I’m a Black, Genderqueer Medical Student: Here’s My Hard-Won Wisdom for Students and Educational Institutions
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.]
A new competition by the XPRIZE Foundation is offering $101 million to researchers who discover therapies that give a boost to people aged 65-80 so their bodies perform more like when they were middle-aged.
For today’s podcast episode, I talked with Dr. Peter Diamandis, XPRIZE’s founder and executive chairman. Under Peter’s leadership, XPRIZE has launched 27 previous competitions with over $300 million in prize purses. The latest contest aims to enhance healthspan, or the period of life when older people can play with their grandkids without any restriction, disability or disease. Such breakthroughs could help prevent chronic diseases that are closely linked to aging. These illnesses are costly to manage and threaten to overwhelm the healthcare system, as the number of Americans over age 65 is rising fast.
In this competition, called XPRIZE Healthspan, multiple awards are available, depending on what’s achieved, with support from the nonprofit Hevolution Foundation and Chip Wilson, the founder of Lululemon and nonprofit SOLVE FSHD. The biggest prize, $81 million, is for improvements in cognition, muscle and immunity by 20 years. An improvement of 15 years will net $71 million, and 10 years will net $61 million.
In our conversation for this episode, Peter talks about his plans for XPRIZE Healthspan and why exponential technologies make the current era - even with all of its challenges - the most exciting time in human history. We discuss the best mental outlook that supports a person in becoming truly innovative, as well as the downsides of too much risk aversion. We talk about how to overcome the negativity bias in ourselves and in mainstream media, how Peter has shifted his own mindset to become more positive over the years, how to inspire a culture of innovation, Peter’s personal recommendations for lifestyle strategies to live longer and healthier, the innovations we can expect in various fields by 2030, the future of education and the importance of democratizing tech and innovation.
In addition to Peter’s pioneering leadership of XPRIZE, he is also the Executive Founder of Singularity University. In 2014, he was named by Fortune as one of the “World’s 50 Greatest Leaders.” As an entrepreneur, he’s started over 25 companies in the areas of health-tech, space, venture capital and education. He’s Co-founder and Vice-Chairman of two public companies, Celularity and Vaxxinity, plus being Co-founder & Chairman of Fountain Life, a fully-integrated platform delivering predictive, preventative, personalized and data-driven health. He also serves as Co-founder of BOLD Capital Partners, a venture fund with a half-billion dollars under management being invested in exponential technologies and longevity companies. Peter is a New York Times Bestselling author of four books, noted during our conversation and in the show notes of this episode. He has degrees in molecular genetics and aerospace engineering from MIT and holds an M.D. from Harvard Medical School.
- Peter Diamandis bio
- New XPRIZE Healthspan
- Peter Diamandis books
- Longevity Insider newsletter – AI identifies the news
- Peter Diamandis Longevity Handbook
- Hevolution funding for longevity
XPRIZE Founder Peter Diamandis speaks with Mehmoud Khan, CEO of Hevolution Foundation, at the launch of XPRIZE Healthspan.
From infections with no symptoms to why men are more likely to be hospitalized in the ICU and die of COVID-19, new research shows that your genes play a significant role
Early in the pandemic, genetic research focused on the virus because it was readily available. Plus, the virus contains only 30,000 bases in a dozen functional genes, so it's relatively easy and affordable to sequence. Additionally, the rapid mutation of the virus and its ability to escape antibody control fueled waves of different variants and provided a reason to follow viral genetics.
In comparison, there are many more genes of the human immune system and cellular functions that affect viral replication, with about 3.2 billion base pairs. Human studies require samples from large numbers of people, the analysis of each sample is vastly more complex, and sophisticated computer analysis often is required to make sense of the raw data. All of this takes time and large amounts of money, but important findings are beginning to emerge.
About half the people exposed to SARS-CoV-2, the virus that causes the COVID-19 disease, never develop symptoms of this disease, or their symptoms are so mild they often go unnoticed. One piece of understanding the phenomena came when researchers showed that exposure to OC43, a common coronavirus that results in symptoms of a cold, generates immune system T cells that also help protect against SARS-CoV-2.
Jill Hollenbach, an immunologist at the University of California at San Francisco, sought to identify the gene behind that immune protection. Most COVID-19 genetic studies are done with the most seriously ill patients because they are hospitalized and thus available. “But 99 percent of people who get it will never see the inside of a hospital for COVID-19,” she says. “They are home, they are not interacting with the health care system.”
Early in the pandemic, when most labs were shut down, she tapped into the National Bone Marrow Donor Program database. It contains detailed information on donor human leukocyte antigens (HLAs), key genes in the immune system that must match up between donor and recipient for successful transplants of marrow or organs. Each HLA can contain alleles, slight molecular differences in the DNA of the HLA, which can affect its function. Potential HLA combinations can number in the tens of thousands across the world, says Hollenbach, but each person has a smaller number of those possible variants.
She teamed up with the COVID-19 Citizen Science Study a smartphone-based study to track COVID-19 symptoms and outcomes, to ask persons in the bone marrow donor registry about COVID-19. The study enlisted more than 30,000 volunteers. Those volunteers already had their HLAs annotated by the registry, and 1,428 tested positive for the virus.
Analyzing five key HLAs, she found an allele in the gene HLA-B*15:01 that was significantly overrepresented in people who didn’t have any symptoms. The effect was even stronger if a person had inherited the allele from both parents; these persons were “more than eight times more likely to remain asymptomatic than persons who did not carry the genetic variant,” she says. Altogether this HLA was present in about 10 percent of the general European population but double that percentage in the asymptomatic group. Hollenbach and her colleagues were able confirm this in other different groups of patients.
What made the allele so potent against SARS-CoV-2? Part of the answer came from x-ray crystallography. A key element was the molecular shape of parts of the cold virus OC43 and SARS-CoV-2. They were virtually identical, and the allele could bind very tightly to them, present their molecular antigens to T cells, and generate an extremely potent T cell response to the viruses. And “for whatever reasons that generated a lot of memory T cells that are going to stick around for a long time,” says Hollenbach. “This T cell response is very early in infection and ramps up very quickly, even before the antibody response.”
Understanding the genetics of the immune response to SARS-CoV-2 is important because it provides clues into the conditions of T cells and antigens that support a response without any symptoms, she says. “It gives us an opportunity to think about whether this might be a vaccine design strategy.”
A researcher at the Leibniz Institute of Virology in Hamburg Germany, Guelsah Gabriel, was drawn to a question at the other end of the COVID-19 spectrum: why men more likely to be hospitalized and die from the infection. It wasn't that men were any more likely to be exposed to the virus but more likely, how their immune system reacted to it
Several studies had noted that testosterone levels were significantly lower in men hospitalized with COVID-19. And, in general, the lower the testosterone, the worse the prognosis. A year after recovery, about 30 percent of men still had lower than normal levels of testosterone, a condition known as hypogonadism. Most of the men also had elevated levels of estradiol, a female hormone (https://pubmed.ncbi.nlm.nih.gov/34402750/).
Every cell has a sex, expressing receptors for male and female hormones on their surface. Hormones docking with these receptors affect the cells' internal function and the signals they send to other cells. The number and role of these receptors varies from tissue to tissue.
Gabriel began her search by examining whole exome sequences, the protein-coding part of the genome, for key enzymes involved in the metabolism of sex hormones. The research team quickly zeroed in on CYP19A1, an enzyme that converts testosterone to estradiol. The gene that produces this enzyme has a number of different alleles, the molecular variants that affect the enzyme's rate of metabolizing the sex hormones. One genetic variant, CYP19A1 (Thr201Met), is typically found in 6.2 percent of all people, both men and women, but remarkably, they found it in 68.7 percent of men who were hospitalized with COVID-19.
Lungs are the tissue most affected in COVID-19 disease. Gabriel wondered if the virus might be affecting expression of their target gene in the lung so that it produces more of the enzyme that converts testosterone to estradiol. Studying cells in a petri dish, they saw no change in gene expression when they infected cells of lung tissue with influenza and the original SARS-CoV viruses that caused the SARS outbreak in 2002. But exposure to SARS-CoV-2, the virus responsible for COVID-19, increased gene expression up to 40-fold, Gabriel says.
Did the same thing happen in humans? Autopsy examination of patients in three different cites found that “CYP19A1 was abundantly expressed in the lungs of COVID-19 males but not those who died of other respiratory infections,” says Gabriel. This increased enzyme production led likely to higher levels of estradiol in the lungs of men, which “is highly inflammatory, damages the tissue, and can result in fibrosis or scarring that inhibits lung function and repair long after the virus itself has disappeared.” Somehow the virus had acquired the capacity to upregulate expression of CYP19A1.
Only two COVID-19 positive females showed increased expression of this gene. The menopause status of these women, or whether they were on hormone replacement therapy was not known. That could be important because female hormones have a protective effect for cardiovascular disease, which women often lose after going through menopause, especially if they don’t start hormone replacement therapy. That sex-specific protection might also extend to COVID-19 and merits further study.
The team was able to confirm their findings in golden hamsters, the animal model of choice for studying COVID-19. Testosterone levels in male animals dropped 5-fold three days after infection and began to recover as viral levels declined. CYP19A1 transcription increased up to 15-fold in the lungs of the male but not the females. The study authors wrote, “Virus replication in the male lungs was negatively associated with testosterone levels.”
The medical community studying COVID-19 has slowly come to recognize the importance of adipose tissue, or fat cells. They are known to express abundant levels of CYP19A1 and play a significant role as metabolic tissue in COVID-19. Gabriel adds, “One of the key findings of our study is that upon SARS-CoV-2 infection, the lung suddenly turns into a metabolic organ by highly expressing” CYP19A1.
She also found evidence that SARS-CoV-2 can infect the gonads of hamsters, thereby likely depressing circulating levels of sex hormones. The researchers did not have autopsy samples to confirm this in humans, but others have shown that the virus can replicate in those tissues.
A possible treatment
Back in the lab, substituting low and high doses of testosterone in SARS-COV-2 infected male hamsters had opposite effects depending on testosterone dosage used. Gabriel says that hormone levels can vary so much, depending on health status and age and even may change throughout the day, that “it probably is much better to inhibit the enzyme” produced by CYP19A1 than try to balance the hormones.
Results were better with letrozole, a drug approved to treat hypogonadism in males, which reduces estradiol levels. The drug also showed benefit in male hamsters in terms of less severe disease and faster recovery. She says more details need to be worked out in using letrozole to treat COVID-19, but they are talking with hospitals about clinical trials of the drug.
Gabriel has proposed a four hit explanation of how COVID-19 can be so deadly for men: the metabolic quartet. First is the genetic risk factor of CYP19A1 (Thr201Met), then comes SARS-CoV-2 infection that induces even greater expression of this gene and the deleterious increase of estradiol in the lung. Age-related hypogonadism and the heightened inflammation of obesity, known to affect CYP19A1 activity, are contributing factors in this deadly perfect storm of events.
Studying host genetics, says Gabriel, can reveal new mechanisms that yield promising avenues for further study. It’s also uniting different fields of science into a new, collaborative approach they’re calling “infection endocrinology,” she says.