Your Brain On Junk Food: ‘Making Us Crazy’ — But Might Fish Help?

By Suzanne E. Jacobs
CommonHealth intern

An urban planner and a biochemist walk into a seafood restaurant.

Okay, that joke’s going nowhere, but last week an urban planner and a biochemist did walk into a classroom at MIT. In a talk titled “Junk Food and the Modern Mind,” the unusual duo explained to a room full of people how seafood’s effects on the human brain could bridge their seemingly disparate fields.

The urban planner was Lynn Todman, a visiting scholar at MIT. Todman has spent the past nine years working to improve mental health and reduce violence among residents of some of Chicago’s roughest neighborhoods.

(Wikimedia Commons)

(Wikimedia Commons)

Last year, Todman held a focus group with adult men in Chicago. At one point, she recalled, one of the men said, “This food is making us crazy,” referring to the unhealthy options common in urban food deserts. Having read up on studies linking nutrition and aggression, Todman took what he said seriously.

“Now, I’ve been doing community based work for a long time, and I know that residents often understand social realities long before we do in the academy, and even though their understanding might be shaped by a series of anecdotes strung together to suggest a trend or pattern, I attribute very real meaning to what residents say about their communities and the observations about the world that they live in,” she said.

Enter Capt. Joe Hibbeln, the biochemist.

Hibbeln, who is also a psychiatrist, works at the National Institutes of Health as a nutritional neuroscientist and is one of the world’s leading experts on the role of fats in brain development.

His claim: a diet rich in omega-3 fatty acids and low in omega-6 fatty acids can make people happier and less aggressive. Continue reading

On Perception (And Pancakes): How The Brain Keeps Vision Stable

By Alexandra Morris
CommonHealth Intern

You probably didn’t think Julia Roberts could teach you much about subtle, yet critical, brain functions.

But, it turns out, she can. Recall Roberts in her iconic film “Pretty Woman.” In one scene, she is eating a croissant. But as the camera pans back to her, the croissant turned into a pancake.

It’s likely that many of us missed that blooper, and now we know why. Scientists have discovered a brain mechanism that smooths our field of vision so that we don’t notice certain subtle visual changes — such as a croissant becoming a pancake in an otherwise identical scene.

In a paper published last month in Nature Neuroscience, researchers from the University of California, Berkeley have identified a brain mechanism that helps to stabilize our field of vision. They call it, a “continuity field” — a process the brain uses to merge similar objects seen within a 15-second timeframe.

“It seems like a very odd thing the brain is doing that could make us less accurate,” said the study’s lead author, Jason Fischer, who is now a postdoctoral fellow in the Department of Brain and Cognitive Sciences at MIT. “But in fact there is this huge benefit to it — and that is stabilizing perception over time.”

To measure this process, researchers showed study participants an image with alternating light and dark bars, or “gratings,” at a random angle every five seconds. The participants were then asked to move a white bar to match the tilt of the grating that had been shown.

Here’s the video:

Researchers found that while the white bars generally aligned with the image, there were subtle differences that were biased toward the previous three or so images. These differences could be attributed to the continuity field.

Imagine, now, for example, you are driving down a highway in the pouring rain and you’re trying to read a road sign. The windshield wipers are moving; the raindrops are hitting your windshield. As you’re looking at the sign, you’re experiencing constant interruptions in your visual stream. In that case, the changes that the continuity field is causing us to miss are the raindrops and windshield wipers — you may even fail to notice them after a while. The continuity field, for the most part, is beneficial — it blocks the stuff we don’t want to see. Continue reading

Why To Exercise Today: It Even Appears To Help Your Eyes

(Wikimedia Commons)

(Wikimedia Commons)

God help us, when will it ever stop? Is there no organ, no medical condition, no tiny part of the human body that is not helped by exercise?

A new mouse study in the The Journal of Neuroscience finds that exercise appears to be good for the retina, and may even slow the development of age-related macular degeneration, which is estimated to affect nearly 2 million older Americans. The key appears to be a helpful protein called brain-derived neurotrophic factor. From the press release:

Moderate aerobic exercise helps to preserve the structure and function of nerve cells in the retina after damage, according to an animal study appearing February 12 in The Journal of Neuroscience. The findings suggest exercise may be able to slow the progression of retinal degenerative diseases.

Age-related macular degeneration, one of the leading causes of blindness in the elderly, is caused by the death of light-sensing nerve cells in the retina called photoreceptors. Although several studies in animals and humans point to the protective effects of exercise in neurodegenerative diseases or injury, less is known about how exercise affects vision.

Machelle Pardue, PhD, together with her colleagues Eric Lawson and Jeffrey H. Boatright, PhD, at the Atlanta VA Center for Visual and Neurocognitive Rehabilitation and Emory University, ran mice on a treadmill for two weeks before and after exposing the animals to bright light that causes retinal degeneration. The researchers found that treadmill training preserved photoreceptors and retinal cell function in the mice.

“This is the first report of simple exercise having a direct effect on retinal health and vision,” Pardue said. “This research may one day lead to tailored exercise regimens or combination therapies in treatments of blinding diseases.” Continue reading

Your Brain On Poverty: Low-Income Childhood Linked To Smaller Brain

Young children living in poverty appear to have smaller brain volumes in critical areas, according to researchers at Washington University School of Medicine. But poverty’s detrimental impact on brain development may be mediated by basic early interventions like compassionate parenting and caregiving, the report says.

(Digital Shotgun/flickr)

(Digital Shotgun/flickr)

Growing up poor is already known to be associated with a higher risk of “poor cognitive outcomes” and school performance, the researchers note. But what’s fairly new here is how outside economic forces play out in the development of a child’s brain. According to the study, published in JAMA Pediatrics Monday:

Poverty was associated with smaller white and cortical gray matter and hippocampal and amygdala volumes. The effects of poverty on hippocampal volume were mediated by caregiving support/hostility on the left and right, as well as stressful life events on the left.

The finding that exposure to poverty in early childhood materially impacts brain development at school age further underscores the importance of attention to the well-established deleterious effects of poverty on child development. Continue reading

The Genetics Of Autism: Inside The Brains Of The Supple Boys

Don’t miss Lynn Jolicoeur’s excellent piece on WBUR this morning about the genetics of autism and the two young Natick boys, Tommy and Stuart Supple, whose gene mutations are the focus of research by Stanford neuroscientist Dr. Thomas Sudhof.

(Jesse Costa/WBUR)

(Jesse Costa/WBUR)

From Lynn’s story:

…The Stanford University neuroscientist — who this year shared the Nobel Prize in medicine for his decades of study into how brain cells communicate — has been studying Tommy and Stuart’s genes, specifically an alteration in one gene, for five years. The Supples hosted Sudhof Wednesday night at a Boston fundraiser in support of his research into the functioning of brain synapses in autism…

According to the Supples, Sudhof’s work is helping conquer the “defeatism” surrounding the neurocognitive disorder.

“He doesn’t think this is unknowable at all. He thinks that it’s very knowable,” Kate Supple said. “We all put so much time and effort into dealing with the symptoms of autism. But you also have to look to deal with the underlying disease.”

For many parents of children with autism, the disorder is a mystery. They have no idea what caused it and focus on therapies to help address the symptoms. But after the blow of both boys being diagnosed before their 2nd birthdays, the Supples sought out private genetic testing without the encouragement of their doctors. Continue reading

Huh? Hunger Hormone May Be Key To Stress Effects On Mental Health

Dr. Ki Goosense and .....

Dr. Ki Goosens and Technical Associate Junmei Yao examine a piece of human brain at the McGovern Institute for Brain Research. They are looking for stress-sensitive genes that are abnormally activated in the amygdala — a brain region that regulates emotion — in people who committed suicide. (Courtesy Justin Knight Photography and McGovern Institute)

(Click the play button above for the audio version of this story.)

Neuroscientist Ki Goosens does her research with black and white rats, but what she has discovered could be very relevant to humans — including her own family.

In the last eight years, three family members have become suicidal in the wake of a “major life stressor” like divorce.

“For years, they were fine, and then it triggers some cascade of vulnerability,” she said. “So I feel a sense of urgency in trying to come up with new ways to think about how we can block the ability of stress to worsen mental illness, to trigger mental illness.”

Goosens and her team at MIT’s McGovern Institute for Brain Research have just published what could be a major lead: A hormone called ghrelin — known as the hunger hormone and made in the stomach — may be a key to post-traumatic stress disorder and other stress-related mental illnesses.

The research is still early, but it raises the possibility that drugs that block ghrelin could be used to block some of the mental harm done by chronic stress.

‘I’m a neuroscientist. I study the brain. But you sort of go where the data take you.’

Goosens and her collaborators at Mass. General Hospital are now planning two studies on ghrelin in humans: One will determine whether ghrelin levels are elevated in people with anxiety disorders; the other will block ghrelin signaling in hopes of preventing stress-related relapses of depression.

Goosens never expected to be using a hunger hormone to understand stress: “If you had asked me five years ago if I would be doing something related to the stomach, I would’ve said, ‘No way, you’re crazy. I’m a neuroscientist! I study the brain,’” she said. “But you sort of go where the data take you.”

She originally set out to explore how stress affects the activity of genes in the amygdala, a part of the brain that processes emotions. Continue reading

Nature: Recipe For A (Primitive Precursor Of A) Human Brain In A Jar


So delicious! No, I don’t mean vat-grown brain pickles. I mean the delicious frisson I get every time real-life science news seems to echo long-beloved science fiction in uncanny ways.

So to today’s very serious report in the prestigious journal Nature: Researchers have found a way to build a sort of a human proto-brain in the lab. (Of course, their work, striking as it is, falls miles short of the classic cinematic depictions of brains in jars, but let’s just take a moment here to recall Steve Martin’s true love in “The Man With Two Brains,” and the ancient black-and-white sci-fi flicks featuring disembodied brains. “Brain in a jar” even has a whole page on

Now to 2013 reality: The scientists, based mainly at the Institute of Molecular Biotechnology in Vienna, used stem cells to engineer a three-dimensional precursor of a human brain, about the size of a pea. They say this miniature proto-brain could help illuminate how the human brain develops — and what can go wrong as it does.

They grew the stem cells into a brain-like structure at about the level of a nine-week-old human embryo’s brain. And they showed that this primitive mini-brain could cast light on a specific disorder: microcephaly, a rare birth defect in which the brain doesn’t grow nearly as big as it should.

The work is still in very early stages, but the researchers say they hope it can also be used to help treat more common brain diseases that begin early in life, including schizophrenia and autism.

They began with human stem cells from adults, and helped them grow and self-organize into a primitive but strikingly brain-like structure, which they call a cerebral organoid. An organoid is a structure like an organ — so this isn’t a full-fledged brain, but if you consider that the human brain is known as the most complex organ in the animal kingdom, it’s still pretty impressive.

So what exactly is the recipe for whipping up a human brain? Continue reading

Tracking Dyslexia In The Preschool Brain

By Karen Weintraub
Guest Contributor

Roughly one child in 10 will struggle to learn to read, but no one can tell which one until he or she starts to fall seriously behind.

At that point – often in 3rd grade – they’ve already taken a hit to their self-esteem and they’re too old for early intervention that can make the biggest difference.

This conundrum has troubled MIT professor John Gabrieli for years.

The area highlighted in yellow, called the arcuate fasciculus, is less robust in children at high risk for dyslexia, according to a new study.

The area highlighted in yellow, called the arcuate fasciculus, is less robust in children at high risk for dyslexia, according to a new study.

Today, the neuroscientist and colleagues published a study that begins to address the problem. They showed on brain scans that kindergartners at risk for dyslexia also had less robust connections between two key language areas on the left side of the brain.

Previously, researchers weren’t sure whether the differences they saw in the brains of people with dyslexia were causes of the condition, or effects of their struggle to read. Because Gabrieli’s group saw the distinction in children too young to read, their brain differences must predate reading problems.

His ultimate hope, of course, is to use these differences to identify children before they begin to struggle, and get them into early intervention programs. Continue reading

‘Total Recall’ For Mice: Scientists Implant False Memories

Arnold Schwarzenegger in "Total Recall" trailer (YouTube)

Arnold Schwarzenegger in “Total Recall” trailer (YouTube)

In “Total Recall,” Arnold Schwarzenegger’s best film ever (in my humble opinion), he plays a construction worker who seeks a “memory implant” from a company that provides them to customers who want a false memory of a wonderful vacation they can’t afford to take.

That’s just the beginning of the complex plot, based on the ingenious Philip K. Dick’s “We Can Remember It For You Wholesale,” but of course I thought of it immediately when I saw this major memory news out of MIT in the journal Science:

Researchers at the RIKEN-MIT Center for Neural Circuit Genetics and MIT’s Picower Institute for Learning and Memory have implanted false memories into mice, potentially illuminating the mechanisms underlying the human phenomenon of “recalling” experiences that never occurred.

In previous work, the researchers had detected a single memory in the brain, genetically tagged the brain cells housing that memory with a light-sensitive protein, and flickered pulses of light to “turn on” the memory at any given moment. The latest work, to be reported in the journal Science, tinkers with that memory to change its contents—in essence, creating a false memory.

Mars, here I come. (Schwarzenegger’s character signs up for a Mars vacation implant.) Actually — sigh — I doubt we’ll be implanting false memories of Mars trips any sooner than we get to Mars for real. But this new work does have more immediate implications for the study of how we make memories — including how we seem to remember things that never actually happened.

For more on how the experiment was conducted, read the Globe’s Carolyn Johnson’s excellent report here. I spoke with Susumu Tonegawa, the MIT brain scientist and Nobel laureate who led the work, about what it could mean. Our conversation, lightly edited:

So in what way is this experiment a “first”?

This is the first time a study allowed for the making of animal models of human false memory.

We knew that false memories existed in humans. So this is the first time that it’s been shown in animals that it’s possible to create a false memory and manipulate it?

That’s exactly right — and that’s important because in humans, all false memory has been studied by psychology. But the human studies had a lot of limitations in terms of understanding what’s going on in the brain. So an animal model is very important.

How would you describe the implications of these animal findings for humans?

First, in terms of practicality, I think we’ve shown how easily false memory can be formed. And also, in terms of underlying brain mechanisms, we have demonstrated that the mechanism for forming false memory is virtually identical to the mechanism underlying the formation of real memory. Continue reading

Study: Your Brain Makes Hundreds Of New Neurons A Day

(Digital Shotgun/flickr)

(Digital Shotgun/flickr)

This just in from the journal Cell: Your hippocampus, a key region for memory in your brain, makes a few hundred new neurons every day.

Does this mean you can now drink Tequila shots with impunity because you can more than make up for the brain cells you damage? Nope, no reason to think so. But the findings in Cell could have implications for future research in areas from antidepressants to Alzheimer’s disease.

Mainly, the new study helps cement the long-controversial claim that new neurons keep a-borning in the human brain all through life. And it does so in a creative new way, using carbon-14 left in humans by above-ground nuclear tests in the mid-20th century to measure the ages of brain cells.

I asked Prof. Joshua Sanes, director of Harvard University’s Center for Brain Science, to explain what the study could mean — why it matters whether our hippocampi keep making new neurons or not. His reply, lightly edited:

The basic dogma of neurobiology has been that you’re born with all the neurons you’re ever going to get, and then everything goes downhill from there.

But there was heated debate about this, and eventually, it was found in experimental animals that you do actually get new neurons throughout life — but weirdly, only in a few places. Where would depend on the species, but for mammals like us, it’s your olfactory bulb — what the heck that is about, nobody has any idea — and the other place is the hippocampus.

The hippocampus has proven to be critical to memory, and I’m not sure whether you’d say memories are stored there, but they certainly seem to be made there. You probably know about the famous patient HM: When he lost his hippocampus, he lost his ability to make memories.

So the idea arose that maybe if you’re making new neurons in the hippocampus, that’s to help you make new memories. In mice, there’s some evidence that favors that idea. I think nobody thinks it’s going to be as simple as that — that every time you need a new memory, you make a new neuron — but there are lots of experiments where they prevent the making of new neurons and somehow degrade memory in mice. And it seems that a lot of the things that a mouse does can affect how many new neurons are made, or at least how many of the new neurons that are made wire up.

One of those things is exercise: if you exercise more, you make, or keep, more new neurons. If you suffer a lot of stress, you make fewer neurons. Depression has been implicated; nobody knows how but there’s some idea that antidepressants can help you make new neurons, and if you’re depressed, you make fewer neurons.

So people have been interested in these new neurons, but nobody knew whether they were made in the human hippocampus, and this new study tells you that they are. Continue reading