Duke Research Blog

Following the people and events that make up the research community at Duke.

Category: Biology (Page 1 of 19)

Teaching a Machine to Spot a Crystal

A collection of iridescent crystals grown in space

Not all protein crystals exhibit the colorful iridescence of these crystals grown in space. But no matter their looks, all are important to scientists. Credit: NASA Marshall Space Flight Center (NASA-MSFC).

Protein crystals don’t usually display the glitz and glam of gemstones. But no matter their looks, each and every one is precious to scientists.

Patrick Charbonneau, a professor of chemistry and physics at Duke, along with a worldwide group of scientists, teamed up with researchers at Google Brain to use state-of-the-art machine learning algorithms to spot these rare and valuable crystals. Their work could accelerate drug discovery by making it easier for researchers to map the structures of proteins.

“Every time you miss a protein crystal, because they are so rare, you risk missing on an important biomedical discovery,” Charbonneau said.

Knowing the structure of proteins is key to understanding their function and possibly designing drugs that work with their specific shapes. But the traditional approach to determining these structures, called X-ray crystallography, requires that proteins be crystallized.

Crystallizing proteins is hard — really hard. Unlike the simple atoms and molecules that make up common crystals like salt and sugar, these big, bulky molecules, which can contain tens of thousands of atoms each, struggle to arrange themselves into the ordered arrays that form the basis of crystals.

“What allows an object like a protein to self-assemble into something like a crystal is a bit like magic,” Charbonneau said.

Even after decades of practice, scientists have to rely in part on trial and error to obtain protein crystals. After isolating a protein, they mix it with hundreds of different types of liquid solutions, hoping to find the right recipe that coaxes them to crystallize. They then look at droplets of each mixture under a microscope, hoping to spot the smallest speck of a growing crystal.

“You have to manually say, there is a crystal there, there is none there, there is one there, and usually it is none, none, none,” Charbonneau said. “Not only is it expensive to pay people to do this, but also people fail. They get tired and they get sloppy, and it detracts from their other work.”

Three microscope images of protein crystallization solutions

The machine learning software searches for points and edges (left) to identify crystals in images of droplets of solution. It can also identify when non-crystalline solids have formed (middle) and when no solids have formed (right).

Charbonneau thought perhaps deep learning software, which is now capable of recognizing individual faces in photographs even when they are blurry or caught from the side, should also be able to identify the points and edges that make up a crystal in solution.

Scientists from both academia and industry came together to collect half a million images of protein crystallization experiments into a database called MARCO. The data specify which of these protein cocktails led to crystallization, based on human evaluation.

The team then worked with a group led by Vincent Vanhoucke from Google Brain to apply the latest in artificial intelligence to help identify crystals in the images.

After “training” the deep learning software on a subset of the data, they unleashed it on the full database. The A.I. was able to accurately identify crystals about 95 percent of the time. Estimates show that humans spot crystals correctly only 85 percent of the time.

“And it does remarkably better than humans,” Charbonneau said. “We were a little surprised because most A.I. algorithms are made to recognize cats or dogs, not necessarily geometrical features like the edge of a crystal.”

Other teams of researchers have already asked to use the A.I. model and the MARCO dataset to train their own machine learning algorithms to recognize crystals in protein crystallization experiments, Charbonneau said. These advances should allow researchers to focus more time on biomedical discoveries instead of squinting at samples.

Charbonneau plans to use the data to understand how exactly proteins self-assemble into crystals, so that researchers rely less on chance to get this “magic” to happen.

“We are trying to use this data to see if we can get more insight into the physical chemistry of self-assembly of proteins,” Charbonneau said.

CITATION: “Classification of crystallization outcomes using deep convolutional neural networks,” Andrew E. Bruno, et al. PLOS ONE, June 20, 2018. DOI: 10.1371/journal.pone.0198883


Post by Kara Manke

Better Butterfly Learners Take Longer to Grow Up

Emilie Snell-Rood studies butterflies to understand the factors that influence plasticity.

The ability of animals to vary their phenotypes, or physical expression of their genes, in different environments is a key element to survival in an ever-changing world.

Emilie Snell-Rood, PhD, of the University of Minnesota, is interested in why this phenomena of plasticity varies. Some animals’ phenotypes are relatively stable despite varying environmental pressures, while others display a wide range of behaviors.

Researchers have looked into how the costs of plasticity limit its variability. While many biologists expected that energetic costs should be adequate explanations for the limits to plasticity, only about 30 percent of studies that have looked for plasticity-related costs have found them.

Butterflies’ learning has provided insight into developmental plasticity.

With her model of butterflies, Snell-Rood has worked to understand why these researchers have come up with little results.

Snell-Rood hypothesized that the life history of an animal, or the timing of major developmental events like weaning, should be of vital importance in the constraints on plasticity, specifically on the type of plasticity involved in learning. Much of learning involves trial and error, which is costly – it requires time, energy, and exposure to potential predators while exploring the environment.

Additionally, behavioral flexibility requires an investment in developing brain tissue to accommodate this learning.

Because of these costs, animals that engage in this kind of learning must forgo reproduction until later in life.

To test the costs of learning, Snell-Rood used butterflies as a subject. Butterflies require developmental plasticity to explore their environments and optimize their food finding strategies. Over time, butterflies get more efficient at landing on the best host plants, using color and other visual cues to find the best food sources.

Studying butterfly families shows that families that are better learners have increased volume in the part of the brain associated with sensory integration. Furthermore, experimentally speeding up an organism’s life history leads to a decline in learning ability.

These results support a tradeoff between an organism’s developmental plasticity and life history. While this strategy is more costly in terms of investment in neural development and energy investment, it provides greater efficacy in adaptation to environment. However, further pressures from resource availability can also influence plasticity.

Looking to the butterfly model, Snell-Rood found that quality nutrition increases egg production as well as areas of the brain associated with plasticity.

Understanding factors that influence an animal’s plasticity is becoming increasingly important. Not only does it allow us to understand the role of plasticity in evolution up to this point, but it allows us to predict how organisms will adapt to novel and changing environments, especially those that are changing because of human influence. For the purposes of conservation, these predictions are vital.

By Sarah Haurin

DNA Breakage: What Doesn’t Kill You…

What doesn’t kill you makes you stronger―at least according to Kelly Clarkson’s recovery song for middle school crushes, philosopher Friedrich Nietzsche, and New York University researcher Viji Subramanian.

During the creation of sperm or eggs, DNA molecules exchange genetic material. This increases the differences between offspring and their parents and the overall species diversity and is thought to make an individual and a species stronger.

However, to trade genetic information — through a process called recombination — the DNA molecules must break at points along the chromosomes, risking permanent damage and loss of genomic integrity. In humans, errors during recombination can lead to infertility, fetal loss, and birth defects.

Subramanian, a postdoctoral researcher in the lab of Andreas Hochwagen at NYU, spoke at Duke on February 26. She studies how cells prevent excessive DNA breakage and how they regulate repair.

Subramanian uses budding yeast to study the ‘synaptonemal complex,’ a structure that forms between pairing chromosomes as shown in the above image. Over three hundred DNA breakage hotspots exist in the budding yeast’s synaptonemal complex. Normally, double-stranded DNA breaks go from none to some and then return to none.

However, when Subramanian removed the synaptonemal complex, the breaks still appeared, but they did not completely disappear by the end of the process. She  concluded that synaptonemal complex shuts down DNA break formation. The synaptonemal complex therefore is one way cells prevent excessive DNA breakage.

The formation of the synaptonemal complex


During DNA breakage repair, preference must occur between the pairing chromosomes in order for recombination to correctly transpire. A protein called Mek1 promotes this bias by suppressing DNA in select areas. Early in the process of DNA breakage and repair Mek1 levels are high, while synaptonemal complex density is low. Later, the synaptonemal complex increases while the Mek1 decreases.

This led to Subramanian’s conclusion that synaptonemal complex is responsible for removing Mek1, allowing in DNA repair. She then explored if the protein pch2 regulates the removal of Mek1. In pch2-mutant budding yeast cells, DNA breaks were not repaired.

Subramanian showed that at least one aspect of DNA breakage and repair occurs through the Mek1 protein suppression of repair, creating selectivity between chromosomes. The synaptonemal complex then uses pch2 to remove Mek1 allowing DNA breakage repair.

Subramanian had another question about this process though: how is breakage ensured in small chromosomes? Because there are fewer possible breaking points, the chance of recombination seems lower in small chromosomes. However, Subramanian discovered that zones of high DNA break potential exist near the chromosome ends, allowing numerous breaks to form even in smaller chromosomes. This explains why smaller chromosomes actually exhibit a higher density of DNA breaks and recombination since their end zones occupy a larger percentage of their total surface area.

In the future, Subramanian wants to continue studying the specific mechanics behind DNA breaks and repair, including how the chromosomes reorganize during and after this process. She is also curious about how Mek1 suppresses repair and has more than 200 Mek1 mutants in her current study.

Kelly Clarkson may prove that heartbreaks don’t destroy you, but Viji Subramanian proves that DNA breaks create a stronger, more unique genetic code.         

Post by Lydia Goff


Researcher Turns Wood Into Larger-Than-Life Insects

Duke biologist Alejandro Berrio creates larger-than-life insect sculptures. This wooden mantis was exhibited at the Art Science Gallery in Austin, Texas in 2013.

Duke biologist Alejandro Berrio creates larger-than-life insect sculptures. This wooden mantis was exhibited at the Art Science Gallery in Austin, Texas in 2013.

On a recent spring morning, biologist Alejandro Berrio took a break from running genetic analyses on a supercomputer to talk about an unusual passion: creating larger-than-life insect sculptures.

Berrio is a postdoctoral associate in professor Greg Wray’s lab at Duke. He’s also a woodcarver, having exhibited his shoebox-sized models of praying mantises, wasps, crickets and other creatures in museums and galleries in his hometown and in Austin, Texas, where his earned his Ph.D.

The Colombia-born scientist started carving wood in his early teens, when he got interested in model airplanes. He built them out of pieces of lightweight balsa wood that he bought in craft shops.

When he got to college at the University of Antioquia in Medellín, Colombia’s second-largest city, he joined an entomology lab. “One of my first introductions to science was watching insects in the lab and drawing them,” Berrio said. “One day I had an ‘aha’ moment and thought: I can make this. I can make an insect with wings the same way I used to make airplanes.”

Beetle carved by Duke biologist Alejandro Berrio.

His first carvings were of mosquitoes — the main insect in his lab — hand carved from soft balsa wood with an X-Acto knife.

Using photographs for reference, he would sketch the insects from different positions before he started carving.

He worked at his kitchen table, shaping the body from balsa wood or basswood. “I might start with a power saw to make the general form, and then with sandpaper until I started getting the shape I wanted,” Berrio said.

He used metal to join and position the segments in the legs and antennae, then set the joints in place with glue.

“People loved them,” Berrio said. “Scientists were like: Oh, I want a fly. I want a beetle. My professors were giving them to their friends. So I started making them for people and selling them.”

Soon Berrio was carving wooden fungi, dragons, turtles, a snail. “Whatever people wanted me to make,” Berrio said.

He earned just enough money to pay for his lunch, or the bus ride to school.

Duke biologist Alejandro Berrio carved this butterfly using balsa wood for the body and legs, and paper for the wings.

His pieces can take anywhere from a week to two months to complete. “This butterfly was the most time-consuming,” he said, pointing to a model with translucent veined wings.

Since moving to Durham in 2016, he has devoted less time to his hobby than he once did. “Last year I made a crab for a friend who studies crustaceans,” Berrio said. “She got married and that was my wedding gift.”

Still no apes, or finches, or prairie voles — all subjects of his current research. “But I’m planning to restart,” Berrio said. “Every time I go home to Colombia I bring back some wood, or my favorite glue, or one of my carving tools.”

Insect sculptures by Duke biologist Alejandro Berrio.

Insect sculptures by Duke biologist Alejandro Berrio.

Explore more of Berrio’s sculpture and photography at https://www.flickr.com/photos/alejoberrio/.

by Robin Smith

by Robin Smith

Obesity: Do Your Cells Have a Sweet Tooth?

Obesity is a global public health crisis that has doubled since 1980. That is why Damaris N. Lorenzo, a professor of  Cell Biology and Physiology at UNC-Chapel Hill, has devoted her research to this topic.

Specifically, she examines the role of ankyrin-B variants in metabolism. Ankyrins play a role in the movement of substances such as ions into and out of the cell. One of the ways that ankyrins affect this movement is through the glucose transporter protein GLUT4 which is present in the heart, skeletal muscles, and insulin-responsive tissues. GLUT4 plays a large role in glucose levels throughout the entire body.

Through her research, Lorenzo discovered that with modern life spans and high calorie diets, ankyrin-B variants can be a risk factor for metabolic disease. She presented her work for the Duke Developmental & Stem Cell Biology department on March 7th.

Prevalence of Self-Reported Obesity Among U.S. Adults by State, 2016

GLUT4 helps remove glucose from the body’s circulation by moving it into cells. The more GLUT4, the more sugar cells absorb.

Ankyrin-B’s role in regulating GLUT4 therefore proves really important for overall health. Through experiments on mice, Lorenzo discovered that mice manipulated to have ankyrin-B mutations also had high levels of cell surface GLUT4. This led to increased uptake of glucose into cells. Ankyrin-B therefore regulates how quickly glucose enters adipocytes, cells that store fat. These ankyrin-B deficient mice end up with adipocytes that have larger lipid droplets, which are fatty acids.

Lorenzo was able to conclude that ankyrin-B deficiency leads to age-dependent obesity in mutant mice. Age-dependent because young ankyrin-B mutant mice with high fat diets are actually more likely to be affected by this change.

Obese mouse versus a regular mouse

Ankyrin-B has only recently been recognized as part of GLUT4 movement into the cell. As cell sizes grow through increased glucose uptake, not only does the risk of obesity rise but also inflammation is triggered and metabolism becomes impaired, leading to overall poor health.

With obesity becoming a greater problem due to increased calorie consumption, poor dietary habits, physical inactivity, environmental and life stressors, medical conditions, and drug treatments, understanding factors inside of the body can help. Lorenzo seeks to discover how ankyrin-B protein might play a role in the amount of sugar our cells internalize.

Post by Lydia Goff

How Earth’s Earliest Lifeforms Protected Their Genes

A colorful hot spring in Yellowstone National Park

Heat-loving thermophile bacteria may have been some of the earliest lifeforms on Earth. Researchers are studying their great great great grandchildren, like those living in Yellowstone’s Grand Prismatic Spring, to understand how these early bacteria repaired their DNA.

Think your life is hard? Imagine being a tiny bacterium trying to get a foothold on a young and desolate Earth. The earliest lifeforms on our planet endured searing heat, ultraviolet radiation and an atmosphere devoid of oxygen.

Benjamin Rousseau, a research technician in David Beratan’s lab at Duke, studies one of the molecular machines that helped these bacteria survive their harsh environment. This molecule, called photolyase, fixes DNA damaged by ultraviolet (UV) radiation — the same wavelengths of sunlight that give us sunburn and put us at greater risk of skin cancer.

“Anything under the sun — in both meanings of the phrase — has to have ways to repair itself, and photolyase proteins are one of them,” Rousseau said. “They are one of the most ancient repair proteins.”

Though these proteins have been around for billions of years, scientists are still not quite sure exactly how they work. In a new study, Rousseau and coworkers, working with Professor David Beratan and Assistant Research Professor Agostino Migliore, used computer simulations to study photolyase in thermophiles, the great great great great grandchildren of Earth’s original bacterial pioneers.

The study appeared in the Feb. 28 issue of the Journal of the American Chemical Society.

DNA is built of chains of bases — A, C, G and T — whose order encodes our genetic information. UV light can trigger two adjacent bases to react and latch onto one other, rendering these genetic instructions unreadable.

Photolyase uses a molecular antenna to capture light from the sun and convert it into an electron. It then hands the electron over to the DNA strand, sparking a reaction that splits the two bases apart and restores the genetic information.

A ribbon diagram of a photolyase protein

Photolyase proteins use a molecular antenna (green, blue and red structure on the right) to harvest light and convert it into an electron. The adenine-containing structure in the middle hands the electron to the DNA strand, splitting apart DNA bases. Credit: Benjamin Rousseau, courtesy of the Journal of the American Chemical Society.

Rousseau studied the role of a molecule called adenine in shuttling the electron  from the molecular antenna to the DNA strand. He looked at photolyase in both the heat-loving ancestors of ancient bacteria, called thermophiles, and more modern bacteria like E. Coli that thrive at moderate temperatures, called mesophiles.

He found that in thermophiles, adenine played a role in transferring the electron to the DNA. But in E. coli, the adenine was in a different position, providing mainly structural support.

The results “strongly suggest that mesophiles and thermophiles fundamentally differ in their use of adenine for this electron transfer repair mechanism,” Rousseau said.

He also found that when he cooled E. Coli down to 20 degrees Celsius — about 68 degrees Fahrenheit — the adenine shifted back in place, resuming its transport function.

“It’s like a temperature-controlled switch,” Rousseau said.

Though humans no longer use photolyase for DNA repair, the protein persists in life as diverse as bacteria, fungi and plants — and is even being studied as an ingredient in sunscreens to help repair UV-damaged skin.

Understanding exactly how photolyase works may also help researchers design proteins with a variety of new functions, Rousseau said.

“Photolyase does all of the work on its own — it harvests the light, it transfers the electron over a huge distance to the other site, and then it cleaves the DNA bases,” Rousseau said. “Proteins with that kind of plethora of functions tend to be an attractive target for protein engineering.”

Post by Kara Manke

Game-Changing App Explores Conservation’s Future

In the first week of February, students, experts and conservationists from across the country were brought together for the second annual Duke Blueprint symposium. Focused around the theme of “Nature and Progress,” this conference hoped to harness the power of diversity and interdisciplinary collaboration to develop solutions to some of the world’s most pressing environmental challenges.

Scott Loarie spoke at Duke’s Mary Duke Biddle Trent Semans Center.

One of the most exciting parts of this symposium’s first night was without a doubt its all-star cast of keynote speakers. The experiences and advice each of these researchers had to offer were far too diverse for any single blog post to capture, but one particularly interesting presentation (full video below) was that of National Geographic fellow Scott Loarie—co-director of the game-changing iNaturalist app.

iNat, as Loarie explained, is a collaborative citizen scientist network with aspirations of developing a comprehensive mapping of all terrestrial life. Any time they go outside, users of this app can photograph and upload pictures of any wildlife they encounter. A network of scientists and experts from around the world then helps the users identify their finds, generating data points on an interactive, user-generated map of various species’ ranges.

Simple, right? Multiply that by 500,000 users worldwide, though, and it’s easy to see why researchers like Loarie are excited by the possibilities an app like this can offer. The software first went live in 2008, and since then its user base has roughly doubled each year. This has meant the generation of over 8 million data points of 150,000 different species, including one-third of all known vertebrate species and 40% of all known species of mammal. Every day, the app catalogues around 15 new species.

“We’re slowly ticking away at the tree of life,” Loarie said.

Through iNaturalist, researchers are able to analyze and connect to data in ways never before thought possible. Changes to environments and species’ distributions can be observed or modeled in real time and with unheard-of collaborative opportunities.

To demonstrate the power of this connectedness, Loarie recalled one instance of a citizen scientist in Vietnam who took a picture of a snail. This species had never been captured, never been photographed, hadn’t been observed in over a century. One of iNat’s users recognized it anyway. How? He’d seen it in one of the journals from Captain James Cook’s 18th-century voyage to circumnavigate the globe.

It’s this kind of interconnectivity that demonstrates not just the potential of apps like iNaturalist, but also the power of collaboration and the possibilities symposia like Duke Blueprint offer. Bridging gaps, tearing down boundaries, building up bonds—these are the heart of conservationism’s future. Nature and Progress, working together, pulling us forward into a brighter world.

Post by Daniel Egitto



How A Zebrafish’s Squiggly Cartilage Transforms into a Strong Spine

A column of green cartilage cells divides into an alternating pattern of green cartilage and red vertebra

Our spines begin as a flexible column called the notochord. Over time, cells on the notochord surface divide into alternating segments that go on to form cartilage and vertebrae.

In the womb, our strong spines start as nothing more than a rope of rubbery tissue. As our bodies develop, this flexible cord, called the notochord, morphs into a column of bone and cartilage sturdy enough to hold up our heavy upper bodies.

Graduate student Susan Wopat and her colleagues in Michel Bagnat’s lab at Duke are studying the notochords of the humble zebrafish to learn how this cartilage-like rope grows into a mature spine.

In a new paper, they detail the cellular messaging that directs this transformation.

It all comes down to Notch receptors on the notochord surface, they found. Notch receptors are a special type of protein that sits astride cell membranes. When two cells touch, these Notch receptors link up, forming channels that allow messages to rapidly travel between large groups of cells.

Notch receptors divide the outer notochord cells into two alternating groups – one group is told to grow into bone, while the other is told to grow into cartilage. Over time, bone starts to form on the surface of the notochord and works its way inward, eventually forming mature vertebrae.

X-ray images of four zebrafish spines

Meddling with cellular signaling on the notochord surface caused zebrafish spines to develop deformities. The first and third image show healthy spines, and the second and fourth image show deformed spines.

When the team tinkered with the Notch signaling on the surface cells, they found that the spinal vertebrae came out deformed – too big, too small, or the wrong shape.

“These results demonstrate that the notochord plays a critical role in guiding spine development,” Wopat said. “Further investigation into these findings may help us better understand the origin of spinal defects in humans.”

Spine patterning is guided by segmentation of the notochord sheath,” Susan Wopat, Jennifer Bagwell, Kaelyn D. Sumigray, Amy L. Dickson, Leonie F. Huitema, Kenneth D. Poss, Stefan Schulte-Merker, Michel Bagnat. Cell, February 20, 2018. DOI: 10.1016/j.celrep.2018.01.084

Post by Kara Manke

Growing “Mini Brains” To Understand Zika’s Effects

You probably remember what the Zika virus is because of the outbreak in 2015 that made global headlines.

microcephaly illustration

An infant with microcephaly (left) with a reduced head circumference, as compared to an infant born with a regular head circumference (right) Picture credit: https://commons.wikimedia.org/w/index.php?curid=63278345

The serious nature of the virus was apparent when hundreds of infants across South America were born with microcephaly – a condition characterized by a very small head circumference as a result of abnormally slow brain growth.

The sudden outbreak of Zika in South America led to a panic of the possibility of spread into the United States as well as beyond – and thus, research into learning more about the disease mechanisms of Zika expanded. However, one of the problems in studying a disease like Zika is the difficulty of modeling a complex organ like the developing brain.

Until now, the current way to model the brain was with a brain organoid – a brain grown in a lab. Organoid structures attempt to mimic whole developing organs – however, current brain organoid technology required the use of a large spinning bioreactor to facilitate nutrient and oxygen absorption to mimic the function of the vascular system in our brains. Large spinning bioreactors are expensive to run and bulky—they require large volumes of expensive media that mimic brain fluid. The size and cost has meant that only a few organoids can be grown and studied at once.

Guo-li Ming, University of Pennsylvania

Dr. Guo-li Ming, a professor of neuroscience from the Perelman School of Medicine at the University of Pennsylvania, set out to work on finding a way to solve this problem. She came down to Duke University last week to give a talk on her findings.  As she spoke, I could feel the minds of the audience firmly captivated by her words. It was truly fascinating stuff – Ming was actually growing brains in the lab!

The work began by finding a way to take the large spinning reactor that the existing brain organoid required and make it smaller. Three clever high school students working in her lab used a 3D printer and a small motor that involved spinning 12 tiny interconnected paddles within 12 small cell culture wells. Each of the wells contain a paddle that is spun by one gear.  All of the individual gears connect to a continually rotating central gear driven by a motor.

Bioreactor schematic

The Spin bioreactor. Source: http://www.cell.com/cell/abstract/S0092-8674(16)30467-6

After many optimizations, the final design was called SpinW,  which ultimately required a mere 2 ml of media per well, resulting in a net 50-fold reduction in media consumption, as well as dramatically reduced incubator space. The large number of wells, combined with dramatically reduced cost of the apparatus and media consumption, allowed for optimal conditions to run multiple test scenarios with ease – essentially meaning that 12 “mini brains” could be tested at the same time.

The design of SpinW costed a mere $400, while the commercial design costs over $2,000, with the added burden of consuming 50 times more media. The success of the design only serves to prove that age doesn’t matter when it comes to great ideas!

A brain organoid infected with Zika virus. ZIKV envelope protein is shown in green; neural progenitor cells marked by SOX2 are shown in red; neurons marked by CTIP2 are shown in blue.
CREDIT: Xuyu Qian/Johns Hopkins University

Dr. Ming and her team used the apparatus to model the Zika virus’s impact on the brain.

The findings indicate that Zika works by killing off neural stem cells, as well as causing a thinning of key brain structures. One of the observations was that, by day 18 of Zika infection of a brain organoid, there was an overall decrease in size, which points to the link of Zika causing microcephaly. The Zika infection of early-stage organoids corresponded to the first trimester of human fetal development.

The brain is the most complex organ in the body, and one of the least understood. The work Dr. Ming and her team has done goes a long way towards helping us understand the way the human brain develops and works, as well modeling its reaction to things like viruses. It was a pleasure and honor to hear Dr. Ming talk to us about her work –I am eager to hear about further developments in this field!

Post by Thabit Pulak

Hearing Loss and Depression Are Connected

Jessica West is a PhD candidate in sociology.

Jessica West, a PhD student in sociology at Duke, has found that hearing loss creates chronic stress but that high levels of social support – from family, friends and others – can help alleviate depression. Given that hearing loss is a growing social and physical health problem, her study suggests a need for increased vigilance regarding hearing loss among older adults, West said.

Her study was published in the November issue of Social Science & Medicine and is available here.

Here, West discusses her research.

Your research examines the correlation between hearing loss and depression. That seems a logical connection: why study it in the way you did?

Despite how common hearing loss is, it is actually quite understudied. A handful of studies have looked at the relationship between hearing loss and mental health over time, but the results from these studies are mixed: some find a relationship between hearing loss and more depressive symptoms, while others do not. On top of the mixed findings, most studies have been based overseas, and studies based in the U.S. have tended to use state-specific datasets, like the Alameda County Study, which drew from Oakland and Berkeley, CA.

I use the Health and Retirement Study, which is nationally representative of adults aged 50 and older in the U.S., and therefore more generalizable to the U.S. population.

I frame hearing loss as a physical health stressor that can impact mental health, and that social support can alter this relationship by preventing a person from experiencing stress or reducing the severity of a reaction to it. To the best of my knowledge, this is the first paper to link hearing loss to health outcomes in this way.

What might surprise people about your findings?

More than one-fifth of the people in my sample have fair to poor hearing (23.12% or 1,405 people in the first wave). Hearing loss is really common in the U.S.

Also, I found that social support is most beneficial in easing the burden of hearing loss among people with significant hearing loss. Overall, this suggests that hearing loss is a chronic stressor in people’s lives and that responses to this stressor will vary by the level of social resources that people have available to them.

What does ‘social support’ mean in real terms? What can the family and friends do for a person with hearing loss to help them?

For people with hearing loss, it’s important that they feel able to lean on, talk to, and rely on family, friends, spouses or partners, and children. And going a step further, people with hearing loss need to know that these important people in their lives truly understand the struggles they face. What this means is that people with hearing loss can benefit quite a lot from having a network of people that they feel comfortable discussing things with or reaching out to when needed.

Do people with hearing loss have adequate mental health resources or care available to them?

My research shows that social support is really important for people with hearing loss. One suggestion I make in my paper is that audiologic – or hearing — rehabilitation programs could include educational training for significant others, like spouses or friends, to emphasize the importance of supporting people with hearing impairment. Audiologists, primary care physicians, family, and friends are all key resources that could be targeted in such rehabilitation programs.

 What is your next project related to hearing loss?

 I am currently working on several projects related to hearing loss. In one, I am looking at the relationship between an individual’s hearing loss and his/her spouse’s mental health outcomes. Few population-based studies have examined the relationship between hearing loss and spousal mental health longitudinally, so I hope this study will shed light on the experience of spousal disability within marriages.

Another project I am working on looks at hearing loss from a life course perspective. In other words, I am looking at people who self-reported hearing loss before the age of 16 and seeing how their hearing loss influenced their marriages, academics and careers. A better understanding of how early life hearing loss influences later life outcomes has implications for earlier identification of hearing loss and/or the use of assistive technology to help people remain socially, academically, and economically engaged.

CITATION: West, Jessica S. 2017. “Hearing Impairment, Social Support, and Depressive Symptoms among U.S. Adults: A Test of the Stress Process Paradigm.” Social Science & Medicine 192(Supplement C):94-101.

 Read the paper 

Guest post by Eric Ferreri, News and Communications

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