12 Minutes to a Better Brain

Exercise as “Brain Food” and Its Impact on How We Le

I am sure we are all familiar with the old adages “Drink your milk, it will make your bones strong” and “Eat your spinach, so your muscles will be big like Popeye’s”.

As common and “parental” as these phrases may seem, they are actually backed by science. The calcium our body absorbs when we drink milk is related to bone strength. The vitamins and minerals in spinach (and many other vegetables) will allow our body to function in a better way, giving us more energy to become strong. There is a new idea circulating in research (as well as mainstream media) and the evidence based recommendation is:

“Get heart pumping exercise to strengthen your BRAIN

Brain

 

Not your heart, not your muscles, not your lungs, though those results will also occur and be beneficial. However the focus of the emerging research I am referring to is showing that aerobic or vigorous exercise likely leads to increases in brain function (also known as “cognition”) and improve a person’s memory, attention, and academic performance overall.

How does this work?

First a little background on how fascinating our brains are…

Remember the days of Play Doh? Molding, mashing, creating- keeping us busy for hours? Remember what happened if you left the Play Doh out of its container for too long (ok maybe it was just me who did this as a little kid?). Let me fill you in- it becomes rock solid. Yup, no more forming dogs and houses and “doh” patties. It was literally unable to be shaped. About 100 years ago that is how scientists viewed our brains, once formed, sort of hard and “un-moldable”. However, many brilliant scientists over the years have thankfully discovered that our brains are not “stuck” after a certain age. Our brains are actually constantly adapting and responding, a concept with a fancy name termed “neuroplasticity”. Neuroplasticity simply means that our brains can change and DO change, depending on what kind of “stuff” we put in it. This type of stuff that influences our brain includes:

  • What we listen to: loud music, background noise; research shows that young children and babies who are exposed to great amounts of noise (White noise, background noise, tv produced noise) may have significant negative effects on their attention and learning later in life.
  • What we see: images that we watch on tv and movies, pictures we look at influence how our brains experience real life. It can be a negative experience if we “feed” our brains with violent, angry or traumatic images on a regular basis. On the other hand when we provide our brains with positive, relaxing and funny input, it can boost our body systems as a whole.
  • What we eat: foods high in antioxidants (berries, greens, and yes, DARK CHOCOLATE) protects the insulation cells in our brain keeping it functioning as fast as we need it to
  • What and how we learn: this is one of the hottest topics in research right now, as we are seeing that even well into adulthood (When brains are LESS likely to change) the connections in our brain can be strengthened with learning new tasks (such as a language, or a picking up a new creative hobby such as painting or drawing), reading new material, or doing word and number puzzles.
  • How we rest: The importance of sleep, and good quality sleep (READ: NO TV, MORE THAN 6 HOURS, etc) is essential to maximizing our brain potential
  • HOW WE MOVE: This is the main point of this post and will be the focus from here on out…

 

Scientists have discovered that when we exercise (especially when we perform aerobic exercise; meaning heart pumping, heavy breathing, maybe even break a sweat type exercise) that our brains respond by releasing an amazing chemical called BDNF. The long and very complex name for this chemical is brain derived neurotrophic factor. But actually, I prefer to refer to it as “Big Deal Neuro Food”.

This extremely powerful little chemical leads to BIG changes in our brain circuitry. Think of your brain as a series of wires, all criss- crossed and interconnected like a web.

 

We have billions of these connections and wires in our brains, each with their own unique path to perform one aspect of our daily lives. We have areas of our brain responsible for our emotions, our memory, our judgements and our attention allowing us to perform complex tasks or read or favorite books. There are circuits that allow a sense of joy to come along with the scent of mom’s fresh baked cookies, or the clear memory of your first best friend. Our brain does SO MANY wonderful things for us. It’s only fair we do some good for it!

 

 

Image from www.noigroup.com

Here is a very simple representation of what happens to the pathways in our brain when we exercise:

Infographic Sarah

 

Keep in mind these pathways can be even stronger when you feed it “good food” from all of the other items listed above (what we see, learn, eat, etc). The other great news is that you do not have to LOVE exercise or be a marathon runner to experience these benefits.

A study conducted on middle school aged children showed that just 12 minutes of vigorous exercise had a positive effect on their attention and academic related performance. This is not just for kids!

A study of healthy adults demonstrated significant improvements in tests for attention and memory after participating in aerobic exercise for 30 minutes. This is great news, as this means that it is accessible for everyone (ie. You do not need fancy equipment or a gym) as well as doable even with a busy schedule. There are so many forms of exercise out there to get our hearts pumping; it can be running, but it can also be so many other things, dancing vigorously, swimming, jumping jacks, kickboxing/ punching bag, biking, hiking, jump rope… the list could go on! As a physical therapist working with patients with spinal cord injury I taught my patients who were unable to move their lower body at all how to get a great aerobic workout with their upper bodies. IT IS POSSIBLE & IT IS NECESSARY.

It saddens me when I hear about physical education and sports programs being cut from schools. We are literally working against ourselves and putting kids at a disadvantage by plunking them in a desk to sit all day and requiring them to be attentive and learn. Our bodies were not made to sit all day (for a great read: Sitting is the New Smoking) and it is certainly not an optimal environment for our brains to get stronger.

As now a professor teaching graduate students, one of the things I encourage MOST often and especially around examination time, is regular vigorous exercise, as well as sleep.

Keep this in mind next time you go outside for some fresh air, you’re in gym class, shooting hoops with friends, and just anytime you are taking time for yourself to get that heart going… you are doing more than just increasing your heart health, your mood and overall well- being; you are BOOSTING YOUR BRAIN!

 

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But WHY Do I Run?

By Meghan Pearson

But WHY Do I Run?

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(As you can see, I always take it seriously…)

Running has always been a part of my life. I began by running around with my neighbors, then played soccer, then ran cross-country, and now, since I am a glutton for punishment, I run marathons. And before you ask, yes, I actually enjoy doing it. Luckily for me, recent science shows I am actually doing interesting things to my brain while I am running.

For the next month, Inner City Science and Faces of STEM will be reporting about exercise and science and the science of exercise. We are going to look at it from a lot of different perspectives, so stay tuned!

Introduction:

Exercise has long been known to have important health effects. We have all been told that it is an important part of life if we want to live long and prosper (ha!), but the why is a little harder to put into words. I am going to start with some basic studies that looked at what effect exercise had on the aging mind.

As we age, our bodies start to fail on us. It’s a slow process, but we have all probably seen or felt it. Maybe the metabolism slows, maybe the brain can’t remember things, or maybe there is the sudden urge to yell at kids to get off the lawn. The last one is a silly example, but you get the idea. Aging stinks. But research is actually starting to pour in that by exercising, we can slow (and sometimes reverse) some of the effects on aging.

Methods and Materials:

As stated above, there is much research in this topic; however, it should be noted as human testing is still very frowned on, most of these studies are done on mice and rats. Why is this still relative? Well, it turns out we are pretty similar to rats and mice (evolution is cool!)

Many scientists are interested in how to best preserve their brain power. In one such study, they began by comparing the learning abilities and new nerve cell growth of mice from four different groups: sedentary young mice, sedentary old mice, exercising young mice, and exercising old mice. They provided the third and fourth groups (the exercisers) with a wheel and monitored their use.

Results:

This is where it gets cool. They then compared how the mice performed on different a specific maze learning test, and it turns out, the mice that exercised did better! But it gets even better. While there was a difference in the performance between the young and old mice, the old mice performed outperformed their sedentary old mice peers, and in some regards, performed similarly to the young mice of the sedentary group. The mice were able to learn more effectively when they exercised. In fact, when the researchers looked at the brains of the mice, they found that the old mice that exercised had increased their neurogenesis. This is the scientific word for they were once again creating new dendrites: nerve cells! The old mice were not able to make as many new cells as their young peers, but the old mice that exercised showed more new growth than the sedentary old mice. They were reversing some of the effects of aging. It should also be noted that the old mice were all kept sedentary until they were 19 months old (remember, the life span of mice is only about two years…). These researchers believe that beginning to exercise sooner may have lessened the effects of aging even more.

Discussion:

So what does this mean for us? Well, it is pretty good motivation to get out the door and go exercise, but it also means that there are some pretty good indicators that exercising could help us feel young for longer. Human application of these studies is never perfect, but it is usually close. The sooner a person starts exercising, the sooner they can begin to have these benefits. So go outside, go to the park, chase your kids around. Give your brain a few extra dendrites so you can feel better for longer!

If you would like to read one of the papers about this topic, I encourage you to read Exercise Enhances Learning and Hippocampal Neurogensis in Aged Mice by Henriette van Praag et al.

Canis lupus familiarus: A ridiculous story of artificial selection

By Dr. Debbie Rook

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“Natural Selection” is a complicated and intricate biological concept that often trips up the most educated and well-read among us. To get to that, we’re first going to start with something we all can relate to and understand- specifically, breeding or “artificial selection”. This means specifically that people are the selecting what traits are passed on to the next generation, instead of nature.

Think of a dog, any dog. You may know a chihuahua down the street or your great aunt’s mastiff. Dogs come in amazingly different varieties, different sizes, weights, strengths, hair, tails, ears, noses… you name it! You probably have heard that the dog came from wild wolves, which even look like a few breeds (huskies and malamutes, mostly). But how did we get there? How is that even possible to get so much change in just a couple of thousand years?

Artificial selection is the answer. Back in the days long ago (around 130,000 years ago), there were likely wolves that hung out around farmers or nomadic tribes because there was easy food to get- whether it be cattle or other farm animals, the rabbits that came to eat crops, or simply leftover scraps that were either discarded or given to the wolves willingly. Over time, the wolves that had a nicer temperament (less biting, better smiles), would be given more scraps (think if a stray dog came up to you at a park- would you share your ham sandwich if it was growling at you or cuddled next to your side?). This was the beginning of a beautiful relationship between the more tame of the wolves and the humans. Now, how was this really selecting? The humans were not breeding these dogs yet, nor were the animals even living with them, so how could that change the population? Simple- food. The nicer dogs are more likely to get scraps from the humans, and therefore more likely to survive the winter and reproduce, while the mean wolves got no scraps and had to fend for themselves. Slowly over time, the scrap-grabbing would change into cohabitation of tame wolves and humans, which would allow those dogs to have even more offspring, because they were being actively cared for by the humans. And that’s how you get dogs! Bring a nice wolf into your house and in a couple (hundred) generations you’ll have yourself a dog (but don’t try this at home…).

So that’s great, a slow change in the population over thousands of years got us from nasty predator wolves to tame live-in dogs. But how did we go from wolf-like dogs (big, sharp teeth, long noses, pointy ears) to all the different kinds today (big/small, variable teeth, long/short/pug noses, pointy/droopy ears)? That is where serious artificial selection comes in, breeding.

Say you are a farmer and need a dog to look after your flock of sheep. You start with the basic wolf-dog and you select for traits that you want. Specifically, you want a dog that is kind to you and your sheep but will scare away other animals. So you take all your dogs and find the ones that meet those criteria best. They won’t be perfect yet, maybe it will sometimes snap at you or a sheep, but otherwise just likes to chase off coyotes. You mate the two together that have the best traits. Those offspring then will have a smaller range of these traits closer to your ideal. It’s possible that in one generation you will have succeeded with at least one of the dogs, but if not you just try again with the next breeding cycle. This also works if you need a dog to pull a sled, or find foxes, or cuddle with your kids, or even carry in your purse. Slowly, over a few generations you can get a lot of change in these animals.

I’ll give you one more example because I think it is so cool. Bull terriers. Bull terriers are known for their noses that are shorter and angled downwards. Here is one:

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This is a very dramatic feature, so you’d think that it would take hundreds or years to get a nose like that from a regular looking dog. BUT…

Here is a bull terrier from 1915.

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And 1918 (for good measure).

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You can see that those noses have changed a lot in the last hundred years. The 1918 picture also shows you a little how this works. If you look at the four dogs, they are all bull terriers and likely related, but there is variation (differences) between the noses. Specifically, the second from the left has a nose that is slightly more downturned than his siblings. If you were trying to make the modern bull terrier, he is the dog you would want to mate to get the next generation.

So you can see that in a few decades you can get dramatic changes in breeds of dog, all by having humans select traits that they like the most. Selective breeding has brought about the multitude of types of dogs that you see today. Hopefully you have a better understanding of this now that you’ve seen it in action!

Next time: nature takes a crack at selecting for different animals, incredible variation, and adaptation occurs.

The Zika Virus (#1)

By Lauren A. R. Tompkins

A collection/series of blog posts entitled:

The Zika virus pandemic – insights from a scientist

The past few weeks (March 2016) have provided major advances in our understanding of Zika virus through publication of several key research studies. In the wake of the global response to the Ebola virus outbreaks, measures to expedite research and prevention strategies for Zika virus are now underway. Emerging infectious diseases, which manifest outbreaks without warning and often without the presence of effective control measures, are dramatically affecting how information is shared between scientists and how prevention strategies, such as vaccines, are regulated. In a time of public health crisis, the scientific community has pulled together with the common goal of a rapid response to combat Zika virus.

 First blog post for this series, entitled: The politics of Zika virus

             On Monday (April 11, 2016), Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (NIAID), and Dr. Anne Schuchat, principal deputy director of the Centers for Disease Control and Prevention (CDC), addressed reporters at a White House briefing. The topic of discussion was Zika virus and an appeal for the necessary funds to prepare for mosquito season, when the virus will likely spread to the southern United States. According to the CDC, at least 346 people from the continental United States have been infected with the virus, mainly through travel-related exposure. However, with the summer months approaching, and mosquito populations expanding with warmer weather, local transmission of Zika virus is likely to occur.

A gridlocked Congress is not an unusual concept to the American people. Still, a “public health crisis of international concern”, as stated by the World Health Organization (WHO) in February of this year, should theoretically hold weight if politicians continually claim to have the best interests of Americans in mind, let alone the public health of all inhabitants of our planet. Unfortunately, Congressional Republicans are tightening their wallets and stubbornly resisting the allocation of necessary funds for combating Zika virus. Rather than listening to knowledgeable scientists and public health officials, pleas for appropriations are falling on deaf ears. Indeed, President Obama has asked Congress, again, for the full $1.9 billion dollars that is required to fuel Zika virus research. On Tuesday (April 12, 2016), Congress approved a bill to provide financial incentives to companies to develop treatments for Zika virus infection, although no funding was provided. Currently, roughly $600 million has been diverted from the Ebola virus funds towards Zika virus research.

Let me pause here to let the following concept sink in: now that Ebola is no longer a potential threat to the United States, it is assumed that the rest of the world can handle the fallout itself…but, that doesn’t seem to be the case. Dr. Margaret Chan, WHO director-general, announced in January that although all known chains of transmission in West Africa had stopped, including the most recent outbreak in Liberia, new flare-ups are likely to occur. This will require a sustained response for prevention of future outbreaks. Indeed, Sylvia Mathews Burwell, U.S. Health and Human Services Secretary, told reporters, “We face two global health challenges, Ebola and Zika, and we don’t have an option to set one aside in the name of the other.” The decision to pull money from the Ebola fund is somewhat analogous to withdrawing military troops from countries where the United States has intervened and then pulled out, for one reason or another, hoping for sustainable change in those regions. Historically, this system doesn’t seem to work, and furthers the global opinion that Americans don’t care about non-Americans.

There is a comical phrase among infectious disease scientists: “ATM diseases” get the money. Essentially, the majority of funding is allocated to AIDS/HIV, tuberculosis, and malaria research, which some say are “sexy diseases” as they engender public attention. We know that these diseases are incredibly important to study and combat, but when funding is limited, research on other diseases stalls. Why don’t we know that much about Zika virus? It didn’t cause outbreaks until recently. This is the problem with emerging pathogens: they burst forth rapidly when we don’t have the tools to control them. The scientific community is now scrambling, working around the clock to learn as much as possible, as quickly as possible. $600 million sounds like a great deal of money, but it is nowhere near enough to fight Zika virus, as Dr. Fauci reiterated on Monday.

Pull-quote: “When the president asked for $1.9 billion, we needed $1.9 billion.” – Dr. Fauci, NIAID

One day several years ago, as a novice virologist, I was star struck when I met Dr. Fauci during one of his routine visits to the laboratories of the NIAID. The first thing I noticed was Dr. Fauci’s notorious New York accent, the second, his calm demeanor, humility, and compassion. His lectures inspired me, giving me great faith in the leaders of our scientific community. Why this faith is lacking in our Congressional leaders is nonsensical to me. If we cannot trust those we have appointed to run programs ethically and passionately, then what is the point of having these leaders?

Pull-quote: “Everything we look at with (Zika) virus seems to be a bit scarier than we initially thought.” – Dr. Schuchat, CDC

The NIAID and CDC, institutions that preserve public health in America, are not the only scientific leaders voicing the urgency of combating infectious disease outbreaks before they become uncontrollable pandemics. The WHO has also emphasized the potential consequences of a Zika virus pandemic. Indeed, although Zika virus is an old virus (it was discovered in 1947), it emerged as a rapidly spreading pathogen causing sizeable outbreaks in recent years. In the span of about one year, 440,000 to 1.3 million Brazilians have been infected with Zika virus, which has spread to at least 33 countries. At this point, the association between Zika virus infection during pregnancy and microcephaly, a condition among infants resulting in a smaller than normal head size, has essentially reached causality. That is, scientists can definitively and causally link the virus to microcephaly. [In subsequent posts, I will present some of the important research rocketing into publication regarding this issue.] In addition to microcephaly, the WHO acknowledges that Zika virus infection likely causes Guillain-Barré syndrome, an autoimmune disorder in which a person’s immune system attacks his/her own nerves.

Science is not devoid of political influence. Granted, financial resources are not endless, but history has shown the rapidity with which infectious diseases can spread and the devastation that follows. We were not prepared for Ebola virus, which claimed the lives of over 11,000 people. Will the necessary funding come for Zika virus research, or are we destined to continually ignore potential public health crises until it’s too late to combat them?

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Hot and Spicy Chemicals

By Dr. Doris Kimbrough

You grab a bag of corn chips and a bowl of salsa out of the refrigerator and settle in to watch TV. The salsa is hotter than you expected and after about five chips, your mouth is on fire. Big gulps of ice water don’t help, so you head back to the kitchen to look for sour cream or a glass of milk. What is going on in your mouth? How can cold salsa from the fridge burn your mouth? Why doesn’t cold water help the way it would for hot soup or hot tea? How does the sour cream or whole milk solve the problem?

To answer these questions we have to look at some special nerve cells (neurons) and the chemicals found in hot peppers. In addition to the nerve cells that help you move (motor) and control body functions (autonomic) you have lots of different kinds of sensory nerve cells. Sensory neurons are responsible vision and hearing and all your other senses. There are many different types of neurons involved in touch. Some can detect pain; others respond to pressure, heat, cold, or itchiness to name a few. The nerve cells that detect heat are the ones we need to focus on for this story.

Heat detecting neurons don’t work at or below normal body temperature; think of them as sleeping until you touch a hot stove when they wake up and tell you “Ouch, pull back! Pull back!” Hot peppers like jalapeños contain a chemical called capsaicin (cap-SAY-shin) that fools these nerve cells. The capsaicin binds to the nerve cells and wakes them up. Your brain gets signals that something is burning you even though nothing that is actually hot (in temperature) is involved. There are other chemicals that can do this: piperine and sabinene are chemicals found in ground pepper and curry spices.

So why doesn’t a nice cold drink of water help with the burning? Capsaicin is a chemical that is hydrophobic—literally: “water fearing”. Capsaicin doesn’t really fear water; it can’t because it is a molecule, which cannot have feelings. However hydrophobic compounds, like capsaicin, do not dissolve in water. Other hydrophobic substances are vegetable oil, wax and gasoline. So when you gulp cold water because spicy salsa is “burning” your mouth, the capsaicin stays bound to your neuron and your brain still gets signals that your mouth is burning. Hydrophobic compounds do dissolve in other hydrophobic substances, like oils or fats. You may have heard the expression, “like dissolves like”. The fat in sour cream and whole milk will dissolve the capsaicin and remove it from the nerve cell. This turns off the signaling to the brain and lets you get on with your life.

About the author: Doris Kimbrough is a chemistry professor at CU Denver. She grew up in Atlanta, GA, and went to college at the College of William and Mary in Virginia and to graduate school at Cornell University in Ithaca, New York. She has loved science and chemistry since she was a little girl when her chemist father let her play (safely!) with stuff in his lab.

For the Love of Derby…I mean Biology

By Abena Watson-Siriboe

Who I really am-

I grew up in a family of scientists. My grandmother obtained her pharmacy degree when few women or even women of color were involved in the field. My grandfather was a Korean War vet and dentist deeply entrenched in his community. My mother is a biologist and father a chemical engineer. You can say that science was in my blood. Growing up, my family made sure to foster my interests by providing me with science kits and even a rat to dissect when I was too young to handle a scalpel. In middle school, I received a microscope that probably dated to the late 60s, but I loved it. I searched my house for things to inspect and was even tempted to take my own blood sample but eventually chickened out. Little did I know that as an adult, I would be inspecting and showing off x-rays of my ankle broken during a roller derby game. Not only am I a scientist, I’m a roller derby player who goes by the name Norah P Neffrin. You can take the nerd out of the lab but you can’t take the science nerd out of the girl.

How I got here-

When I first started my undergraduate degree, I was a philosophy major with aspirations of going to medical school. As my studies progressed and I took courses such as cellular biology and neuroscience, I realized that medical school wasn’t in the cards. I wanted to be a researcher. So, much to my parent’s pleasure, I changed my major to Biological Sciences and decided on a minor in neuroscience. One of my teachers expressed to her class that she was looking for students to conduct research in her neuroscience lab. I immediately jumped at the chance and was immediately smitten. My research involved the response of a brain region called the Supra Optic Nucleus (SON) to dehydration in rats. Most of my days were spent treating, sacrificing and preparing rat brain tissue. I would go home and my mother complained that I smelled like rat, but I loved every minute of it.

My time conducting research during undergrad inspired me to get a Masters degree, but it also required moving across the country away from family. I continued to work in the neuroscience field but my work focused on a smaller scale. My work focused on a transporter responsible for sequestering molecules such as serotonin and norepinephrine into vesicles. Small changes in the genetic script of this protein have been linked to mental conditions such as bipolar disorder. It was my hope to provide some insight into the role this protein plays in such a complicated condition. During my MS, is when I started roller derby, hence the derby name, a play on norepinephrine. Oddly, most people don’t get it.

What I do now-

Currently, I work in a biophysical laboratory at CU, Denver. My lab examines membrane binding proteins, some of which are present in the brain and or pancreas. We use varying techniques to determine what parts and under what conditions does the protein bind to the membrane. Some of the proteins we work with contribute to membrane fusion whilst others prevent it. My protein of interest prevents vesicles that contain insulin from being released by specialized pancreatic cells, potentially playing a role in diabetes. By understanding how this protein works, our work can inform potential drug targets. In addition to my work in the lab, I still play roller derby with a league ranked #9 in the world. But these days I skate under my legal name.

Passion for the subject-

As a kid, I was obsessed with how things worked, especially the natural world. It still amazes me that we’re made of atoms, molecules, cells, organs that all work together mostly in harmony. Even more amazing is how small changes can disrupt an equilibrium and result in conditions such as bipolar disorder or diabetes. It’s this wonder and hunger for answers that keeps me motivated and impassioned.