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March 8, 2017

How Do EpiPens Work?

This is the latest post in my #BrainBits series, where I'll answer your burning neuroscience questions in 60 seconds or less. If you have a question you'd like me to answer, you can e-mail me, tweet me, or submit your questions anonymously here.

EpiPen has made a splash in the headlines in recent months. Last summer, the pharmaceutical company Mylan drew widespread criticism when it was revealed that a 500% price hike had been placed on the epinephrine autoinjector. After Congressional investigations, Mylan agreed to introduce a cheaper generic version of the drug, as well as fund programs to help patients afford the costs.

An EpiPen, with its safety cover. Source: Tokyogirl79 (Wikimedia Commons)

But the damage has already been done: since the beginning of 2017, physicians have been prescribing alternatives to EpiPen at a rate 6X higher than in 2016. Without insurance, a generic version called Adrenaclick costs just $10 for a two-pack at CVS.

A young boy with anaphylaxis. 
Source: James Heilman, MD 
(Wikimedia Commons)
So how do EpiPens, and other brands of epinephrine autoinjectors, work in the first place?

Millions of people keep epinephrine autoinjectors on hand due to their risk of anaphylaxis. Anaphylaxis is a serious type of allergic reaction — most commonly to particular foods, animal stings or bites, and medications — that can start within minutes of exposure to the allergen. Symptoms include shortness of breath, throat or tongue swelling, vomiting, lightheadedness, and a drop in blood pressure.

Why such a severe reaction? In response to the the allergen, inflammatory mediators such as histamine cause contraction of smooth muscles (such as the lungs), blood vessel dilation and fluid leakage, and changes in heart rate. A person can die from anaphylaxis if their heart stops beating, or if they are unable to breathe due to swelling of the airway.

EpiPens work by rapidly injecting a dose of epipinephrine (also called adrenaline), which reverses the effects of anaphylaxis.

Epinephrine. Source: Roland Mattern (Wikimedia Commons)
Epinephrine, which plays an important role in our fight-or-flight response, relaxes the smooth muscles of the airways and lungs, and rapidly increases blood pressure by constricting blood vessels. (It's the same hormone that makes us feel like we can run a marathon when, instead, we have to sweat through a public speech to a large, scary audience.) The pen is injected directly into the thigh muscle, as the intramuscular route is faster than subcutaneous administration (like how insulin is delivered).

Have you used an epinephrine autoinjector before? What was the experience like? Let me know in the comments.

February 16, 2017

Why Does Drinking Milk Ease the Pain of Eating Spicy Food?

This is the latest post in my #BrainBits series, where I'll answer your burning neuroscience questions in 60 seconds or less. If you have a question you'd like me to answer, you can e-mail me, tweet me, or submit your questions anonymously here.

You can find me with a plate of hot wings, and a glass of milk.
Source: falovelykids (Pixabay)
I'm pretty wimpy when it comes to eating spicy foods — but if I must indulge in some peppery Chinese food or a plate of hot wings, you'll surely see a glass of milk close to my reach.

Chili peppers contain an active component called capsaicin, which is part of the vanillioid family (the same family that includes the vanilla bean). Capsaicin binds to a receptor called the vanilloid receptor subtype 1 (TRPV1).

While TRPV1 receptors are found in several different organs throughout the body, activation of the TRPV1 receptor on the tongue produces the sensation of heat or abrasion, causing that characteristic burning sensation. Eating a chili pepper does not actually cause a chemical burn — but it certainly feels like it.

So why does milk soothe the savage serrano?

The chemical structure of capsaicin (below) reveals a long hydrocarbon tail, shown in black (carbon) and white (hydrogen):
Chemical structure of capsaicin. (Source: Jacopo Werther/Favourites/Chemistry, Wikimedia Commons)

That hydrocarbon tail means that oily or soapy compounds can act as a detergent to dissolve capsaicin, but water cannot. It's similar to how you can't clean grease off of a cooking pan simply with water, but dish soap will get the job done.

Source: Unsplash (Pixabay)
Milk from mammals contains a protein called casein (the same protein which creates curds in sour milk). Casein is a lipophilic (literally, "fat-loving") protein, which means that it acts as a detergent on capsaicin, thanks to that fatty hydrocarbon tail.

Alcohol also dissolves capsaicin well (wings and beer, anyone?), although its concentration in most alcoholic beverages is often too low to have much of an effect. (On the other hand, casein represents roughly 80% of the protein in cow's milk.)

But remember: it must be mammal's milk! Plant-based milks — such as soy, rice, coconut, or almond — do not contain casein.

Fun fact: Interestingly, in birds, the TRPV1 receptor does not respond to capsaicin, which means that the seeds of chili pepper plants can be dispersed widely. Biologists believe that some species of peppers, such as ghost peppers, have evolved to contain such high levels of capsaicin in order to deter animals from eating them — unless they are also able to help disperse the seeds!

Learn more about the Scoville Scale and how spiciness is quantified here.

Do you have a favorite home remedy for combating the pain of spicy foods? Let me know in the comments!

January 11, 2017

Does the Mercury in Vaccines Cause Autism? What's the Safest Immunization Schedule for Infants?

This is the latest post in my #BrainBits series, where I'll answer your burning neuroscience questions in 60 seconds or less. If you have a question you'd like me to answer, you can e-mail me, tweet me, or submit your questions anonymously here.

With the recent news of President-Elect Trump's talks with Robert F. Kennedy, Jr. to potentially head a new commission on vaccine safety and scientific integrity, many in the scientific and healthcare communities are understandably rattled. Kennedy is a well-known skeptic of vaccine safety, and has previously described the vaccine/autism allegations as such:

“They get the shot, that night they have a fever of a hundred and three, they go to sleep, and three months later their brain is gone. This is a holocaust, what this is doing to our country.”

Source: James Gathany, Judy Schmidt, USCDCP
Mercury is toxic to the human body. It's important, however, to understand how the mercury present in immunizations is different than the mercury in, say, the scary old thermometer in your medicine cabinet.

Thimerosal is a vaccine preservative. Since the early 20th century, small amounts of thimerosal have been used in vaccines to prevent the growth of fungi and bacteria. Thimerosal is mainly composed of ethylmercury. When we hear concerns of mercury toxicity (for example, with the consumption of fish), we are primarily concerned about the compound methylmercury.

Methylmercury (left) and ethylmercury (right). Image source: Wikimedia Commons (public domain)

Ethylmercury is metabolized and excreted by the body much faster than methylmercury (half-life of 1 week vs. 6 weeks), meaning methylmercury is more likely to "build up" in the body. You consume higher, longer-lasting, more concerning doses of mercury when you eat a serving of fish than when you get a vaccine.

Many independent epidemiological studies over the last two decades have concluded that the low doses of thimerosal in vaccines are not harmful to infants, and the compound is not present in routine childhood vaccination schedules in the U.S., E.U., and several other countries. All this said, the current scientific consensus is that there is no compelling evidence linking vaccinations and autism; mercury poisoning does not resemble autism, and rates of autism diagnosis continue to rise despite the removal of thimerosal in many vaccines.

Furthermore, there is no evidence to suggest that the American Academy of Pediatrics' recommended immunization schedule is harmful, or that young children's bodies can't "handle" it. Spacing out vaccines only increases the amount of time by which children are vulnerable to contracting vaccine-preventable diseases. The parents' choice to delay their children's immunizations is what caused the measles outbreak in Disneyland in 2015, with nearly 150 cases.

It's estimated that the MMR (measles, mumps, and rubella) vaccine has saved 17.1 million lives worldwide since 2000. Herd immunity is important for the health of the entire community, as not all children can be vaccinated or will respond satisfactorily to immunizations.

Further reading:

December 4, 2016

What's Next for Me?

Presenting research at the European Sleep Research Society's
meeting in Bologna, Italy this past September. Great
experience — and my first time abroad!
Since defending my dissertation in June, I've remained in the same sleep research laboratory as a postdoctoral researcher — expanding upon the findings of my dissertation, attending conferences (in Italy!) to present my work, and collecting data for a new pilot study in the sleep clinic.

As many of you know, I've known for a few years now that I wanted to use my extracurricular writing and communication experience toward a career in science policy. During my time as a student, I sought out advocacy projects that allowed me to interact with lawmakers, such as Capitol Hill Days in D.C. with the Society for Neuroscience and inviting my Congressman to tour our laboratory.

I was thrilled this past summer to see advertisements about the William Penn Fellowship, a brand new program designed for recent grad school graduates interested in public service. Working full-time with the Pennsylvania state government, fellows are paired with state agencies "to complete impactful projects based on their personal interests and skillsets."

After two months of preparing my application and interviewing, I'm excited to announce that I'll be serving as one of ten inaugural William Penn Fellows! Beginning next summer, I'll be working in the Department of Drug and Alcohol Programs (DDAP) working on policies related to the opioid epidemic in Pennsylvania.


I'm incredibly excited and feel empowered knowing that I can use my science degree to help others and be a voice in government — especially now, where I feel it's needed more than ever. I'm also thrilled for this opportunity to learn and grow in a career that I know so little about, yet have wanted for so long. Without a doubt, 2017 will bring some amazing changes and challenges.

I want to sincerely thank you, the readers of this blog, for keeping me "in business" and engaged with my science writing. Your unending support is the reason I've stuck with it all these years, giving me the experience I needed to hone my skills outside of academia.

You can learn more about the William Penn Fellowship here.

(And don't fear. The brain blogging will continue!)

October 21, 2016

What are Migraines, and What Do They Feel Like?

This is the latest post in my #BrainBits series, where I'll answer your burning neuroscience questions in 60 seconds or less. If you have a question you'd like me to answer, you can e-mail me, tweet me, or submit your questions anonymously here.
Sasha Wolff (Wikimedia Commons)

I am lucky to have never experienced a migraine before. *knocks on wood*

But 15% of the world's population suffers from migraines, and those folks will easily rattle off all of the painful symptoms: pulsating pain — sometimes localized to one side of the head — often accompanied by sensitivity to light, sound, or smell. Some also experience nausea. About 1/3 of migraine sufferers perceive auras before the onset of pain, or brief periods of strange visuals, scents, or confusing thoughts.

In more lay terms, Huffington Post columnist Lisa Belkin once described a migraine as feeling "like you are trying to give birth through your forehead."

But what exactly causes migraines, and how are they different from headaches?

It's important to know that although the brain perceives pain from all parts of the body, the brain itself does not feel pain. The brain lacks nociceptors, or specialized sensory nerve fibers that transmit pain signals, which are present in our skin, muscles, and joints.

Headaches, then, are not pain in the brain, but rather activation of nociceptors located in the layers between the brain and the skull: the pia mater and dura mater (collectively, the meninges):

The pia mater (yellow) and dura mater (gray), collectively called the meninges, cushion and 
protect the brain from the skull. OpenStax (Wikimedia Commons)

As you can see from the image above, these layers are highly vascularized, or contain many blood vessels. Common headaches are triggered by fatigue, stress, head injury, or medications which, one way or another, lead to dilation of blood vessels, blood vessel spasms, or inflammation of the meninges.

While the source of pain in migraines is similar to that of headaches, migraines are actually thought to originate in the brain. Many specialists believe auras are caused by sudden increased, then decreased, neural activity in the cortex (outer layer) of the brain.

The activation of these nerves releases a number of proteins, such as serotonin, which can cause inflammation to the meninges as well as dilate blood vessels. A family of migraine medications called triptans work by constricting blood vessels and blocking serotonin. Many people report that "triggers," such as certain foods or changes in the weather, will reliably cause the onset of their migraines, though it is not entirely clear why this happens.

Do you suffer from migraines? Are there specific things that "trigger"  your migraines? What treatments work for you (or don't work)? Let me know in the comments.

October 13, 2016

[Bringing it Back] #BrainBits: 60-Second Neuroscience - Submit Your Questions!

Last year, I experimented with fun, short posts through a segment called #BrainBits, where I'd answer your burning "why?" questions in a post that would take 60 seconds or less to read.

Hey Paul Studios (Flickr)
You can read all #BrainBits posts here, which include, among others:

  • Why does coffee make me poop?
  • What is déjà vu ?
  • Why do I get hangry?
  • What are hiccups?

I'm bringing it back!

You can e-mail me your questions, tweet me (@GainesOnBrains), comment below, or submit your questions anonymously here

And make sure you're subscribed to Gaines, on Brains (see sidebar on the right) to get my regular blogs, including the #BrainBits posts, sent to your inbox.

Stay neuroscience-y!

October 6, 2016

Scientists Should Advocate for their Own Research

Why (and how) scientists should advocate for their research with journalists and policymakers


iStock/BPLANET
Long gone are the days of the lone investigator who discovered a new scientific truth, published the finding in a journal, and continued doing bench research. Nowadays, scientists have to wear any number of different hats: experimenter, data analyst, teacher, mentor, negotiator, financial planner, writer, boss, philosopher, and speaker.

We have to be team players, but also self-motivated. We have to pay meticulous attention to detail while also under- standing how our research fits into the bigger picture. A good scientist performs well in many of these roles, but one person can’t be good at everything.

I am a postdoctoral researcher whose favorite hat is “writer.” It’s exciting to craft my message, put years’ worth of work down on paper, and add my own results to the literature of a decades-old research field. Scientific publications give us the potential to change the status quo in how other researchers approach their own work—and that’s a big deal.

But when we pour all our energy into communicating only with other scientists, we miss the mark on targeting two other crucial audiences who can help us make an even bigger impact: journalists and policymakers.

To read the rest of this op-ed at The Scientist, click here.

August 11, 2016

#PhelpsFace and the Neuroscience of Getting “in the Zone”

Social media exploded earlier this week with a bevy of tweets and memes featuring a rather unimpressed Olympian – and this time, it wasn’t McKayla Maroney.

On Monday night, cameras captured a hooded Michael Phelps appearing to brood and snarl in the direction of South African swimmer Chad le Clos, who was shadowboxing in preparation for the 200-meter butterfly semifinal.

#PhelpsFace. (NBC; gif via Imgur)

Thus, #PhelpsFace was born.

Despite the intense focus we’ve seen since the Sydney games in 2000, Phelps’ ADHD presented him with a struggle early on. As his mother Debbie described in a 2008 article with The New York Times, “In kindergarten I was told by his teacher, ‘Michael can’t sit still, Michael can’t be quiet, Michael can’t focus.’” Attending regular swim practices – sometimes more than four hours’-worth each day – gave him an outlet for his boundless energy and a lesson in self-discipline.

In fact, many of Phelps’ pre-swim rituals align with what scientists have recently been learning about how we focus to get our heads in the game.


June 5, 2016

#PhDin2016: I'm Defending in 2 Days!

It's here, guys.

This 194-page beast went to the committee on May 12. (No, I had nothing more
to say, but another 6 pages would have been awesome.)

April 28, 2016

#PhDin2016: April Re-cap

Wow, how am I writing my April update already? This month flew by so quickly.

I do have exciting news, though. I FINISHED MY RESULTS CHAPTERS on Thursday, April 21 at 6:52pm. Yes. This was very momentous. I can also tell you exactly what I ate, wore, etc. etc. on that day. THIS WAS VERY EXCITING, PEOPLE.

This is the face of someone who literally *just* wrote the last sentence of their Results section:


April 25, 2016

The False Dream of Less Sleep

During a typical week in college, I slept four or five hours a night. Between evening classes, club meetings, and writing lab reports, I was lucky if I made it to bed by midnight before my 5  a.m. alarm wailed each morning for rowing practice.


I never actually felt too terribly tired, which was the strange part. Naturally, I likened myself to Winston Churchill, Thomas Edison, Nikola Tesla, and other greats who claimed to need just a few hours of sleep each night. Little did I know, the damage was already being done.

It wasn’t until I started researching sleep for my PhD in neuroscience that I realized only a handful of people actually succeed at getting by on just a few hours of rest—and they’ve got genetics on their side.

Read the rest at PrimeMind here.