I’m a Black, Genderqueer Medical Student: Here’s My Hard-Won Wisdom for Students and Educational Institutions
Advice follows for how to improve higher education for marginalized communities.
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.
In the last 12 years, I have earned degrees from Harvard College and Duke University and trained in an M.D.-Ph.D. program at the University of Pennsylvania. Through this process, I have assembled much educational privilege and can now speak with the authority that is conferred in these ivory towers. Along the way, as a Black, genderqueer, first-generation, low-income trainee, the systems of oppression that permeate American society—racism, transphobia, and classism, among others—coalesced in the microcosm of academia into a unique set of challenges that I had to navigate. I would like to share some of the lessons I have learned over the years in the format of advice for both Black, Indigenous, and other People of Color (BIPOC) and LGBTQ+ trainees as well as members of the education institutions that seek to serve them.
To BIPOC and LGBTQ+ Trainees: Who you are is an asset, not an obstacle. Throughout my undergraduate years, I viewed my background as something to overcome. I had to overcome the instances of implicit bias and overt discrimination I experienced in my classes and among my peers. I had to overcome the preconceived, racialized, limitations on my abilities that academic advisors projected onto me as they characterized my course load as too ambitious or declared me unfit for medical school. I had to overcome the lack of social capital that comes with being from a low-resourced rural community and learn all the idiosyncrasies of academia from how to write professional emails to how and when to solicit feedback. I viewed my Blackness, queerness, and transness as inconveniences of identity that made my life harder.
It was only as I went on to graduate and medical school that I saw how much strength comes from who I am. My perspective allows me to conduct insightful, high-impact, and creative research that speaks to uplifting my various intersecting communities. My work on health equity for transgender people of color (TPOC) and BIPOC trainees in medicine is my form of advocacy. My publications are love letters to my communities, telling them that I see them and that I am with them. They are also indictments of the systems that oppress them and evidence that supports policy innovations and help move our society toward a more equitable future.
To Educators and Institutions: Allyship is active and uncomfortable. In the last 20 years, institutions have professed interest in diversifying their members and supporting marginalized groups. However, despite these proclamations, most have fallen short of truly allying themselves to communities in need of support. People often assume that allyship is defined by intent; that they are allies to Black people in the #BLM era because they, too, believe that Black lives have value. This is decency, not allyship. In the wake of the tragic killings of Breonna Taylor and George Floyd, and the ongoing racial inequity of the COVID-19 pandemic, every person of color that I know in academia has been invited to a townhall on racism. These meetings risk re-traumatizing Black people if they feel coerced into sharing their experiences with racism in front of their white colleagues. This is exploitation, not allyship. These discussions must be carefully designed to prioritize Black voices but not depend on them. They must rely on shared responsibility for strategizing systemic change that centers the needs of Black and marginalized voices while diffusing the requisite labor across the entire institution.
Allyship requires a commitment to actions, not ideas. In education this is fostering safe environments for BIPOC and LGBTQ+ students. It is changing the culture of your institution such that anti-racism is a shared value and that work to establish anti-racist practices is distributed across all groups rather than just an additional tax on minority students and faculty. It is providing dedicated spaces for BIPOC and LGBTQ+ students where they can build community amongst themselves away from the gaze of majority white, heterosexual, and cisgender groups that dominate other spaces. It is also building the infrastructure to educate all members of your institution on issues facing BIPOC and LGBTQ+ students rather than relying on members of those communities to educate others through divulging their personal experiences.
Among well-intentioned ally hopefuls, anxiety can be a major barrier to action. Anxiety around the possibility of making a mistake, saying the wrong thing, hurting or offending someone, and having uncomfortable conversations. I'm here to alleviate any uncertainty around that: You will likely make mistakes, you may receive backlash, you will undoubtedly have uncomfortable conversations, and you may have to apologize. Steel yourself to that possibility and view it as an asset. People give their most unfiltered feedback when they have been hurt, so take that as an opportunity to guide change within your organizations and your own practices. How you respond to criticism will determine your allyship status. People are more likely to forgive when a commitment to change is quickly and repeatedly demonstrated.
The first step to moving forward in an anti-racist framework is to compensate the students for their labor in making the institution more inclusive.
To BIPOC and LGBTQ+ Trainees: Your labor is worth compensation and recognition. It is difficult to see your institution failing to adequately support members of your community without feeling compelled to act. As a Black person in medicine I have served on nearly every committee related to diversity recruitment and admissions. As a queer person I have sat on many taskforces dedicated to improving trans education in medical curricula. I have spent countless hours improving the institutions at which I have been educated and will likely spend countless more. However, over the past few years, I have realized that those hours do not generally advance my academic and professional goals. My peers who do not share in my marginalized identities do not have the external pressure to sequester large parts of their time for institutional change. While I was drafting emails to administrators or preparing journal clubs to educate students on trans health, my peers were studying.
There were periods in my education where there were appreciable declines in my grades and research productivity because of the time I spent on institutional reform. Without care, this phenomenon can translate to a perceived achievement gap. It is not that BIPOC and LGBTQ+ achieve less; in fact, in many ways we achieve more. However, we expend much of our effort on activities that are not traditionally valued as accomplishments for career advancement. The only way to change this norm is to start demanding compensation for your labor and respectfully declining if it is not provided. Compensation can be monetary, but it can also be opportunities for professional identity formation. For uncompensated work that I feel particularly compelled to do, I strategize how it can benefit me before starting the project. Can I write it up for publication in a peer-reviewed scientific journal? Can I find an advisor to support the task force and write a letter of reference on my behalf? Can I use the project to apply for external research funding or scholarships? These are all ways of translating the work that matters to you into the currency that the medical establishment values as productivity.
To Educators and Institutions: Compensate marginalized members of your organizations for making it better. Racism is the oldest institution in America. It is built into the foundation of the country and rests in the very top office in our nation's capital. Analogues of racism, specifically gender-based discrimination, transphobia, and classism, have similarly seeped into the fabric of our country and education system. Given their ubiquity, how can we expect to combat these issues cheaply? Today, anti-racism work is in vogue in academia, and institutions have looked to their Black and otherwise marginalized students to provide ways that the institution can improve. We, as students, regularly respond with well-researched, scholarly, actionable lists of specific interventions that are the result of dozens (sometimes hundreds) of hours of unpaid labor. Then, administrators dissect these interventions and scale them back citing budgetary concerns or hiring limitations.
It gives the impression that they view racism as an easy issue to fix, that can be slotted in under an existing line item, rather than the severe problem requiring radical reform that it actually is. The first step to moving forward in an anti-racist framework is to compensate the students for their labor in making the institution more inclusive. Inclusion and equity improve the educational environment for all students, so in the same way one would pay a consultant for an audit that identifies weaknesses in your institution, you should pay your students who are investing countless hours in strategic planning. While financial compensation is usually preferable, institutions can endow specific equity-related student awards, fellowships, and research programs that allow the work that students are already doing to help further their careers. Next, it is important to invest. Add anti-racism and equity interventions as specific items in departmental and institutional budgets so that there is annual reserved capital dedicated to these improvements, part of which can include the aforementioned student compensation.
To BIPOC and LGBTQ+ Trainees: Seek and be mentors. Early in my training, I often lamented the lack of mentors who shared important identities with myself. I initially sought a Black, queer mentor in medicine who could open doors and guide me from undergrad pre-med to university professor. Unfortunately, given the composition of the U.S. academy, this was not a realistic goal. While our white, cisgender, heterosexual colleagues can identify mentors they reflect, we have to operate on a different mentorship model. In my experience, it is more effective to assemble a mentorship network: a group of allies who facilitate your professional and personal development across one or more arenas. For me, as a physician-scholar-advocate, I need professional mentors who support my specific research interests, help me develop as a policy innovator and advocate, and who can guide my overall career trajectory on the short- and long- term time scales.
Rather than expecting one mentor to fulfill all those roles, as well as be Black and queer, I instead seek a set of mentors that can share in these roles, all of whom are informed or educable on the unique needs of Black and queer trainees. When assembling your own mentorship network, remember personal mentors who can help you develop self-care strategies and achieve work-life balance. Also, there is much value in peer mentorship. Some of my best mentors are my contemporaries. Your experiences have allowed you to accumulate knowledge—share that knowledge with each other.
To Educators and Institutions: Hire better mentors. Be better mentors. Poor mentorship is a challenge throughout academia that is amplified for BIPOC and LGBTQ+ trainees. Part of this challenge is due to priorities established in the hiring process. Institutions need to update hiring practices to explicitly evaluate faculty and staff candidates for their ability to be good mentors, particularly to students from marginalized communities. This can be achieved by including diverse groups of students on hiring committees and allowing them to interview candidates and assess how the candidate will support student needs. Also, continually evaluate current faculty and staff based on standardized feedback from students that will allow you to identify and intervene on deficits and continually improve the quality of mentorship at your institution.
The suggestions I provided are about navigating medical education, as it exists now. I hope that incorporating these practices will allow institutions to better serve the BIPOC and LGBTQ+ trainees that help make their communities vibrant. I also hope that my fellow BIPOC and LGBTQ+ trainees can see themselves in this conversation and feel affirmed and equipped in navigating medicine based on the tools I provide here. However, my words are only a tempering measure. True justice in medical education and health will only happen when we overhaul our institutions and dismantle systems of oppression in our society.
[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