Blind sight: The next generation of sensory substitution technology

Conventional wisdom says that you see with your eyes. But new technology is changing the way we think about sensation and perception, showing that instead of relying on these orbs for vision, we instead really see using the activity in our brains.

My newest piece for Discover Magazine explores three amazing devices that are restoring sight to the blind, circumventing the malfunctioning sensory organs and tapping into the healthy neuro-circuitry underneath. High-tech computers in Google Glass-like devices are converting visual information into auditory and tactile stimuli, allowing the blind to see, drive, navigate, and mountain climb using their ears, fingertips, and even their tongues, the brain translating this information back to the visual cortex.

Check out the full piece here, including a video of one of the devices in action.

Spending more time in the dark could boost hearing in old age

Your brain can do amazing things, not least of which is change. Specifically, neurons can adapt and grow new connections to help compensate for a loss in function in other areas. This has been most dramatically shown in children who have an entire hemisphere of their brain removed, usually to treat extreme cases of epilepsy, the other side taking over so that they can still walk, talk and function normally. Another common example of this type of neural plasticity is the improvement of other senses, particularly hearing, after the loss of sight.

In my latest article for The Guardian, I review a study that reports improvements in hearing in mice that have been visually sensory deprived for a week — meaning they were locked in a darkened room. Amazingly, cells in a sensory relay-station part of the brain reorganized to strengthen their hearing after this temporary loss of sight, even in older mice, which were previously thought to be exempt from this ability. While it’s still early days, this finding opens up the possibility for less invasive ways to treat hearing loss in old age.

Check out the full piece here.

How a pregnant mother’s diet could change a child’s brain

Scientists have pursued every possible avenue to try to figure out why we keep getting fatter. They’ve explored our genes, our brains, our hormones and our gut bacteria, not to mention our fatty, sugary diets and sedentary lifestyles. Now, a recent study has come out blaming our expanding waistlines and poor health on our parents’ behaviors before we were born.

My newest article is up on The Atlantic, discussing recent research on the impact a mother’s diet has on her offspring’s health, affecting our brains and subsequently our bodies. This line of research isn’t new — other studies have shown links between a woman’s health during pregnancy and her child’s weight later in life — but this is one of the first to provide a potential explanation for this phenomenon by looking in the brain at some crucial hunger hormones.

However, you can’t blame all of your problems on your parents; what you eat still has a major impact on how these brain changes manifest:

Now, I’m all for shifting blame away from myself and onto my parents, but I feel that, like every possible explanation behind the obesity epidemic, this is only one piece of the puzzle. Genes undoubtedly play a role in body mass, fat percentage, and metabolism, but so does what you eat and how many calories you burn through physical activity…The problem of obesity, like so many health and social issues we face today, is that there isn’t just a single contributor to the problem. If there were, it would have been solved by now.

Check out the entire piece here.

Seeing left, smelling right

We’ve all heard about the “left-brain/right-brain” hype, which, to be honest, is really just a bunch of malarkey. Supposedly, a bigger right hemisphere means you’ll be a great artist, and a larger left indicates a penchant for science. If the dancer spins clockwise, you’re right-brained, while if you’re left-brained she twirls counter-clockwise.

Fortunately, all of these neural conspiracy theories have been largely debunked. However, the fact does remain that we do have two hemispheres that are connected but divided – a cortical “separate but equal,” if you will. And oftentimes, one of these hemispheres is larger than the other, the smaller being situated slightly behind. Now, again, this is not to say that the bigger hemisphere is better, simply that they are asymmetric, and presumably this asymmetry has evolved for a reason.

Researchers from University College London have investigated the purpose of this neural asymmetry on a much smaller scale using the zebrafish, a common animal model used for investigating basic but deceptively complex brain-related phenomena thanks to their simplified central nervous system. Published in the journal Current Biology, the researchers discovered that neuronal asymmetry lends itself towards enhanced processing of sensory information in the zebrafish, and that a symmetrical brain can result in an impairment of the processing of visual or olfactory stimuli.

The researchers focused on the habenula – an area located near the thalamaus that is a type of way station in the brain, processing sensory information. The habenula receives inputs from around the brain and helps to designate the appropriate neurochemical output for neurons further down the line. However, cells in the left and right habenula react differently to different types of stimuli, resulting in separate projections to other areas of the brain.

In the current study, cells in the right habenula were largely responsible for receiving odor information, while the left-sided neurons processed visual information. Very few neurons responded to both types of stimuli. These left and right neurons also had distinct outputs, the left heading to the dorsal, or top, interpeduncular nuclei (IPN), while the right had outputs to the ventral, or bottom, IPN. These ventral and dorsal IPN neurons subsequently had their own distinct outputs as well, meaning the entire operation of processing visual and olfactory information was distinct, divided between the two hemispheres.

The real test of any scientific phenomenon though, is what happens when you disrupt this process (scientists really just like to mess things up to see what will happen). Will the other hemisphere take over, or will that function be entirely lost?

To find out, the researchers “shocked” the fish with cold – meaning when the fish were still embryos, they exposed them to extreme cold with the hopes of disrupting their typical gene expression and thus their cell development. In fact, using cold shock was so successful, it resulted in a complete reversal of many of the fishes’ neurons, meaning that what was right was now left, and left was right. Not only did this lead to a switch in the processing of sensory information, but the entire assembly line from the habenula neurons on down was reversed, a mirrored reflection of the fishes’ normal cell functions. Light information was now processed on the right side, however, the projections to the IPN remained the same. So light processed on the right side projected to the dorsal IPN, whereas previously the dorsal IPN had been activated by the left habenula light response.

The final step was to find out what happens when asymmetry is completely lost, to ascertain whether there was a functional benefit to this lateralization (again, scientists really just like to mess with a perfectly good brain process). To do this, the researchers manipulated the fishes’ neurons so that the habenula cells were either all right or all left. That isn’t to say that all the neurons were located on either the left or the right side, but rather the cells acted like they were all “right” neurons or “left” neurons, receiving inputs and creating outputs from and to their respective sources.

This complete lateralization resulted in a loss of the opposite side’s function, meaning the “double-left” fish had exceptional vision but were unable to process odors, while the “double-right” fish were blind to the light but had a super-power sense of smell.

Finally, even fish that were raised in complete darkness still showed this laterality when it came to processing visual information, meaning that the brain’s left-right organization was dependent on gene expression, not the cells’ experience or exposure to light.

From this, the researchers concluded that it doesn’t actually matter which side the cells are on, so long as each type of cell and its connections are in place. But a loss of those neurons, even if others are in their place, leads to complete functional disruption. And really, this makes sense; it is not the location of the cell but its connections that truly matter, dictating its function.

Yet another instance of science proving cool stuff that, if we really thought about it, we already kind of figured to be true.

Also posted on Mind Read.

The White Stuff

Whether it goes in our mouths or up our noses, we’re drawn to the powdery chemical confectionaries that can both give us pleasure and cause us harm — The White Stuff

I’m very excited to announce a new project I’m launching today on Beacon Reader, The White Stuff, where I’ll be writing about our favorite vices: food and drugs. I’m trying to bring some sense into the ongoing debate about what we put into our bodies, and my goal is to provide unbiased research-based reporting on the latest science and policy news on addiction, nutrition and everything in between.

Beacon is a new kind of journalism platform that, instead of being financed with ads or commissions, lets you fund my work directly. In addition to my own writing, you’ll get access to exclusive content from all of the other amazing journalists on the site who write about politics, technology, global issues, sports and more.

However, I need help getting the project off the ground. In order for the project to launch, I need 25 people to subscribe in the next 14 days. If you like what you’ve read on Brain Study, please help with my new endeavor by subscribing and sharing my project page for The White Stuff (there’s even a snazzy promo video).

I’ll still be writing from time to time on Brain Study, but most of the action is going to be over on Beacon, so if you want to stay up-to-date, please subscribe!

Anxiety about certain things can be hereditary

It looks like we might be able to start putting the nature-nurture debate to bed. Epigenetics – the new hot-button research topic in both science and the media – is the ability of genes to be influenced by our experiences, altering our genetic make-up in real time. By changing the chemical signals that course through your brain and body, you can actually turn genes on or off, a process that can then influence your future actions. Thus, in some ways, epigenetics can be thought of as the bridge between nature and nurture—your behavior and environment affecting your biology, and vice versa.

I have an article in The Atlantic this week exploring epigenetics through a couple recent studies investigating inherited learning – where a parent’s experience alters their own genetic make-up, and this change is then passed on to their child. Admittedly, this all sounds a bit too much like Lamarckism, and scientists are quick to caution that the field is still in its infancy, so it’s hard to tell just how important this will be for our understanding of genes and behavior. But in the mean time, some of things we’re discovering about our parents’ unseen influence on us are pretty damn cool.

Check out the full Atlantic piece here.

Can synesthesia in autism lead to savantism?

I’ve got a new piece out on the Scientific American MIND blog network today on the fascinating link that’s been discovered between synesthesia – a “crossing of the senses” where one perceptual experience is tied to another, like experiencing sound and color together – and autism spectrum disorder.

Individuals with autism have significantly higher rates of synesthesia than the rest of the population, and the two are potentially linked by a unique way in which the brain is wired. White matter tracts that traverse our brains, connecting one area to another, are thought to be increased in both conditions. This results in an abnormal wiring of the brain that may lead in more close-range connections, but fewer long-distance ones. And it’s possible that these extra connections may also contribute to some of the extraordinary cognitive abilities seen in some autistic individuals with savant syndrome.

For more on the story, check out the full piece on here.

Do you have an addictive personality?

You’ll have to bear with me if this is a bit of a self-indulgent post, but I have some exciting news, Brain Study-ers: I’ve officially submitted my dissertation for a PhD in psychology!

In light of this – the culmination of three years of blood, sweat, tears and an exorbitant amount of caffeine – I thought I’d write this week on part of my thesis work (I promise to do my best to keep the jargon out of it!)

One of the biggest questions in addiction research is why do some people become dependent on drugs, while others are able to use in moderation? Certainly some of the risk lies in the addictive potential of the substances themselves, but still the vast majority of individuals who have used drugs never become dependent on them. This then leads to the question, is there really such a thing as an “addictive personality”, and what puts someone at a greater risk for addiction if they do choose to try drugs?

We believe that there are three crucial traits that comprise much of the risk of developing a dependency on drugs: sensation-seeking, impulsivity and compulsivity.

Sensation-seeking is the tendency to seek out new experiences, be they traveling to exotic countries, trying new foods or having an adrenaline junkie’s interest in extreme sports. These people are more likely to first try psychoactive drugs, experimenting with different sensations and experiences.

Conversely, impulsivity is acting without considering the consequences of your actions. This is often equated with having poor self-control – eating that slice of chocolate cake in the fridge even though you’re on a diet, or staying out late drinking when you have to be at work the next day.

While impulsivity and sensation-seeking can be similar, and not infrequently overlap, they are not synonymous, and it is possible to have one without the other. For example, in research we conducted on the biological siblings of dependent drug users, the siblings showed elevated levels of impulsivity and poor self-control similar to that of their dependent brothers and sisters, but normal levels of sensation-seeking that were on par with unrelated healthy control individuals. This led us to hypothesize that the siblings shared a similar heightened risk for dependence, and might have succumbed to addiction had they started taking drugs, but that they were crucially protected against ever initiating substance use, perhaps due to their less risk-seeking nature.

The final component in the risk for addiction is compulsivity. This is the tendency to continue performing a behavior even in the face of negative consequences. The most classic example of this is someone with OCD, or obsessive-compulsive disorder, who feels compelled to check that the door is locked over and over again every time they leave the house, even though it makes them late for work. These compulsions can loosely be thought of as bad habits, and some people form these habits more easily than others. In drug users, this compulsive nature is expressed in their continued use of the substance, even though it may have cost them their job, family, friends and health.

People who are high in sensation-seeking may be more likely to try drugs, searching for that new exciting experience, but if they are low in impulsivity they may only use a couple of times, or only when they are fairly certain there is a small risk for negative consequences. Similarly, if you have a low tendency for forming habits then you most likely have a more limited risk for developing compulsive behaviors and continuing an action even if it is no longer pleasurable, or you’ve experienced negative outcomes as a result of it.

Exemplifying this, another participant group we studied were recreational users of cocaine. These are individuals who are able to take drugs occasionally without becoming dependent on them. These recreational users had similarly high levels of sensation-seeking as the dependent users, but did not show any increase in impulsivity, nor did they differ from controls in their self-control abilities. They also had low levels of compulsivity, supporting the fact that they are able to use drugs occasionally but without having it spiral out of control or becoming a habit.

We can test for these traits using standard questionnaires, or with cognitive-behavioral tests, which can also be administered in an fMRI scanner to get an idea of what is going on in the brain during these processes. Behaviorally, sensation-seeing roughly equates to a heightened interest in reward, while impulsivity can be seen as having problems with self-control. As mentioned above, compulsivity is a greater susceptibility to the development of habits.

In the brain, poor self-control is most commonly associated with a decrease in prefrontal cortex control – the “executive” center of the brain. Reflecting this, stimulant-dependent individuals and their non-dependent siblings both showed decreases in prefrontal cortex volume, as well as impairments on a cognitive control task. Conversely, recreational cocaine users actually had an increase in PFC volume and behaved no differently from controls on a similar task. Thus, it appears that there are underlying neural correlates to some of these personality traits.

It is important to remember that we all have flashes of these behaviors in differing amounts, and it is only in extremely high levels that these characteristics put you at a greater risk for dependence. Also, crucially it is not just one trait that does it, but having all three together. Most notably though, neuroscience is not fatalistic, and just because you might have an increased risk for a condition through various personality traits, it does not mean your behavior is out of your control.

Oh, and I’ll be going by Dr. D from now on.

—

Ersche, KE et al., Abnormal brain structure implicated in stimulant drug addiction. Science 335(6068): 601-604 (2012).

Ersche, KE et al., Distinctive personality traits and neural correlates associated with stimulant drug use versus familial risk of stimulant dependence. Biological Psychiatry 74(2): 137-144 (2013).

Smith, DG et al., Cognitive control dysfunction and abnormal frontal cortex activation in stimulant drug users and their biological siblings.Translational Psychiatry 3(5): e257 (2013).

Smith DG, et al., Enhanced orbitofrontal cortex function and lack of attentional bias to cocaine cues in recreational stimulant users.Biological Psychiatry Epub ahead of print (2013).

You are what you eat

Anyone who’s ever tried to cure the blues with Ben and Jerry’s knows that there is a link between our stomachs and our moods. Foods high in fat and sugar release pleasure chemicals like dopamine and opioids into our brains in much the same way that drugs do, and I’d certainly argue that french fries and a chocolate milkshake can perk up even the lousiest of days.

This brain-belly connection works in the opposite direction, too. Ever felt nauseous before giving a big presentation? Or had butterflies in your stomach on a first date? It’s this system relating feedback from your brain to your gut causing those sensations and giving you physical signals that something big is about to happen.

However, instead of trying to suppress those feelings (or running to the bathroom every five minutes) it now appears that we can use this brain-body loop to our advantage. Formally referred to as the microbiome-gut-brain axis, bacteria that live in our stomach and intestines can affect our responses to stress and anxiety, and research in recent years has shown that probiotic bacteria – like those found in many strains of yogurt – can help to reduce anxiety and elevate mood in addition to helping us “stay regular”.

Previous research has shown reduced fear and stress responses during anxiety-inducing tests in mice who were fed broth with an added probiotic. This included less freezing in the face of fear, greater exploration of new environments, and fewer indicators of depression during a behavioral despair test (cheerful, huh?). These chilled out mice also had lower levels of corticosterone – a major stress hormone – after being tested, corroborating these behavioral findings.

Now, recent research from a team of doctors at UCLA’s School of Medicine and *CONFLICT OF INTEREST ALERT* funded by Danone, the yogurt company, has for the first time provided support for this brain-stomach connection in humans. These researchers looked at the effect eating yogurt (or as they like to call it, a “fermented milk product with probiotic”) every day for four weeks had on neural responses to pictures of negative faces. This type of task usually causes an increase in activity in emotion and somatosensory regions of the brain, like the amygdala and the insula, indicating an unpleasant or stressful reaction to the images. Compared to control individuals who had eaten just a normal fermented milk product, those who had eaten the probiotics had decreased activity in these brain areas, suggesting they were not as affected by the pictures.

Curiously though, there was no difference between the groups in probiotic levels found in stool samples taken (yes, they tested their poop), and none of the participants reported feeling any changes in their levels of stress, anxiety or depression during the study. However, there were significant differences in brain activity between the groups while they were resting, including in the areas identified during the task. Altogether, it looks like even small amounts of probiotics (i.e., not enough to change your gut levels) can still have a significant affect on our brain activity, even without noticeably changing our moods.

This interaction between our guts and our gray matter is thought to be facilitated by the vagus nerve traveling down the base of the brain into the stomach, transmitting sensory information and chemical signals from internal organs back up to the brain. Supporting this theory, when this nerve was cut in the first study the positive effects of the probiotics disappeared, and the test mice were back to their normally anxious selves.

It doesn’t appear that non-fermented milk products have the same positive effects on the brain, so it looks like I’ll be switching my usual Ben and Jerry’s to frozen yogurt for the next few weeks while I finish writing up my PhD thesis. Maybe it’ll help with my growing “thes-ass” too!

(Originally posted on Mind Read)

(“Thes-ass” coinage credit to Anna Bachmann)

An unconventional treatment for depression: Sleep deprivation

I watched a good ‘psychological thriller’ the other night – Side Effects by Steven Soderbergh – that centers on a woman’s debilitating depression and critiques the pharmaceutical industry’s untoward influence over clinicians (it turns into a plot-twisty crime thriller, but that’s beside the point). The film got me thinking about our reliance on psychotropic medications to treat psychological distress, and how helpless we are when these pills don’t work.

I’ve written before on the over-medicalization of psychiatric disorders and the pharmaceutical industry’s role in this controversy, but this time the topic got me thinking about possible alternative treatments for depression, other than cognitive-behavioral therapy or mood-altering medications.

One innovative method for treating depression that has received attention is sleep deprivation. Acute sleep deprivation has been touted as having a 60% success rate in immediate relief from depression; however, this effect is temporary, only lasting until you finally do nod off.

At first this might seem surprising, after all, think about how cranky and irritable you feel after a poor night of sleep. But complete deprivation (i.e. missing an entire night’s sleep, or more than 12 hours) can actually have the opposite effect. Remember that loopy, giggly, hysterical feeling you used to get staying up all night at a sleepover, or at 5am in the library while studying for exams? It is believed that this phenomenon is at least partially caused by an alteration in activation and connectivity in our frontal cortex, potentially offsetting the harmful effects chronic depression can have on this area.

It is still relatively unknown how or why exactly this works though. A recent study from Tuft’s University attempted to answer this question by testing sleep deprivation and its efficacy as an anti-depressant in depressed mice. First, researchers confirmed that depressed animals who were sleep-deprived for 12 hours displayed significantly less depressive symptoms than control depressed mice. Then, for the first time, they were able to link this effect to the activation of a certain type of brain cell, astrocytes, that release a particular protein, adenosine.

Adenosine is important in sleep regulation, and its absence has also been implicated in a greater risk for depression. Adenosine release is increased the longer you’re awake (to a point), making you feel less aroused and more tired, and acting as part of your normal sleep-wake cycle. A beneficial side effect of its release now also appears to be an alleviation of depressive symptoms. However, after 72 hours of sleep deprivation there was no change in adenosine levels, as the astrocyte cells had largely shut down by this point. Thus, there was no effect of more extreme sleep deprivation on feelings of depression. Also, as soon as you do catch up on some zzz’s your adenosine levels return to normal and the anti-depressant effects disappear.

Adenosine’s effect on depression potentially works by altering the electrical signals in your brain, causing an immediate change in mood and behavior. Other fast-acting, unconventional treatments for depression, like deep brain stimulation and electro-shock therapy, are thought to work in a similar manner, impacting the brain’s electrical currents. These treatments also last much longer, suggesting that there may be a way to channel adenosine’s electrical effect into a longer-term solution.

I should be clear that I am in no way against using psychotropic medication to treat psychiatric disorders; in fact, in many instances these pills are absolutely essential. But in cases where these medications don’t work, or where their Side Effects are too severe (seriously, go see the movie!), it is important to have well-researched alternatives to the standard course of treatment. Also, it’s always nice to know how to get a good natural high every now and then, if you can stay up that long.

(Originally posted on Mind Read)