Health

Can concussions cause fear of movement?

Megan M Rogers — Mon, 23 Mar 2026 17:42:11 +0000

Can concussions cause fear of movement? Megan M Rogers Mon, 03/23/2026 - 11:42

Colorado Arts and Sciences Magazine

CU Boulder neuroscience student Alexander Wiegman's research finds that a history of concussions doesn't necessarily lead to later kinesiophobia.

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Python blood could hold the secret to healthy weight loss

Lisa Marshall — Thu, 19 Mar 2026 20:23:30 +0000

Python blood could hold the secret to healthy weight loss Lisa Marshall Thu, 03/19/2026 - 14:23

Lisa Marshall

A ball python. Photos by Patrick Campbell/CU Boulder

CU Boulder researchers have discovered an appetite-suppressing compound in python blood that helps the snakes consume enormous meals and go months without eating yet remain metabolically healthy.

The research, a collaboration with scientists at Stanford Medicine and Baylor universities, could inform new weight loss therapies that promote satiety without the nausea and muscle loss that can come with existing drugs.

Professor Leslie leinwand, left, and PhD candidate Skip Maas look on at Maas's pet pythons during their visit to the lab. In addition to keeping pet pythons, Maas studies python metabolism.

The findings were published in the journal Natural Metabolism on March 19.

“This is a perfect example of nature-inspired biology,” said senior author Leslie Leinwand, a distinguished professor of Molecular, Cellular and Developmental Biology who has been studying pythons in her lab for two decades. “You look at extraordinary animals that can do things that you and I and other mammals can’t do, and you try to harness that for therapeutic interventions.”

Metabolic superheroes

Pythons can grow as big as a telephone pole, swallow an antelope whole, and go months or even years without eating—all while maintaining a healthy heart and plenty of muscle mass. In the hours after they eat, Leinwand’s research has shown, their heart expands 25% and their metabolism speeds up 4,000-fold to help them digest their meal.

To get a better sense of what makes these superpowers possible, Leinwand teamed up with Jonathan Long, an associate professor of pathology at Stanford School of Medicine who studies metabolic byproducts in the blood, or metabolites, to learn how mammals take in and expend energy.

Long’s lab recently examined the blood of another curious creature—the racehorse—for insight on how the animals can endure those all-out sprints.

“If we truly want to understand metabolism, we need to go beyond looking at mice and people and look at the greatest metabolic extremes nature has to offer,” said Long.

For the new study, the team measured blood samples from ball pythons and Burmese pythons, fed once every 28 days, immediately after they ate a meal.

In all, they found 208 metabolites that increased significantly after the pythons ate. One molecule, called para-tyramine-O-sulfate (pTOS) soared 1,000-fold.

Further studies, done with Baylor University researchers, showed that when they gave high doses of pTOS to obese or lean mice, it acted on the hypothalamus, the appetite center of the brain, prompting weight loss without causing gastrointestinal problems, muscle loss or declines in energy.

The study found that pTOS, which is produced by the snake’s gut bacteria, is not present in mice naturally. It is present in human urine at low levels and does increase somewhat after a meal.

But because most research is done in mice or rats, pTOS has been overlooked.

“We’ve basically discovered an appetite suppressant that works in mice without some of the side-effects that GLP-1 drugs have,” said Leinwand, referring to drugs like Ozempic and Wegovy, which act on the hormone glucagon-like petide-1 (GLP-1).

Nature-inspired weight loss therapies

Leinwand noted that these new drugs were inspired by another reptile, the Gila monster. Gila monster venom contains a hormone similar to human GLP-1.

Those drugs are now used by millions, but studies show that as as many as half of people who use them stop taking them within a year.

“We believe there is still room for therapeutic growth in this market,” said Leinwand.

She, Long and her CU Boulder colleagues have formed a start-up, Arkana Therapeutics, to work toward commercializing some of the lessons they are learning from pythons.

They imagine a day when chemically synthesized analogs of the rare metabolites found in pythons could be turned into therapies to help people.

Ball pythons. Credit: Patrick Campbell/CU Boulder

Weight loss isn’t the only therapeutic goal they are eyeing.

Age-related muscle loss, or sarcopenia, impacts nearly everyone to some degree as they get older, and people who have health problems that make it hard for them to exercise are hit particularly hard. To date, there are no therapies to halt or reverse sarcopenia.

The snakes may offer insight into how to do that, too, Leinwand said.

In future research, the team hopes to explore how pTOS works in people and catalogue the function of the other metabolites that increase after pythons eat. Some metabolites the researchers identified in their study soar by 500% to 800%.

“We’re not stopping with just this one metabolite,” said Leinwand. “There’s a lot more to be learned.”

Scientists have discovered a novel metabolite in pythons that quells appetite without causing gastrointestinal side effects or muscle wasting. The findings could lead to new weight loss therapies with fewer side effects.

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Study probes 'new normal' for older adults post-COVID

Megan M Rogers — Wed, 18 Mar 2026 18:49:55 +0000

Study probes 'new normal' for older adults post-COVID Megan M Rogers Wed, 03/18/2026 - 12:49

Colorado Arts and Sciences Magazine

Researchers from CU Boulder have found that the pandemic reshaped how people age 55 and older interact with their communities while highlighting the importance of "social infrastructure."

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CU researchers study potential links between hearing loss and dementia

Megan M Rogers — Tue, 17 Mar 2026 16:45:55 +0000

CU researchers study potential links between hearing loss and dementia Megan M Rogers Tue, 03/17/2026 - 10:45

Coloradan , Lisa Marshall

A CU Boulder lab is exploring how age-related hearing loss rewires the brain—and whether hearing aids can undo the damage.

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Could 3D-printed livers make transplant lists a thing of the past?

Lisa Marshall — Tue, 17 Mar 2026 16:19:38 +0000

Could 3D-printed livers make transplant lists a thing of the past? Lisa Marshall Tue, 03/17/2026 - 10:19

Lisa Marshall

Jonathan Makhoul, a research assistant in the Burdick lab, holds a gel infused with human liver cells and printed with blood-vessel-like channels. Patrick Campbell/CU Boulder

It weighs 3 to 4 pounds, includes seven different cell types and features an intricate web of blood vessels that help it filter toxins, guard against pathogens, metabolize nutrients and carry out hundreds of other biological functions.

The human liver, experts say, is an architectural wonder. But its complexity has also made it immensely difficult to replicate in the lab.

Now, a multi-institution team, including scientists at the University of Colorado Boulder, MIT, Harvard and Columbia universities, is taking on the challenge. Supported by a new five-year, up to $25 million award from the Advanced Research Projects Agency for Health (ARPA-H) Personalized Regenerative Immunocompetent Nanotechnology Tissue (PRINT) program, they’re working to develop 3D-printed liver tissue made of human cells and able to be transplanted into anyone without their body rejecting it.

An AI generated illustration of a liver. Adobe Stock photo

“There are many patients out there that either never get a transplant or are stuck on the waiting list for years,” said Jason Burdick, a professor of chemical and biological engineering whose lab at CU’s BioFrontiers Institute will lead the 3D printing part of the project.

“If there were an off-the-shelf alternative, once a patient needs a liver they could get a transplant almost immediately,” he said. “That’s our goal.”

Organs on demand

91��Ѽ 4.5 million U.S. adults have been diagnosed with liver disease, and about 52,000 die annually of liver failure. At any given time, roughly 15,000 people in the U.S. are on the transplant list, with waits ranging from 30 days to more than five years.

Patients who do get a transplant from a cadaver or living donor must take drugs to keep their immune system from rejecting it. Those medications come with their own health challenges, and sometimes the body rejects their new liver anyway.

Above, research associate Matt Davidson looks at a liver organoid under the microscope. Below, Left to Right: Makhoul, research associate Megan Cooke, Professor Jason Burdick and Davidson in the lab.

In 2024, ARPA-H launched the Personalized Regenerative Immunocompetent Nanotechnology Tissue (PRINT) program, an ambitious, fast-track endeavor driven by a single question: “What if we could bioprint any organ on demand?” The PRINT program is led by ARPA-H Program Manager Ryan Spitler, Ph.D.

In January, the agency announced the ImPLANT project team (short for Immunoshielded Printed Liver Assist NeoOrgan for Transplant). Led by Harvard University’s Wyss Institute, the project brings together a dream team of the world’s leading experts in synthetic biology, transplant immunology, vascular engineering and 3D bioprinting to develop life-like replacements for the body’s largest organ.

“We all recognize the moonshot nature of the program and are thankful that ARPA-H is making it possible,” said Chris Chen, M.D., PhD, the ImPLANT project’s principal investigator (PI) at the Wyss Institute.

How to make an organ

Standing at a microscope in the Burdick Biomaterials and Biofabrication lab, research associate Matt Davidson zooms in on a tray of spherical cell clusters known as ‘liver organoids.’

In the room next door, research assistant Jonathan Makhoul switches on a glistening white 3D printer which uses a sharp tool, akin to a sewing machine needle, to print delicate channels deep within a vat of gelatin-like liquid known as a hydrogel.

While these are early days, the effort to manufacture a liver is well underway.

The process goes like this:

Through a technique pioneered at MIT, induced pluripotent stem cells — adult skin or blood cells that have been modified to have the capacity to become any kind of cell— are programmed to become all the different types of liver cells. (Soon, researchers hope to be able to genetically engineer those cells to also evade immune rejection by patients, making them universally compatible.)

Burdick’s team takes clusters of those cells, or liver organoids, and amasses them into larger, tissue-like structures. Then they deploy a novel 3D-printing technique called ‘suspension printing’, pioneered in his lab.

“Rather than building up a three-dimensional structure layer by layer, like most 3D printers do, we can now take a bath of material— in this case organoids suspended within a hydrogel — and print an ink directly into that three-dimensional volume,” said Burdick.

Once the ‘ink’ is washed away and cells migrate to those channel walls, it leaves intricate webs of blood vessels behind.

Producing liver tissue at scale

Ultimately, when a patient needs a new liver, that tissue could then be implanted and sutured in place, its vessels lining up with those connecting it to the rest of the body.

Much like patients seeking a knee replacement today, those seeking a new liver could basically order the part off the shelf.

Of the up to $25 million allocated to the team, about $3.5 million will go to CU Boulder.

Within a few years, the team hopes to be embarking on animal studies.

Meanwhile, collaborators at Columbia will be developing new bioreactor technologies and manufacturing processes to produce liver cells, organoids and tissues at scale.

If all goes according to plan, clinical trials could be underway within five to 10 years, said Burdick.

“We are all experts in our own fields with many years of research behind us,” said Burdick. “Now that we can combine all of our expertise with enough funding and support to really push the program forward, I’m confident that we can develop new therapies based on 3D printed livers to truly help patients.”

"Research reported in this publication was supported by the Advanced Research Projects Agency for Health (ARPA-H) under Award Number D25AC00322-00. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Advanced Research Projects Agency for Health."

Supported by an up to $25 million federal award, a dream team of experts is working to develop the world’s first off-the-shelf engineered liver tissue.

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Why do we get a skip in our step when we're happy? Thank dopamine

Daniel William Strain — Fri, 27 Feb 2026 19:01:00 +0000

Why do we get a skip in our step when we're happy? Thank dopamine Daniel William… Fri, 02/27/2026 - 12:01

Daniel Strain

Subject "reaches" for a target on a computer screen, while Alaa Ahmed and Colin Korbisch follow the data. (Credit: Jesse Morgan Petersen/CU Boulder College of Engineering and Applied Science)

New research by engineers at CU Boulder aims to get to the bottom of why, as the saying goes, you get a “skip in your step” when you’re happy.

The study highlights the central role that dopamine, a brain chemical associated with reward, seems to play in making people move faster when they want something. The findings could one day help scientists understand and even diagnose a range of human medical conditions, including Parkinson’s disease and depression.

“Anecdotally, we just feel that this is true,” said senior author Alaa Ahmed, professor in the Paul M. Rady Department of Mechanical Engineering at CU Boulder. “When you go to the airport to pick up your parents, you may run to greet them. But if you’re picking up a colleague, you’re probably just going to walk.”

In the new study, she and Colin Korbisch, a former graduate student at CU Boulder, set out to unravel the pathways in the brain that control those sorts of behaviors.

The researchers designed a simple experiment: They asked human subjects to “reach” for a target on a computer screen using a joystick-like device. Those targets dealt out rewards—in this case, a simple flash of light and a beeping sound.

The team discovered that how those rewards exceeded, or failed to meet, expectations changed how the subjects moved, in some cases giving them a little more oomph as they reached.

Colin Korbisch and Alaa Ahmed in the lab. (Credit: Jesse Morgan Petersen/CU Boulder College of Engineering and Applied Science)

A subject completes a reaching task in Ahmed's lab. (Credit: Jesse Morgan Petersen/CU Boulder College of Engineering and Applied Science)

Those patterns aligned closely with what scientists know about the behavior of dopaminergic neurons—cells in the brain that release dopamine and shape a huge range of human behavior.

The researchers published their findings Feb. 27 in the journal Science Advances.

“Movements are a window to the mind,” Korbisch said. “Normally, you can’t go into the brain and see what the dopaminergic neurons are doing, but movement could reflect those neural computations that are so difficult to disentangle.”

Juice time

Scientists have known for decades that dopamine plays a critical role in helping animals learn.

In the 1990s, for example, neuroscientist Wolfram Schultz conducted seminal studies on dopaminergic activity in primates.

He and his colleagues trained monkeys to expect a reward—maybe a drop of apple juice—when they heard a bell ring. Those same monkeys began to experience a spike in dopamine every time the heard the bell, even before they got their juice.

But when the monkeys heard the bell and didn’t receive any juice, the disappointment also registered in the brain: The animals still experienced an initial spike in dopamine, but that activity dipped when they failed to receive their reward.

Scientists call this pattern a “reward prediction error.” In a sense, the brain is teaching itself which options are worth pursuing, and which can be ignored.

In the current study, Ahmed and Korbisch wanted to see whether those same patterns might affect how we move.

Reach for it

The team had good reason to think they might. Ahmed explained that people with Parkinson’s disease lose many of the dopaminergic neurons in their brains. They also have a lot of trouble moving.

To explore the link between dopamine and movement, the researchers asked human subjects to use the joystick to make a series of reaches toward one of four targets at each corner of a screen. One target gave a reward every time the subjects hit it, while another target never gave rewards. The other two fell in between.

As the team expected, the subjects tended to reach a little faster toward the targets that were more likely to offer a reward.

But the group also discovered something intriguing: If the subjects reached for a target that was unlikely to give a reward, and they unexpectedly got one, their reaching motion suddenly sped up—even after they had already gotten the reward.

This increase in vigor occurred just 220 milliseconds after the subjects heard the beep. The effect was subtle and not something you could spot with the naked eye. But the findings indicate that a pleasant surprise may give people a little extra pep.

The researchers can’t show definitively what is behind that burst of energy. But Ahmed and Korbisch suspect that their subjects were receiving a second jolt of dopamine from the unexpected treat.

When the subjects were certain they were going to get a reward, in contrast, they didn’t seem to get a second surge in dopamine after the beep.

"Importantly, this effect wasn't tied to reward reception alone," Korbisch said. "If the outcome was certain and known to the individual, we saw no further increase in vigor."

Past experience mattered, too. If patients got a string of rewards in a row, they started moving faster overall. If they got nothing but bad luck, they slowed down.

Ahmed noted that many medical conditions affect how people move. People with depression, for example, tend to move more slowly than others. She envisions that, one day, medical professionals could use these sorts of trends to help their patients—following how people move across months or years to track their health.

“If you’ve had a good day, you’ll go faster. If you’ve had a bad day, you’ll move slower,” Ahmed said. “It’s basically that skip in your step.”

Humans tend to move faster when they think they're going to get a reward. A new experiment explores the pathways in the brain that may be behind these patterns.

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Startup brings cancer care technology to Lab Venture Challenge

Megan M Rogers — Thu, 26 Feb 2026 21:54:01 +0000

Startup brings cancer care technology to Lab Venture Challenge Megan M Rogers Thu, 02/26/2026 - 14:54

Doctoral student William Frantz is developing microscopic droplets designed to help doctors track radiation therapy in real time. His pitch at the Lab Venture Challenge highlighted how the technology could make cancer treatment more precise and less harmful, particularly for pediatric patients.

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Karolin Luger wins Vilcek Prize in Biomedical Science

Megan M Rogers — Thu, 05 Feb 2026 16:53:42 +0000

Karolin Luger wins Vilcek Prize in Biomedical Science Megan M Rogers Thu, 02/05/2026 - 09:53

Colorado Arts and Sciences Magazine

The CU Boulder biochemist has been awarded for her career dedication to the study of nucleosomes and groundbreaking discoveries.

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The other 'Alzheimer's protein': The quest to prevent toxic tau buildup in the brain

Lisa Marshall — Tue, 03 Feb 2026 22:00:04 +0000

The other 'Alzheimer's protein': The quest to prevent toxic tau buildup in the brain Lisa Marshall Tue, 02/03/2026 - 15:00

Lisa Marshall

In the quest to cure Alzheimer’s, the protein known as beta-amyloid has long taken center stage, driving development of a long list of drugs aimed at breaking up “amyloid plaques” in the brain.

But mounting research shows a lesser-known protein called tau, which forms toxic hairball-like tangles inside neurons, plays an equally vital role in fueling this and other neurodegenerative diseases.

New CU Boulder research published in the journal PNAS offers fresh insight into how tau tangles form and spread. In a companion paper, published in the journal Neuron, the researchers propose a new strategy for preventing this process and show the approach can halt or reverse neurodegeneration in mice.

The findings could ultimately pave the way toward a "neuronal vaccine" that stops neurodegeneration before it can spread.

“If we really want to treat Alzheimer’s and many of these other diseases, we have to block tau as early as possible,” said senior author Roy Parker, distinguished professor of biochemistry and director of the BioFrontiers Institute. “These studies are an important step forward in understanding why tau aggregates in cells and how we can intervene.”

A good protein gone bad

First discovered 50 years ago, tau helps brain cells keep their shape and shuttles important molecules around within them. When it malfunctions, tau can turn toxic and spread through the brain killing neurons.

This process underlies more than two dozen neurodegenerative diseases called ‘tauopathies.’ In Alzheimer’s, which affects 7 million people in the U.S., amyloid beta forms plaques that kick-start the spread of tau tangles.

“By the time you treat an Alzheimer’s patient, even if you can completely get rid of amyloid plaque in the brain, it’s often too late because tau has already done its damage and is continuing to spread,” said Parker.

Other "tauopathies" include chronic traumatic encephalopathy (CTE), often found among football players with head trauma; and some forms of frontotemporal dementia, a cruel and fast-moving disease that causes personality changes and memory loss in adults as young as 40.

Roy Parker, director of the BioFrontiers Institute at CU Boulder.

91��Ѽ one in 1,000 children who get measles will acquire a fatal tauopathy called subacute sclerosing panencephalitis (SSPE) six to 10 years after infection, noted Parker.

“That’s the one that scares me the most, as so many people think measles is not a big deal,” Parker said.

To date, there are no FDA approved drugs to target tau. But Parker’s lab and others are making progress toward that goal.

A 'vaccine' for brain cells

Previous studies looking at postmortem brain tissue of Alzheimer’s patients have found that tau aggregates include unusual proteins containing disordered chains of an amino acid called serine.

This led Parker’s team to wonder whether these “polyserines” somehow drive tau to, essentially, turn bad.

Through a series of experiments described in the PNAS paper, he and his students found that when polyserine makes its way to a budding seed of tau inside a brain cell, it can prompt tau to misfold, clump and spread toxic aggregates to other neurons like a virus.

They also found that when mice with a predisposition to tauopathies have more polyserine on board, they get sicker faster.

“In experiments in human neurons in the test tube, fruit flies, animals and human tissue, we have now shown that overexpression of polyserine increases tau aggregation,” said Parker. “The question now is: How do you target this process to prevent or treat disease?”

In one clever strategy, described in the Neuron paper, they turned polyserine—which naturally gravitates toward tau aggregates—into a sort of Trojan horse.

They administered polyserine, attached to a different protein expressly engineered to bust up tau tangles, to mice. They found that this led to a striking decrease of tau aggregates in the brain, diminished production of new seeds of toxic tau and decreased anxiety and memory deficits in the animals.

“Essentially, if we use this strategy in a mouse that is prone to tau aggregation, it either doesn’t get disease or it slows it way down,” said Parker.

In future work, his lab hopes to get a better sense of why polyserine forms in the first place and what else goes wrong inside cells to turn typically beneficial tau into a lethal threat to neurons.

He imagines a day when his lab’s research can inform development of a preventative treatment, given to people predisposed to tauopathies far earlier in the disease process.

“The holy grail here would be a safe, cheap therapy that is well-tolerated and can be given to people who need it before they have a lot of symptoms,” he said. “Understanding how the cellular environment influences this process, and how to interfere with it, is a huge part of getting there.”

Toxic protein clusters known as tau aggregates underlie dozens of neurodegenerative diseases, or "tauopathies." New research illuminates why they form and spread and how to stop them.

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Tau protein clusters known as tau aggregates underlie dozens of neurodegenerative diseases known as "tauopathies."

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Toxic clusters of the protein tau underlie dozens of neurodegenerative diseases known as 'tauopathies.'

Creating pathways to accessible heart health

Emma Holst — Tue, 03 Feb 2026 17:33:00 +0000

Creating pathways to accessible heart health Emma Holst Tue, 02/03/2026 - 10:33

Emma Holst

February is American Heart Month, a time when people are encouraged to focus on their cardiovascular health.

According to the World Health Organization (WHO), cardiovascular diseases (CVDs) are the leading cause of death globally. Risk factors for poor cardiovascular health include tobacco use, an unhealthy diet, physical inactivity and physiological factors like high blood pressure.

Researchers Sanna Darvish (left) and Sophia Mahoney (right)

At CU Boulder’s Integrative Physiology of Aging Laboratory led by Doug Seals and Matt Rossman, researchers are studying cardiovascular aging.

Sanna Darvish, a doctoral student of integrative physiology, is working toward reducing CVD risk in underrepresented and ethnic populations. “We hope that by studying vascular dysfunction in vulnerable, underrepresented groups, we can better understand the mechanisms contributing to their exacerbated CVD and identify effective interventions,” explained Darvish.

In a study published in 2024, Darvish and integrative physiology doctoral graduate Sophia Mahoney explored the intersection of ethnicity and race, socioeconomic factors and cardiovascular health.

“I think the public knows men have a high risk of heart attacks, but this is mostly because women and other groups have been historically understudied in biomedical research,” said Darvish. “Most people don’t realize that CVD risk is actually higher in older women compared with older men, and this is exacerbated in Black and Indigenous women.”

One tactic to help combat CVD risk is to stay informed. A conversation with Darvish explored what interventions her research has identified to improve heart health and what steps the laboratory has taken to address accessibility challenges for those from underrepresented groups.

What interventions have you found effective in improving heart health among different populations?

Aerobic exercise is the standard-of-care clinical strategy for reducing CVD in older adults across all racial and ethnic groups. This is emphasized by organizations such as the American Heart Association that recommend 150 minutes of moderate intensity aerobic exercise or 75 minutes of vigorous aerobic exercise per week, plus at least two strength training sessions.

These exercises might include hiking, swimming or yoga. If integrating a workout into your week presents a challenge, remember that some daily activities are also considered forms of exercise. These might include mowing the lawn and gardening, shoveling snow or walking to the store and carrying groceries.

Could you share any trends or patterns you’ve observed regarding exercise and heart health in specific communities?

Most studies have been conducted in largely non-Hispanic white populations. There are a few studies, as outlined in our review paper, that have found that aerobic exercise training improves vascular function among Black Americans, Hispanics, Indigenous Americans, Southeast Asians and Native Hawaiians.

It is important to note that there are many barriers to performing aerobic exercise training, especially in underrepresented groups, including cost, time, limited resources and a lack of motivation and health literacy. These barriers provide justification to identify potential alternative interventions that also improve vascular function but overcome these barriers. Our laboratory is currently studying a few lifestyle and supplement-based interventions that are proving to be effective at improving vascular function in older adults.

What heart health statistics have you found most significant in your work?

Importantly, around age 55–60, women supersede men with higher CVD risk. Accumulating evidence demonstrates this is largely due to menopause and the diminished estrogen production that follows reproductive aging.

I think that increasing education and overall health literacy in the general public about the risks of CVD in women and underrepresented communities is important because many people don’t realize that certain factors, such as menopause or race or ethnicity, do substantially increase the risk for many chronic diseases.

We don’t fully understand the mechanisms of increased CVD risk in these groups. It is our job as researchers to identify those risks and mechanisms so physicians and public health officials can better help their patients live healthier lives.

What challenges have you faced in studying the intersection of socioeconomic factors and cardiovascular health?

Studying underrepresented groups is quite challenging in Boulder because we have a relatively homogenous community in terms of race, socioeconomic profile, education status, etc. This makes it difficult to study people who are representative of the U.S. demographic. However, neighboring cities and counties do have more diverse populations, so we do recruit a decent number of people from outside Boulder to participate in our clinical trials.

Could you share any steps that CU Boulder or your lab has taken to address these challenges?

Recently, our laboratory has emphasized pouring more resources into strategies that may help participation in research be more accessible for individuals of underrepresented groups.

To better accomplish these goals, we have done some reflection as a laboratory and identified specific internal and external methods to improve diversity in our clinical trials. A majority of our lab has completed a training focused on creating inclusive research environments for participants and colleagues, and all lab members complete a mandatory implicit bias training when they join the lab. A large focus of our discussions is dismantling biases we have against the aging community, which is even more discriminatory against aging people of color.

In terms of making our clinical trials more directly accessible, we compensate participants for their time and travel, offer free transportation assistance for those who lack safe and reliable transport, and we offer meal vouchers for participants. We think these steps can be easily adopted by other research groups on campus who are seeking to diversify their clinical research participant cohorts.

Sanna Darvish discusses the interventions her research has identified to improve heart health and the steps the Integrative Physiology of Aging Laboratory has taken to address accessibility challenges for people in underrepresented groups.

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