What’s the COVID vaccine situation?

Image credit: National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH)

Many experts are saying that social distancing may have to continue until we have a COVID19 vaccine. That may not necessarily mean we have to stay home, but it does mean we may need to continue wearing masks and banning large public gatherings for the next year or more.  So let’s talk about why vaccines are important, the status of a COVID vaccine, why it can take so long, and what might happen if we don’t get one.

Why is a COVID19 vaccine so important? 

Vaccines are the best remedy against viruses.

First, they prevent infections–meaning that the virus doesn’t have a chance to reproduce and spread in the first place. If we prevent a virus from infecting people, we don’t need medicine.

Second, making drugs that can stop a virus infection (antivirals) is difficult. This is because viruses are very simple parasites. Most of what they do involves hijacking cells to make more of themselves. Because they use your body to do their thing, there aren’t many ways to interfere with their lifecycle without harming your body, too. This is different from bacteria. Bacteria are more complex life forms, so we can create drugs (antibiotics) that stop their unique parts from working.

What’s the current COVID19 vaccine status?

In a nutshell: a vaccine is in development, but is very likely to take at least a year. That’s because research is still in the early stages. There is a vaccine in clinical trials (being tested in people), but it sounds like researchers don’t expect this early candidate to be “the one”.

The 12-18 month timeframe is actually very quick for a virus that is brand new. Even the flu vaccine takes 6 months to develop and produce, and we already have a tried-and-true system in place for making large batches of it. We don’t have such a system for making large batches of coronavirus vaccines. We don’t even have a great candidate yet for a vaccine. We do have leads, though.

There are two coronavirus that have previously caused outbreaks and serious illnesses known as SARS and MERS. After the SARS outbreak in 2003, scientists started the research to understand how these deadly coronaviruses caused infection and how the immune system might react. So, even though COVID19 is caused by a new coronavirus, the research on SARS and MERS gives us a head start. 

How are vaccines made?

As I mentioned, the time consuming part of making a vaccine is collecting data. By data, I mean the results from numerous tests. We can’t make these tests faster, but we can have a bunch of labs doing different tests at the same time. So, something like 70 – 100 different vaccine candidates are being tested in various labs right now. From there, it comes down to weeding out a few of the most promising candidates to move forward with.

How do they know when they have a good candidate? A good vaccine must cause a strong “immune response,” which usually means that antibodies are created. Other immune responses may be effective as well, but the immune system is very complicated, so I won’t (can’t really) elaborate further (see Fundamentals of Vaccine Immunology). Antibodies are important Y-shaped proteins that can stick to a virus, prevent it from getting into cells, and tell the immune system to destroy it.

Image credit: John Keith, National Institutes of Health

To find out whether the vaccine candidates create a good immune response, scientists inject them into lab animals (such as mice, rats, or primates); later, the scientists test the response. They will collect the animals’ blood to see whether there are antibodies there, and they will infect the animals with virus to see whether they get sick.

Why do the clinical trials take so long?

If everything works as predicted, the order of things will look like this:

• First, potential vaccine candidates are tested as described above, which they say this will take 3-6 months. This is happening now.
• The next step is safety testing in humans (these are called phase I clinical trials). For these tests, scientists test differently sized dosages of the vaccine to make sure they don’t have side effects.
• After that test, they do a next round of testing in a larger group of people. These tests (phase II clinical trials) further monitor the vaccine’s safety and alo check whether the vaccine causes an immune response. The data from this type of study is used to plan the next phase.
• Next would be a phase III clinical trial, with larger groups of people, more close monitoring for side effects, more evaluating of immune response, and likely lots of monitoring of subjects’ health and activities to see whether they are exposed to the virus and whether they get sick.

I’ve heard that they are likely going to be doing some of these phases in an overlapping way to get data more quickly in this unique situation. However, no matter what steps they skip, scientists still must collect enough data to convincingly show that the vaccine is safe and effective before it will be approved by the FDA. Only then can it go into production.

So, this whole testing phase is what may take 12-18 months. But then production will have to be figured out, so that will also take time – months, likely.

What if we don’t get a vaccine?

With all of this to think about, it is still possible that we don’t get a vaccine in that time. Some things in science and nature are just stupidly tricky. The coronavirus that causes COVID19 seems likely to continue to spread and cause local outbreaks for the next year or so. Many people will contract it, over time, which will likely provide them at least some immunity. Eventually the spread may slow down, as population immunity increases. Unfortunately, it is possible for the virus to mutate and begin to dodge that immunity, like the flu virus does. But, that virus will be different, and may not be as severe or spread as easily.

There are many possibilities. But I’m optimistic that we will go on with society and culture for the next year, even if it’s a little different. They may implement contact tracing to do so. Maybe antibody testing will improve. We will learn to not touch our face, we will carry/provide hand sanitizer everywhere, we will wash our hands well and often, and we will get used to wearing face masks in crowds, especially when we have a cough or tickle in our throat. There are so many people working on solutions, and I think the right attitude is openmindedness and willnessness to listen to health experts.

Maybe I’ll do another post soon about possibilities for what the immediate future might look like.

FURTHER READING

https://www.self.com/story/coronavirus-vaccine

https://www.livescience.com/coronavirus-covid-19-vaccine-timeline.html

https://www.nih.gov/health-information/nih-clinical-research-trials-you

https://time.com/5819887/coronavirus-vaccines-development-who/

https://www.sciencemag.org/news/2020/03/record-setting-speed-vaccine-makers-take-their-first-shots-new-coronavirus#

An updated guide to the coronavirus drugs and vaccines in development

The 7 Best Things In the Smithsonian’s Deep Time Exhibit

(So much more than dinosaurs)

As part of the DC science writers group, last Friday I got a sneak peek of the revamped Fossil Hall at the National Museum of Natural History. Visitors have had to live without the most popular exhibit, their “hall of prehistoric monsters,” for about five years. But (I’d argue) it was worth the wait.

Fossils are meant to bring us face to face with the evidence of evolution. Ammonites and dinosaurs are part of a larger, way more awesome story of how the living, breathing, Earth has changed over eons. Obviously, it’s not easy to get that point across—the time scale is BILLIONs of years. That’s why it’s called “deep time.”

The Smithsonian’s Deep Time exhibit has done a fantastic job of setting up Earth’s history in a three dimensional space. Walking in, you may first notice the treasured giants, such as the large extinct mammals, sea creatures, and dinosaurs, including a T-rex munching on a triceratops. Then you may notice that there are smaller fossils all around the giants, representing plants and small animals that coexisted and served as food and other aspects of life. You may also notice discussion of the climate, because climate dictates the adaptations needed for survival. Together, the elements of each display work to describe the ecosystems in our distant past.

The hall is organized by time, and after entering, you move backwards through millions of years. But along a part of the hall, there is a whole section about the present. Humans are making a huge impact on the earth now (through climate, among other things) and it can be hard to appreciate big-picture changes on a scale we can understand. That’s why deep time is the perfect context to set up the explanation.

So, of all of the awesomeness I saw in the exhibit, these 7 things were my favorite.

1 – Fossil skeletons are arranged as looking-at-you-hungrily, frozen-in-time monsters. 

These aren’t some lifeless dinosaur bones. In one case, not shown because a hundred other articles have shared photos of it already, there is a display of the “nation’s T-rex” eating a triceratops.

2 – The displays include beautiful plant fossils, for context (i.e., ecosystems).

The displays talk about the animals along with the plants, along with the climate, and how it fits together.

3 – It really goes into deep time, including the evolution of eukaryotic cells!

At what feels like the “end” of the exhibit, there is discussion of the evolution of cells and the first life on earth. This image is from an animation. I’m a cell biologist, so—meet me in this section.

4 – There are stromatolites! And a giant millipede.

Stromatolites are stone structures made by ancient cyanobacteria, which are believed to have played a major role in putting oxygen in our atmosphere. So, KIND OF a big deal.

And, I love telling people about the giant insects of the carboniferous – a period when there was more oxygen in the air, which allowed insects to grow huge. The oxygen was higher because of high rates of photosynthesis.

5 – It addresses the big questions and misconceptions of climate change.

In the discussion of climate, people sometimes bring up the major climate changes in the past and how that implies that global warming is a natural process. Well first of all, extinctions are “normal” too, then. But second of all, read all about what we know and why it matters in the exhibit.

6 – The section on human impacts has positive, actionable messaging.

This interactive display lets you chose how you can help, by doing what you already enjoy. Then it tells you how many other people chose it, too. Very inspiring. I chose trees, and it told me to plant some more. This is just an example of the positive and hopeful messages.

7 – Parts of the overall exhibit design made me into a giddy little girl.

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Not only was the content really good, but the exhibit is just so fun. There are some sweet diaramas; some rousing quotes; a striking wall of asteroid doom; and clever ways to get people thinking about evolution.

The hall is now open, starting today! I’d definitely suggest coming to see it, but probably in the winter, on a weekday, when you can avoid the crowds and enjoy it like I did.

Ancient viruses in our DNA that might cause disease – wait, what?

I love when my friends or family come to me to talk about science! I got an email from my awesome friend Sarah Martin who wrote:

I want my favorite biochemist to tell me about how a virus can incorporate itself permanently into the human genome and I want to know more about the school of thought that evolution is driven by infection…

The news item she sent me reports: Ancient Virus May Cause Crippling Disease ALS, Study Finds. The study introduces a possible link between a devastating disease and a human endogenous retrovirus, which is not your average virus. It also mentions the role of human endogenous retroviruses in evolution. These are pretty complex ideas for one little news article, so let’s talk about the details and I’ll try not to ramble…

Research implicating an “ancient virus”

Let’s discuss this study first. ALS (Amyotrophic lateral sclerosis) is an incurable neurogenerative disease where motor neurons gradually die, causing a person to lose most of the important functions of their body within a few years. The cause in most cases is completely unknown.

There are many research groups out there studying ALS, viruses, and everything in between. Certain clues inspired this particular group at the National Institute for Neurological Disorders and Stroke to look for retroviruses in ALS patients. These clues included a discovery of “retrovirus activity” in the blood of some ALS patients, and the fact that some HIV patients suffer from nerve degeneration similar to ALS.

In their research, they found that some patients with ALS had elevated levels of a retrovirus called HERV-K. This virus was found specifically in the cortical and spinal neurons in some of the ALS patients, while none was found in the healthy control individuals tested.

“Look at this study! What if…”

Like most studies, this research does not yet explain the cause of ALS but does help direct further research into how ALS might be tackled. This finding is interesting for those affected with ALS because it provides a potential target for therapy. If a virus causes the disease, then drug development efforts can focus on stopping the virus.

A really interesting thing about this retrovirus is that it lives in our DNA – we are born with it. It’s something called a “human endogenous retrovirus”, or HERV – and it became part of our DNA between 2-5 MILLION years ago. Let’s talk about THAT!

Ancient virus baggage                                                            

First things first: what is a virus? A virus is basically a package of genetic material that has evolved a way to replicate itself. They aren’t considered living organisms, like other small pathogens such as bacteria, and they really are quite simple in their build (and elegant, if you ask me). How they work isn’t as simple though, and there are different types of viruses. Some have DNA, but some have RNA instead; some work by inserting themselves into your DNA (retroviruses like HIV), and some work by just using your proteins and leaving your DNA alone. The one thing they all have in common, though, is they need to take over the machinery in your cells to replicate.

A retrovirus like HIV works by inserting itself into your DNA. Crazy, right? That’s why it’s so hard to cure! In this case, it is immune cells, or white blood cells, where the HIV takes residence. It’s safe from detection in there, and its genes are read in the same way your own genes are read by the cell’s machinery.

[overly simplified visual]

What’s the difference between a retrovirus like HIV, and this “endogenous retrovirus” called HERV-K? Well, the main difference is that a person gets HIV from outside their body; but we are born with these endogenous retroviruses.

An endogenous retrovirus used to be a virus like HIV that, at one point, infected a human and inserted its DNA into our ancestors’ cells. But not just any cells – in this case, it was inserted in cells of the germ line. What do I mean germ line? We have DNA (coding our genes) in every cell in our body. But the DNA that gets passed down to our kids is specifically the stuff in eggs and sperm. So, say I catch a retrovirus – it could insert itself into the DNA in some of my cells, but it can only be passed on to future generations if it inserts into the cells specifically located inside my ovaries. A virus like HIV doesn’t do that because it has an affinity for immune cells, (which is why it causes immunodeficiency).

Even though these special circumstances are required, integration of retroviruses into the germ line has happened often enough throughout our evolutionary history that 1% of our entire genome is made up of these “virus fossils”.

Research into endogenous retroviruses is revealing that they may play potential roles in some diseases. Aside from ALS, evidence has implicated their involvement in cancer and certain autoimmune diseases as well.

On the other hand, because they have been part of our DNA (and other animal’s DNA) for MILLIONS of years, their presence has undoubtedly had a number of effects, negative OR positive – one of them being our own evolution.

How could a virus fossil play a role in evolution? 

Evolution is the changing of a population of organisms to adapt to its environment. This adaptation comes about from variation within our genes – often times, spontaneous mutations that happen to allow one organism to be better off than another of its population. Because that one is better suited to the environment, it tends to survive and reproduce more, and thus its genes tend to get passed on more often.

Random mutations are usually one-letter changes in our DNA code. Often these changes don’t make a difference, or they could have a slightly negative effect, or they could have a slightly positive effect, depending on where it happens within a gene. Now think about a retrovirus – this would be a whole string of DNA (a set of virus genes) inserted directly into your set of genes. Obviously this sounds like it would be bad – but could it be good? It would have to for it to play a role in our evolution, right?

For this newly inserted DNA chunk to be a “bad” thing for an organism, it would have to cause early death or prevent reproduction. Otherwise, it would be passed along.  As it gets passed along, mutations occur that prevent the virus from actually working like a virus anymore – which is a good thing for the organism.

Let’s consider an example: evolution of the placenta. A current super-interesting model states that a retrovirus at some point in our past actually helped in the evolution of mammals about 150 million years ago. The placenta allows a developing fetus to gain nutrients from the mother by attaching to the wall of the uterus, and it does this by creating a layer of fused cells. It also protects the developing fetus, with its proteins from both mother and “foreign” ones from the father, from immune attack. Cell fusion and immune suppression are attributes common to viruses. Research into placental development in recent decades uncovered virus-like particles at the placenta interface in monkeys, and then potential endogenous retrovirus sequences, and finally the discovery of the protein, syncytin, which came from a gene within an endogenous retrovirus sequence. Subsequent studies of this protein in mice showed its vital role in embryonic development – when they deleted it from mice, the placenta did not form properly and the embryos died.

How do we know that it played a role in evolution?  Mammals share similar traits, like placental development, because we evolved from common ancestors and share common genes. Our genes have become slightly different over time from genes of other mammals, but they are still similar enough to recognize as the same. And, we find similar syncytin sequences in primates and other mammals.

DNA sequences have more information than just who you are… they can tell us who we were, and how living things – and non-living things like viruses – are all connected.

Conclusions

The research goes on!

 

Featured image: Flickr, B0009743 DNA double helix, illustration; Credit: Maurizio De Angelis, Wellcome Images

Shauna’s academic journey

Cross-posted from PhD Over Easy

The flip side of the PhD

I’ve been doing academic research for about ten years now, and recently decided to leave. Until this year, I was actively asserting my plans to pursue a career in academic research. I wanted to be a professor with a lab. I had remained enthusiastic about research through the tough times, and leading my own lab with control over grand questions and a niche to fill in the expanse of human knowledge seemed like the perfect career to strive for, even if it was still far into the future. But as a first-year postdoc entering my 30s, the truth of what that ambition entailed finally settled in: as an average-at-best scientist, I’d need at least 5 to 10 more years as a productive postdoc (or staff scientist under a PI) with a couple of those years filled with job applications, concerns about the two-body problem, and if an academic job offer…

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Supermassive Black Holes!

It was 2003, and a dark and stormy night. I was in my room on the phone with my best friend being a typical high schooler, avoiding my grandparents, and watching a science special on PBS. The show was “Horizon: Supermassive Black Holes.” The reason I remember that night is because we were gasping at the scientific revelations together like complete in-tune nerds. Now on Netflix, I watched it again the other day and got excited all over again about black holes, so I’m going to tell you about them. The super massive ones. Cue dramatic music.

Image credit: John Hook via Getty Images

First of all, what is a black hole?

A black hole is an object so dense, with gravity so strong, that even light doesn’t move fast enough to escape. In other words, the “escape velocity” from a black hole is faster than the speed of light.

If we can’t see black holes, how do we know anything about them? Much of what is known about black holes is based on what is observed around these super massive dark objects, such as how fast local stars are orbiting. There are only theories about what lies at the center of a black hole. Physicists call it a singularity, and the laws of physics there don’t quite add up. Will you find a tunnel to another universe? Some crazy ball of multidimensional universe string? You would probably find crushing forces, in any case.

Two kinds of black holes have been identified so far – stellar black holes and supermassive black holes. Stellar black holes are just your run-of-the-mill black holes that get featured in Star trek and movies like Interstellar. They are the result of stars that lived out their lives, then exploded and collapsed. They are usually described as having the mass of a couple of suns (solar masses). Supermassive black holes are millions of times bigger. We’re not really talking about “size” here, though, in the way you might think of it. Because we can’t see its size. All comparisons are based on its mass, which can be calculated by the way it affects the movement of surrounding matter.

Where do they come from?

The first cool thing about supermassive black holes is that scientists still aren’t sure where they came from or how they formed. However, the commonly accepted theory among astronomers goes like this: in the early universe, after matter started to form into dust and gas and the universe began to cool, the matter coalesced into the first stars. These stars were much larger and burned hotter than the stars today. Consequently these giant stars burned out relatively quickly and then exploded, like stars do at the end of their life, and the matter that they expelled became other stars. The leftover star material collapsed into a giant black hole that fed on the surrounding matter.

Where are they found?

This was the interesting question of the Netflix special.

Radio image of a quasar taken by the Very Large Array. Image credit: NRAO/AUI

It all started with research into quasars. Quasars are one of the brightest objects in the universe. Originally quite mysterious, eventually astronomers determined that these amazingly luminous objects were actually located in the center of very distant galaxies. What’s more, the incredible amount of light and radiation emitted from a quasar is the result of a feeding supermassive black hole.
The matter falling into the hole – like liquid down a drain – reaches speeds nears the speed of light. Because this matter moves so fast, it becomes superheated and gives off intense energy, effectively pushing away some of the matter just out of reach of the black hole’s grasp. These super energized particles shoot off in high-energy jets with a brightness that outshines all of the surrounding stars.

Since “active” supermassive black holes were found to be sitting at the center of these galaxies with light-emitting quasars, scientists decided to compare these distant active galaxies with quiet, inactive galaxies to get an idea of how massive the black hole was at the center. Quiet galaxies like our own Milky Way have dark centers that astronomers assumed contained nothing of interest, which means the rotation of the stars at the center would have a predictable speed and pattern.

What the scientists found, however – and cue dramatic music – was that these quiet galaxies do not, actually, have a quiet center. There was something there. Something so massive that the stars were circling the center at incredible speeds, and yet it was invisible.

It could only mean one thing: there were supermassive black holes at the center of these quiet galaxies. In the heart of our own galaxy, in a region called Sagittarius A*, is giant destructive force. The more galaxies they looked at, the more evidence they found that almost ALL galaxies have supermassive black holes at their core.

Andromeda Galaxy. Image credit: NASA / JPL-Caltech

Where do they fit into the universe?

An interesting question arose with the finding that super massive black holes reside in the center of galaxies: Why?

The most fun question to ask in science is the why. It’s also usually the most complicated question to answer. Why are there supermassive black holes at the center of galaxies? One really interesting theory is that the black holes were there first, and gave rise to the galaxy. The data to support this theory is based on the speed of the stars moving around the outer edge of the galaxy. These stars are too far away to be affected by the central black hole. However, when measured, astronomers found the velocity of stars in the rotating galaxies to be equivalent to the velocity if the black hole was indeed influencing them. This means that at some point in the past, those stars were close enough to be affected by the mass of the black hole.

This finding supported the theory that supermassive black holes play an important role in the evolution of galaxies. As I described so far, it’s thought that supermassive black holes formed in the early universe. When supermassive black holes consume matter, it swirls around so fast that it actually flings some of the outer material away, out of reach. Thus, the theory goes that these feeding black hole giants were consuming gas and matter, growing larger, while flinging high energy particles and radiation away from themselves that would become orbiting stars. The supermassive black holes do not continuously feed, though, as sometime the surrounding matter gets pushed far enough away to be out of range, and the black hole will go quiet for a time. Someone described this nicely as it being as if the black hole was “burping.”

The evolution of galaxies also involves explosions and collisions and a lot of other destructive cosmic events. But just think about the idea that black holes could play a creative role. These destructive monsters actually gave birth to galaxies, and within one of those galaxies the earth was born. The most terrifying, destructive force in the universe could be responsible for life, as we know it.

Artist’s impression of a quasar. Image credit: NASA / CXC / M. Weiss / Nahks Tr’Ehnl / Nurten Filiz Ak.

Giant squid: separating myth from facts

See my new article about the giant squid at The Super Fins site!

Also, I highly recommend this TED Talk by one of the scientists on the expedition that filmed the giant squid under water and contributed to the special on the Discovery Channel.

Female giant squid specimen on display at the National Museum of Natural History’s Sant Ocean Hall. From wikimedia commons. Credit: Don Hurlbert, Smithsonian Institution

The Super Fins!

Hello!

I am going to be writing some articles for a cool new aquatic news website called The Super Fins.

Check out my first piece! 

Meet the Notothenioid Fish: Antarctic Icefish Uses Antifreeze in Blood to Survive

Notothenioid fish
(Photo credit: Icefish larvae by Uwe Kils is licensed under CC BY-SA 3.0 photo resized)

“2 Scientists Walk Into a Bar…”

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“We are scientists, ask us anything!” reads the poster at the table in Small Bar in University Heights. Two friendly guys, Prithwish and Jim, greet me with smiles and enthusiasm about what questions I might have for them. I thought I detected a hint of disappointment when I brought up that I am also a scientist. “Two scientists walk into a bar” is a community program run by the Reuben H. Fleet Science Center in San Diego, and the premise is to set up scientists at bars around the city, allowing the general public to interact and ask any questions. They have it about every six months. I was so excited when I first heard about this event, and I came to find out how it was going and what it was like. I love the idea of providing science conversation to anyone who wants to join it in a laid-back beer-buzzed environment.

Prithwish Pal and Jim Crute (Photo from Jim)

During my two hours at Small Bar, we scientists spent most of the time speaking with a group of four elementary school teachers who were on a “Two scientists” bar crawl. They mentioned that they like to discuss science when they go out to the bar anyway, but that they usually have a lot of questions, so this was a great opportunity to have those questions answered by scientists. They brought up what they had spoken about with the previous two scientists, asked us what we worked on, when and how we became interested in science, and at some point I started word-vomiting random stuff about virus evolution that I think is super interesting but I don’t remember how I got started on that. The teachers were very enthusiastic listeners. The other short conversation was with some twenty-somethings at the table next to us, who noticed Prithwish taking down the sign and decided to jump in quick to ask about hallucinogenic drugs and whether a zombie apocalypse could happen.

I asked Prithwash what motivated him to volunteer, and he said he was excited about the chance to do science outreach for adults, since there seems to be a good amount targeted for kids. Another friend I know who participated said he was excited about it because it combined his two favorite things, beer and science. That’s definitely one reason I was interested, but I’m also excited about science communication opportunities. The Fleet Science Center has been providing a lot of cool events for kids and adults as well as local teachers. I started volunteering there because I love that they provide so much science for the community, and want to support that mission.

Perhaps interactions like this between the general public and scientists will allow some communication barriers to dissolve. Often when I have told people I study science, they look at me like I have some special ability. I think the main “ability” that has led me to pursue science is the reverence I have for nature and its processes, which helps me to remember them and want to learn more. To understand anything you have to want to understand it. One of the benefits of addressing adults in science outreach events is that they have enough life experience to realize the benefits to understanding scientific concepts, especially related to health and technology and current events.

Another benefit that this type of event provides is the chance to dispel “scientist” stereotypes. Maybe not the nerdy stereotype, but if there’s still a stuffy-academic stereotype out there, this event should take care of it. Most of us love getting tipsy and discussing big questions of the day. It’s what we usually do at the bar anyway. Or maybe that’s just me. But I love talking science, especially with people who want to know more about it. Events like this show me that there are a lot of other scientists out there who feel the same way.

I had been daydreaming about the chance to advocate for vaccines or explain GMOs at the bar, but discussing the realistic causes of a potential zombie apocalypse was pretty fun too. Prithwish mentioned that he was also hoping for more challenging questions. But there are a lot of factors to consider, and we were in a small bar. That’s why it’s great that there were 24 other bars participating that night, with 50 total scientists, and I hope to find out what it was like at some of the other bars. The most we can hope for with any science communication event is just the chance to at least connect with people, and what better place than the pub to connect over ideas in science?

“Fake it ‘til you make it” – with body language

I’m excited about communicating science. As an introvert, I am proud to admit I am practicing my verbal communication skills with my local Toastmasters group. They are awesomely supportive people! I wrote this for our newsletter, and thought I’d share.

I was very jittery before my thesis defense.

2/2/2015

One of my main goals when I joined Toastmasters was to improve my confidence when speaking to people. When I spoke, I feared that people would not take me seriously and that I sounded unintelligent. It’s funny, but because I lacked confidence, it showed in my words and produced the exact outcome I feared. Since coming to this realization, I have been gathering as much information as possible to improve my confidence and presentation skills. An enormously enlightening video I came across was the TED talk from Amy Cuddy about her social psychology research on “power poses”.

When we feel confident, our body language translates this feeling into making ourselves bigger. One example is when a runner wins a race and throws their arms into the air. The opposite is true when we feel ashamed or uncomfortable and we hunch up, cross our legs or our arms, and make ourselves smaller. Cuddy’s research shows that that body language can actually translate both ways – while feeling powerful leads us to making ourselves bigger, making ourselves bigger can actually lead us to feel more powerful. Featured in Toastmaster Magazine issue August 2014 and a Ted talk from 2012, Cuddy tells us “don’t just fake it ‘til you make it – fake it ‘til you become it.” She found that forcing yourself to take on a “power pose” raises your testosterone and lowers your cortisol, increasing confidence and lowering stress.

Since very large “power poses” would be awkward and distracting in normal situations, Cuddy recommends doing power poses before interviews or presentations. I highly recommend Amy Cuddy’s TED talk. You can find it at https://www.ted.com/speakers/amy_cuddy. I was cognizant of a few ums and uhs since I am now a toastmaster, but otherwise her message is eye opening and her inspirational personal story really makes the talk memorable. It has been viewed more than 23 million times. And I encourage all of us, especially those without a self-confident presence, to try power posing before speeches – and to put on that confident face until we are not faking it anymore!

Science Communication Advice from Alan Alda

 

This one is for the scientists!

I saw Alan Alda speak this evening at UCSD about “Helping the public get beyond a blind date with science.” He made a case for telling your science story in personal, simple, engaging language. He also told us about the efforts at the Center for Communicating Science at Stony Brook University to prepare graduate students with communication tools. He was funny and grandfatherly and such a good presenter himself. I’d like to share the insights I gained about getting people to listen to and understand you, especially with science.

I got there late, because UCSD parking sucks, so this photo is from quite far away.

Be conversational, not lecture-y

One of Alda’s first important points was that scientists communicate differently when they are speaking one-on-one with someone instead of presenting a lecture. It is not only the jargon-y fanciness of the words that differs, but the speaker’s tone will tend to be colder and less personal in lecture mode. And when scientists speak about science, we often fall into lecture mode out of habit.

He uses the analogy of falling in love to explain how we can engage the public. Right now science is a “blind date” to the public– an unfamiliar person in the room making them uncomfortable. Alda says “there are three parts to falling in love – and if you haven’t heard of them before, it’s because I made them up,” and these are 1) attraction, 2) infatuation, and 3) commitment.  As an analogy, these stages to love translate to: 1) first impressions when you are communicating, such as welcoming body language, a warm tone, and personal language; 2) memorability, which happens when your audience has an emotional response (any emotional response helps someone to remember that moment); 3) commitment, and I didn’t catch this one from Alda, but I think commitment means your audience will remember scientists to be trustworthy, comfortable sources for information and discussion.

Be a story-teller                                

Tonight Alda told us a lot of stories. Because of this style, we laughed and followed each point he made easily and willingly. And one of his main points was that people like to hear stories.

What makes a good story? This is definitely not something we learn as scientists, except to make “a story” out of our data so it fits into the bigger picture. But he made a point to show that it simply involves an objective (that matters) and the obstacles that must be faced to attain that objective. Alda’s example used a woman from the audience, and she had to carry an overfilled glass of water across the stage without spilling (or her village would die). Our objective would seem to be the significance section of our proposals, so we already have that part floating in our grant-writing brains, and it mustn’t be left out of our public communications. The names of the proteins can be. And words longer than three syllables.

Another important thing about stories is the emotional element, as I mentioned, since people remember things when they have an emotional response to them. Use emotion words. Socialization is our greatest strength as a species, and so much can be gained from plain communication with each other.

 Where does communicating science fit into science?

This issue seems like an ongoing discussion.

Why do we need to be better at telling the public about our science? For one, the general public contributes to science through taxes and thus it is a voter’s issue. Informed voters are crucial to a better society. Obviously. Two, we want them to trust us when we recommend things like vaccines. Three, we should be smart enough to recognize when we need to improve ourselves, eh?

The public aside, Alda brought up a good point about scientists from different fields not clearly communicating with each other. This language barrier is no secret among scientists, as there is a sense of pride among at least the younger scientists that may prevent asking about jargon clarification instead of big picture questions. I’ll admit I avoid neuroscience talks.

The moral of this story is that we need to practice talking about science as people and not scientists. It’s not easy, which is why Alda has created an institute to teach it to grad students, while they are still being molded into scientists. I’ve heard a number of other scientists say, ”why should we bother explaining things to the public when we have important things to do in lab?” But it is more about being prepared for interactions with a lay-audience, and like I said, being able to communicate clearly with other scientists. Just think of the ideas that could come out of increased understanding among different science fields! Increased understanding of what scientists do, how they do it, leading to increased interest by the next generations, and to top it off, better scientific ideas flowing between scientists? Why wouldn’t we want better science communication?

 

A recent interview with Alan Alda: http://www.theatlantic.com/education/archive/2015/01/science-in-the-words-of-alan-alda/384218/

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