Democratize the White Coat by Honoring Black, Indigenous, and People of Color in Science
Celebrating BIPOC's achievements in science are a strong first step to make science a guiding force for all.
This article is part of the magazine, "The Future of Science In America: The Election Issue," co-published by LeapsMag, the Aspen Institute Science & Society Program, and GOOD.
Journalists, educators, and curators have responded to Black Lives Matter by highlighting the history and achievements of Black Americans in a variety of fields, including science. The movement has also sparked important demands to address longstanding scientific inequities such as lack of access to quality healthcare and the disproportionate impact of climate change and environmental pollution on neighborhoods of Black, Indigenous, and people of color (BIPOC). Making such improvements requires bringing BIPOC into science and into positions of leadership in laboratories, graduate schools, medical practices, and clinical trials. The moment is right to challenge scientific gatekeepers to respond to Black Lives Matter by widening the pathways that determine who becomes a scientist, a researcher, or a clinician.
The scientific workforce has long lacked diversity, which in turn discourages Black people from pursuing such careers. Causes include a dearth of mentors and role models, preconceived notions that science is exclusive to white males, and subpar STEM education. Across race, gender, class, ability, and all other dimensions that inform how an individual navigates the world, from the familial to the global level, seeing role models who resemble you impacts what you strive for and believe possible. As Marian Wright Edelman stated, "You can't be what you can't see"—a truth with ever-increasing resonance since the U.S. is projected to be minority-white by 2045.
Black Americans have paved the way for the nation to lead in science and technology, despite marginalization and exclusion from textbooks. Physicist Dr. Shirley Ann Jackson invented the technology behind Caller I.D. and Call Waiting. Otis Boykin's patents made televisions and radios what they are today. Thanks to the 2017 movie Hidden Figures, millions of Americans know about Katherine Johnson, the NASA mathematician whose calculations were essential to the successful trajectory of the Apollo 11 mission.
However, highlighting past role models who were Black achievers is not enough and paints too static a picture—especially when examples of transformative work by contemporary BIPOC scientists serving BIPOC communities abound. Cognitive neuroscientist Dr. Jonathan Jackson founded the Community Access, Recruitment, & Engagement (CARE) Research Center with the goal to break down barriers so that people of color participate in clinical trials. Geneticist Dr. Nanibaa' Garrison's research creates ethical frameworks to overcome genomic injustices so Indigenous populations can benefit from genetic research. Computer scientists Joy Buolamwini and Dr. Timnit Gebru's research drew attention to reinforced racial bias in artificial intelligence, leading Microsoft, Amazon, and IBM this summer to halt use of their facial recognition software.
"Integration does not mean equality if the space being integrated isn't exuberantly down for the cause."
In order to honor concretely the ubiquitous public statements and commitments to justice and equity that flooded everyone's inboxes in early June, we must include traditionally underrepresented voices in all phases of science and its applications. For guidance, we would benefit from listening to activists leading, for example, climate marches and protests over toxic water. Indeed, science is at the core of the issues for which young BIPOC are mobilizing. We need to sit down with these individuals to gain their input on how the narratives, practices, and opportunities in science should change. As Zeena Abdulkarim, a youth climate change organizer working with Zero Hour, explains: "Minority communities are exposed to what the privileged and people in power are not; therefore these communities know the right steps to take in the change we need for the kickstart of true social and environmental justice."
Two other Black youth, for example, used the platform of the laboratory while in high school to mobilize for change. Elle Lanair Lett, now specializing in epidemiology as an M.D.-Ph.D. student in Philadelphia, was prompted by family prevalence of diabetes to research the genetics of pancreatic cells. Dr. Otana Jakpor, now an ophthalmology resident in Michigan, was motivated by the pollution in her hometown of Riverside, California, to research the pulmonary effects of indoor air purifiers, with findings that influenced California ozone regulations. Both became finalists in a national science fair, propelling them on paths toward science careers. These young scientists demonstrate how people's communities and lived experiences can shape trajectories of science research, which, in turn, determines which visions for society are materialized and popularized.
We can also gain insight from another childhood science fair veteran, self-proclaimed "Black STEMinist" Augusta Uwamanzu-Nna, who graduated from college in May and works as a bioengineer. In her view, "we need to shift the burden away from Black people and onto individuals who have contributed to our current reality—fundamentally requiring understanding, open-mindedness, a lack of bias, cultural competency, anti-racism, anti-homophobia, and many, many other things."
Celebrating BIPOC's accomplishments in science and cultivating new leadership today are strong first steps to make science a guiding force for all. Ms. Uwamanzu-Nna keenly reminds us, "Integration does not mean equality if the space being integrated isn't exuberantly down for the cause." Indeed, educational institutions, scientific companies, and medical centers must acknowledge and embrace their role in democratizing science in order for society to realize racial and scientific justice.
[Editor's Note: To read other articles in this special magazine issue, visit the beautifully designed e-reader version.]
Gene Transfer Leads to Longer Life and Healthspan
In August, a study provided the first proof-of-principle that genetic material transferred from one species to another can increase both longevity and healthspan in the recipient animal.
The naked mole rat won’t win any beauty contests, but it could possibly win in the talent category. Its superpower: fighting the aging process to live several times longer than other animals its size, in a state of youthful vigor.
It’s believed that naked mole rats experience all the normal processes of wear and tear over their lifespan, but that they’re exceptionally good at repairing the damage from oxygen free radicals and the DNA errors that accumulate over time. Even though they possess genes that make them vulnerable to cancer, they rarely develop the disease, or any other age-related disease, for that matter. Naked mole rats are known to live for over 40 years without any signs of aging, whereas mice live on average about two years and are highly prone to cancer.
Now, these remarkable animals may be able to share their superpower with other species. In August, a study provided what may be the first proof-of-principle that genetic material transferred from one species can increase both longevity and healthspan in a recipient animal.
There are several theories to explain the naked mole rat’s longevity, but the one explored in the study, published in Nature, is based on the abundance of large-molecule high-molecular mass hyaluronic acid (HMM-HA).
A small molecule version of hyaluronic acid is commonly added to skin moisturizers and cosmetics that are marketed as ways to keep skin youthful, but this version, just applied to the skin, won’t have a dramatic anti-aging effect. The naked mole rat has an abundance of the much-larger molecule, HMM-HA, in the chemical-rich solution between cells throughout its body. But does the HMM-HA actually govern the extraordinary longevity and healthspan of the naked mole rat?
To answer this question, Dr. Vera Gorbunova, a professor of biology and oncology at the University of Rochester, and her team created a mouse model containing the naked mole rat gene hyaluronic acid synthase 2, or nmrHas2. It turned out that the mice receiving this gene during their early developmental stage also expressed HMM-HA.
The researchers found that the effects of the HMM-HA molecule in the mice were marked and diverse, exceeding the expectations of the study’s co-authors. High-molecular mass hyaluronic acid was more abundant in kidneys, muscles and other organs of the Has2 mice compared to control mice.
In addition, the altered mice had a much lower incidence of cancer. Seventy percent of the control mice eventually developed cancer, compared to only 57 percent of the altered mice, even after several techniques were used to induce the disease. The biggest difference occurred in the oldest mice, where the cancer incidence for the Has2 mice and the controls was 47 percent and 83 percent, respectively.
With regard to longevity, Has2 males increased their lifespan by more than 16 percent and the females added 9 percent. “Somehow the effect is much more pronounced in male mice, and we don’t have a perfect answer as to why,” says Dr. Gorbunova. Another improvement was in the healthspan of the altered mice: the number of years they spent in a state of relative youth. There’s a frailty index for mice, which includes body weight, mobility, grip strength, vision and hearing, in addition to overall conditions such as the health of the coat and body temperature. The Has2 mice scored lower in frailty than the controls by all measures. They also performed better in tests of locomotion and coordination, and in bone density.
Gorbunova’s results show that a gene artificially transferred from one species can have a beneficial effect on another species for longevity, something that had never been demonstrated before. This finding is “quite spectacular,” said Steven Austad, a biologist at the University of Alabama at Birmingham, who was not involved in the study.
Just as in lifespan, the effects in various organs and systems varied between the sexes, a common occurrence in longevity research, according to Austad, who authored the book Methuselah’s Zoo and specializes in the biological differences between species. “We have ten drugs that we can give to mice to make them live longer,” he says, “and all of them work better in one sex than in the other.” This suggests that more attention needs to be paid to the different effects of anti-aging strategies between the sexes, as well as gender differences in healthspan.
According to the study authors, the HMM-HA molecule delivered these benefits by reducing inflammation and senescence (cell dysfunction and death). The molecule also caused a variety of other benefits, including an upregulation of genes involved in the function of mitochondria, the powerhouses of the cells. These mechanisms are implicated in the aging process, and in human disease. In humans, virtually all noncommunicable diseases entail an acceleration of the aging process.
So, would the gene that creates HMM-HA have similar benefits for longevity in humans? “We think about these questions a lot,” Gorbunova says. “It’s been done by injections in certain patients, but it has a local effect in the treatment of organs affected by disease,” which could offer some benefits, she added.
“Mice are very short-lived and cancer-prone, and the effects are small,” says Steven Austad, a biologist at the University of Alabama at Birmingham. “But they did live longer and stay healthy longer, which is remarkable.”
As for a gene therapy to introduce the nmrHas2 gene into humans to obtain a global result, she’s skeptical because of the complexity involved. Gorbunova notes that there are potential dangers in introducing an animal gene into humans, such as immune responses or allergic reactions.
Austad is equally cautious about a gene therapy. “What this study says is that you can take something a species does well and transfer at least some of that into a new species. It opens up the way, but you may need to transfer six or eight or ten genes into a human” to get the large effect desired. Humans are much more complex and contain many more genes than mice, and all systems in a biological organism are intricately connected. One naked mole rat gene may not make a big difference when it interacts with human genes, metabolism and physiology.
Still, Austad thinks the possibilities are tantalizing. “Mice are very short-lived and cancer-prone, and the effects are small,” he says. “But they did live longer and stay healthy longer, which is remarkable.”
As for further research, says Austad, “The first place to look is the skin” to see if the nmrHas2 gene and the HMM-HA it produces can reduce the chance of cancer. Austad added that it would be straightforward to use the gene to try to prevent cancer in skin cells in a dish to see if it prevents cancer. It would not be hard to do. “We don’t know of any downsides to hyaluronic acid in skin, because it’s already used in skin products, and you could look at this fairly quickly.”
“Aging mechanisms evolved over a long time,” says Gorbunova, “so in aging there are multiple mechanisms working together that affect each other.” All of these processes could play a part and almost certainly differ from one species to the next.
“HMM-HA molecules are large, but we’re now looking for a small-molecule drug that would slow it’s breakdown,” she says. “And we’re looking for inhibitors, now being tested in mice, that would hinder the breakdown of hyaluronic acid.” Gorbunova has found a natural, plant-based product that acts as an inhibitor and could potentially be taken as a supplement. Ultimately, though, she thinks that drug development will be the safest and most effective approach to delivering HMM-HA for anti-aging.
A new study provides key insights in what causes Alzheimer's: a breakdown in the brain’s system for clearing waste.
In recent years, researchers of Alzheimer’s have made progress in figuring out the complex factors that lead to the disease. Yet, the root cause, or causes, of Alzheimer’s are still pretty much a mystery.
In fact, many people get Alzheimer’s even though they lack the gene variant we know can play a role in the disease. This is a critical knowledge gap for research to address because the vast majority of Alzheimer’s patients don’t have this variant.
A new study provides key insights into what’s causing the disease. The research, published in Nature Communications, points to a breakdown over time in the brain’s system for clearing waste, an issue that seems to happen in some people as they get older.
Michael Glickman, a biologist at Technion – Israel Institute of Technology, helped lead this research. I asked him to tell me about his approach to studying how this breakdown occurs in the brain, and how he tested a treatment that has potential to fix the problem at its earliest stages.
Dr. Michael Glickman is internationally renowned for his research on the ubiquitin-proteasome system (UPS), the brain's system for clearing the waste that is involved in diseases such as Huntington's, Alzheimer's, and Parkinson's. He is the head of the Lab for Protein Characterization in the Faculty of Biology at the Technion – Israel Institute of Technology. In the lab, Michael and his team focus on protein recycling and the ubiquitin-proteasome system, which protects against serious diseases like Alzheimer’s, Parkinson’s, cystic fibrosis, and diabetes. After earning his PhD at the University of California at Berkeley in 1994, Michael joined the Technion as a Senior Lecturer in 1998 and has served as a full professor since 2009.
Dr. Michael Glickman