.

5. Remember, it’s not always a bad thing
It sometimes helps to remember that stress is a natural phenomenon…as natural as digestion or sleep. Though stress (or sadness, or worry) can sometimes get out of hand, our bodies have evolved these responses to help us, and there’s nothing “wrong” with you just because you’re feeling annoyed or down in the dumps today. Instead of trying to make the feeling go away, sometimes the best thing to do is acknowledge it, and think about what’s triggering it. You might surprise yourself with an insight.

So, those tips are pretty simple, right? Try some of ’em out, and let me know which ones worked best for you. After all, that’s why scientists study this stuff – to help us all understand more about what our minds are up to.

Stress Intervention

Scientists have discovered a way to shut down the brain’s “stress process” before it gets going, says a new study.

Stress, or just a very acute case of the munchies? It's hard to say.

By blocking the brain’s ability to manufacture certain chemicals called neurosteroids, researchers have managed to temporarily cut off a biological process crucial for stressful behavior – and for many stressful feelings as well.

Animals from amphibians all the way up to humans produce a hormone called corticosterone in their adrenal glands. Corticosterone levels become elevated under stress, and this hormone is a major ingredient in a number of stress-related biological processes, from feelings of nervousness to aggressive behavior.

Corticosterone does most of its direct work within a brain pathway known as the hypothalamic-pituitary-adrenal axis (also called the HPA or HTPA axis). To be honest, the word “pathway” is a bit of an oversimplification – the HPA is actually a whole set of neurochemical feedback circuits involved in regulating digestion, immune response, and mood, among other things.

The HPA’s activity is mostly regulated by a neurotransmitter chemical called gamma-Aminobutyric acid (GABA to its friends). GABA is typically an inhibitory neurotransmitter, which means it prevents electrochemical signals from being passed beyond a certain point. It often works closely with a neurosteroid called tetrahydrodeoxycorticosterone (THDOC), which helps its inhibitory effects spread even more widely throughout the HPA.

But when we come under stress, everything changes: the adrenal glands start cranking out extra-large doses of THDOC and sending them up into the HPA. And here’s where things get weird – those conditions trigger a certain electrochemical shift that causes GABA and THDOC to activate the HPA rather than inhibit it.

As the Journal of Neuroscience reports, the discovery of that neurochemical mechanism is the first half of a two-part breakthrough made Jamie Maguire‘s team at Tufts University:

We have identified a novel mechanism regulating the body’s response to stress by determining that neurosteroids are required to mount the physiological response to stress.

But how did they discover this mechanism, you ask? Well, since the team suspected that neurosteroidogenesis – the production of neurosteroids like THDOC – was a crucial component in stress-related HPA activation, they got a bright idea: they wondered if a drug that blocked neurosteroidogenesis might be able to stop the brain’s stress response before it could even get into gear.

As it turned out, they were right – they cut off the THDOC rush by administering a drug called finasteride – which you might’ve heard of under the brand name Propecia. Yep, the baldness drug:

Blocking neurosteroidogenesis with finasteride is sufficient to block the stress-induced elevations in corticosterone and prevent stress-induced anxiety-like behaviors in mice.

In other words, the researchers found that finasteride does more than just control stress – it blocks the chemical cascade that causes stress-related feelings and behavior. As far as they can tell, it prevents animals from experiencing stress at all – at least temporarily.

This has the potential to develop into a far more powerful treatment than benzodiazepines like Xanax and Ativan, which work by helping GABA inhibit more activity than it normally would. By contrast, a finasteride-like drug would make it almost impossible to feel stressed, even if you tried – meaning this drug might also be used to treat diseases like epilepsy and major depression, which have been linked to excessive activation of the HPA.

Right now, Maguire’s team is focused on isolating more of the exact neural connections that play roles in disorders like these. That means it may be a few years before this “wonder drug” becomes available. In the meantime, I wouldn’t recommend swallowing handfuls of Propecia when you’re feeling stressed – the drug needs to be applied in a pretty targeted way to make this work, which means a major part of pharmaceutical development will be the creation of an effective chemical delivery system.

Even so, it’s exciting to think that before long, depression and anxiety may be as easy to prevent as, say, polio and malaria are today. The thought’s enough to get my hormones pumping, anyway.

Stress and Balance

Our responses to threatening situations depend on two fear-regulation circuits, a recent study shows.

"I wish this job wasn't so heavy on the glutamate."

A well-balanced sense of fear is crucial to our survival: too much, and we’d descend into panic attacks every time we were startled. Too little, and we might not react when survival is crucial. As it turns out, this balance is maintained by two opposing brain circuits, both involving corticotropin-releasing hormone (CRH) and its type 1 receptor (CRHR1).

The body releases CRH in response to stressful stimuli. This substance creates some pretty interesting effects in different parts of the brain – in areas like the forebrainhippocampus, and thalamus, it triggers the release of the excitatory neurotransmitter glutamate, which contributes to anxiety behavior.

But as a new paper in the journal Science shows, CRH helps with a completely different set of responses in the midbrain – it directly triggers the release of dopamine, which reduces fear and increases confidence. This means CRH and its type 1 receptors are involved in a self-regulating circuit that can both spread and reduce feelings of stress:

These results define a bidirectional model for the role of CRHR1 in anxiety and suggest that an imbalance between CRHR1-controlled anxiogenic glutamatergic and anxiolytic dopaminergic systems might lead to emotional disorders.

In other words, these two CRH-triggered systems exist in a delicate balance – and a disruption of that balance could lead to excessive fear reactions on the one hand, or to indifference on the other.

This means it’s probably time for psychiatrists to take another look at anti-anxiety drugs that target the brain’s CRH circuits:

The over-activity of the CRH system in patients with mood disorders is not general but probably limited to certain regulatory circuits in the brain, thus causing imbalanced emotional behavior.

This means that instead of just thinking of CRH as a “stress hormone,” we should probably be looking at these regulatory circuits as whole systems, and examining their interactions with one another.

So the next time you’re feeling panicky, try to remind yourself that it’s just your glumatergic neurons acting up – and those lovely dopaminergic circuits should kick in any second.

Working Off Worry

Want to get rid of gloomy thoughts? Try working some physical activity into your daily routine, says a new study.

Even adorable kitties need an endorphin boost sometimes.

For people who struggle with depression and anxiety, the research shows, exercise can be just as effective as antidepressant medication. It often prevents symptoms from getting worse – and in some cases, it even helps cure the problem.

Doctors have known for decades that a little physical activity can help distract you from your worries, boost positive feelings, and even relieve anxiety and depression. But in recent years, research has shown that exercise’s hidden effects reach much deeper: it tells your body to produce endorphins – natural chemicals that act similarly to morphine – to produce a natural high. And studies have shown that regular exercise can even make you smarter, by increasing blood flow to the brain and triggering neurogenesis – the birth of new neurons.

But as this new paper in the Journal of Clinical Psychiatry reports, a team led by UT Southwestern’s Dr. Madhukar Trivedi has discovered something even more exciting – a regular dose of exercise can work just as well as antidepressant medication:

Many people who start on an antidepressant medication feel better after they begin treatment, but they still don’t feel completely well or as good as they did before they became depressed. This study shows that exercise can be as effective as adding another medication.

In other words, patients who exercised instead of adding a second drug often improved just as much as people who did add another drug.

By the time the 12-week study was finished, almost 30 percent of the patients who exercised had achieved full remission of their depression, and another 20 percent showed significant improvement. That’s close to 50 percent of depressed patients whose moods measurably improved thanks to exercise.

It’s also intriguing that different types of exercise seem to have different effects on people with various characteristics:

Moderate exercise was more effective for women with a family history of mental illness, whereas intense exercise was more effective with women whose families did not have a history of the disease. For men, the higher rate of exercise was more effective regardless of other characteristics.

So if you’re a woman with crazy parents, you might benefit most from a quick jog on the treadmill – but it looks like I’m gonna have to run a Warrior Dash if I want to stop sulking.

Anyway, the good news is, it doesn’t take much of an investment to start seeing the benefits of exercise – most doctors recommend somewhere between 30 and 60 minutes, three times a week. Even taking a short walk on your lunch break can cheer you up.

Unless you’re perambulating on one of these things – I don’t think that counts.

Facing Fear

New neuroscientific studies are shedding light on the allure of dark forests and eerie old houses…and cliff diving.


In psychology, this drive to explore the unusual is one manifestation of the behavior pattern known as “sensation-seeking” – the tendency to pursue intense, novel experiences out of curiosity, or just for the sheer joy of excitement.

Though the behavior of sensation-seekers has been thoroughly studied, the exact reasons for that behavior – and the neuroscience behind those reasons – are only now beginning to be unraveled. As a report in the journal Psychological Science explains, the brains of people who seek out thrills and mysteries actually behave differently from those of more cautious people.

Now, for me, this is about is about as awesome as life gets – my two great loves are weird mysteries and neuroscience, and I’ve spent most of my adult life exploring the the enigma of why the human mind is so fascinated by enigmas. But anyway, on to the data!

A group of researchers led by Dr. Jane Joseph at the University of Kentucky used fMRI to study subjects’ neurophysiological responses to various types of “strongly arousing” stimuli. They discovered that these stimuli activate different cerebral regions, depending on whether or not the subject was a  sensation-seeker:

Regardless of whether the pictures were pleasant (e.g., mild erotica) or unpleasant (e.g., a snake poised to strike), the high-sensation seekers showed early and strong activation in the insula [a cerebral area involved in what might be called “raw” emotions and sensations, such as excitement, pride, hunger, and lust]. In contrast, in the low-sensation seekers, insula activity barely rose above baseline levels.

The brains of these more conservative subjects responded with increased activity in the anterior cingulate cortex (ACC), an area involved in anticipation of errors and conflicts. What’s interesting is that ACCs of sensation-seekers eventually reached similar levels of activation, but took much longer to get there. It’s possible that their brains were responding first with sheer excitement, and only later considering the possibility of danger or failure:

“If you look at the data, you can see that the insula response in the lows starts to rise, just as in the highs, but then the anterior cingulate kicks in and almost seems to deflect the insula response in the low-sensation seekers,” Joseph said.

Sensation-seeking behavior can sometimes be linked with the personality trait known as novelty-seeking, which plays out as an impulsive tendency to explore new stimuli, even to the point of irresponsibility or personal harm. While a moderate amount of novelty-seeking can be evolutionarily beneficial – we might call it “bravery” in such cases – an excess is obviously dangerous.

Some studies suggest that novelty-seeking may be linked to a deficiency in midbrain D2 receptors, which process the “reward” and “motivation” chemical dopamine. Studies on another type of dopamine receptor seem to show an almost opposite effect: sensation-seeking may be linked with higher numbers of D4 dopamine receptors.

The exact mechanisms at work here are still uncertain: it may be that when it’s harder for someone to feel the joy of a thrill, they’ll go further than normal to get it; it’s also been suggested that D2 receptors act as “brakes” on dopamine release, so a deficiency of them would actually allow more dopamine to pump around.

Still, many of us who don’t qualify as real-life novelty-seekers still love to watch thrilling or scary movies now and then. In those cases, the ACC may actually be helping us enjoy the show:

Thrill-seekers may be able to use cognitive parts of the brains to recognize that the scary movie or ride isn’t really going to hurt them … They can put the brakes on the flight and avoidance response and experience the emotional salience of the fear.

The difference between cliff divers and horror fans, it seems, may be less a matter of taste, and more a matter of response threshold. In other words, the safer we feel, the more fun it is to be scared.


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