December 27 | 2017
Slowing Aging Could Transform Society As We Know It
Neil Savage writes about science and technology from Lowell, Massachusetts. His work has appeared in Nature, Discover, Scientific American, Cell, IEEE Spectrum, and Chemical & Engineering News, among others. A former newspaper reporter, he received an MS in Science Journalism from Boston University.neilsavagewrite
A young woman portrayed next to her old counterpart.
(© Valentina R./Fotolia)
People's lives have been getting longer for more than a century. In 1900, in even the wealthiest countries, life expectancy was under 50, according to the World Health Organization. By 2015, the worldwide average was 74, and a girl born in Japan that year could expect to live to 87. Most of that extra lifespan came from improvements in nutrition and sanitation, and the development of vaccines and antibiotics.
<p><strong>People's lives have been getting longer for more than a century. In 1900, in even the wealthiest countries, life expectancy was under 50, according to the World Health Organization. By 2015, the worldwide average was 74, and a girl born in Japan that year could expect to live to 87. Most of that extra lifespan came from improvements in nutrition and sanitation, and the development of vaccines and antibiotics.</strong> </p>
<blockquote>The question is, how will slowing aging change society?</blockquote>
<p>But now scientists are trying to move beyond just eliminating the diseases that kill us to actually slowing the aging process itself. By developing new drugs to tackle the underlying mechanisms that make our bodies grow old and frail, researchers hope to give people many more years of healthy life. The question is, how will that change society?</p><p>There are several biological mechanisms that affect aging. One involves how cells react when they're damaged. Some die, but others enter a state called senescence, in which they halt their normal growth and send out signals that something's gone wrong. That signaling causes inflammation at the sight of a wound, for instance, and triggers the body's repair processes. Once everything is back to normal, the senescent cells die off and the inflammation fades. But as we age, the machinery for clearing senescent cells becomes less efficient and they begin to pile up. Some researchers think that this accumulation of senescent cells is what causes chronic inflammation, which has been <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616233/" target="_blank">implicated</a> in conditions such as heart disease and diabetes.</p>
<blockquote>The first clinical trial in humans of senolytic drugs is happening now.</blockquote>
<p>In 2015, researchers at the Mayo Clinic in Minnesota and the Scripps Research Institute in Florida tested the first so-called senolytic drugs, which cause senescent cells to die. After the scientists treated mice with a combination of an anti-cancer drug and a plant pigment that can act as an antioxidant, some of the senescent cells shrank away and caused the mouse's heart function to revert to that of a much <a href="https://www.ncbi.nlm.nih.gov/pubmed/25754370" target="_blank">younger mouse</a>.</p><p>"That suggests that senescence isn't just a consequence of aging, it's actually a driver of aging," says Paul Robbins, a professor of molecular medicine at Scripps and one of the researchers involved. Other animal studies have found that reducing the number of senescent cells improves a variety of age-related conditions, such as frailty, diabetes, liver disease, pulmonary fibrosis, and osteoporosis.</p><p>Now the same researchers are moving those tests to humans in the first clinical trials of senolytic drugs. In July 2016, the Mayo Clinic launched what may be the first <a href="https://clinicaltrials.gov/ct2/show/NCT02848131?term=dasatinib%2C+quercetin&rank=2" target="_blank">clinical trial</a> of senolytic therapy, studying the effect of the two drugs, called dasatinib and quercetin, on people with chronic kidney disease, which they hope to complete in 2021. Meanwhile Mayo and Scripps researchers have identified six different biochemical pathways that give rise to senescence, along with several drug candidates that target those pathways. Robbins says it's likely that different drugs will work better for different cells in the body.</p>
<blockquote>Would radical life extension lead to moral deterioration, risk aversion, and an abandonment of creativity?</blockquote>
<p>In Robbins' work, treating mice with senolytic drugs has extended their median lifespan—the age at which half the animals in his experiment have died—by about 30 percent, but hasn't extended the maximum lifespan. In other words, the oldest mice treated with the drugs died at the same age as mice who hadn't been treated, but more of the mice who received senolytics lived to that ripe old age. The same may turn out to be true for humans, with more people living to the limits of the lifespan—estimated by some to be about 115—but no one living much longer. On the other hand, Robbins says, it's early days for these therapies, and it may turn out that delaying aging actually does push the limit of life farther out.</p><p>Others expect more radical extensions of human life; British gerontologist Aubrey DeGray talks about people living for 1000 years, and people who call themselves transhumanists imagine replacing body parts as they wear out, or merging our minds with computers to make us essentially immortal. Brian Green, an ethicist at Santa Clara University in California, finds that concept horrifying. He fears it would make people value their own lives too highly, demoting other moral goods such as self-sacrifice or concern for the environment. "It kind of lends itself to a moral myopia," he says. "Humans work better if they have a goal beyond their own survival." And people who live for centuries might become averse to risk, because with longer lives they have more to lose if they were to accidentally die, and might be resistant to change, draining the world of creativity.</p>
<blockquote>Most researchers are focused on "extending the 'healthspan,' so that the people who live into their 90s are vigorous and disease-free."</blockquote>
<p>He's not too worried, though, that that's where studies such as the Mayo Clinic's are headed, and supports that sort of research. "Hopefully these things will work, and they'll help us live a little bit longer," Green says, "but the idea of radical life extension where we're going to live indefinitely longer, I think that is very unrealistic."</p><p>Most of the researchers working on combatting aging don't, in fact, talk of unlimited lifespans. Rather, they talk about extending the "healthspan," so that the people who live into their 90s are vigorous and disease-free up until nearly the end of their lives.</p><p>If scientists can lengthen life while reducing the number of years people suffer with dementia or infirmity, that could be beneficial, says Stephen Post, a professor of medicine and director of the Center for Medical Humanities, Compassionate Care, and Bioethics at Stony Brook University in New York. But even increasing the population of vigorous 90-somethings might have negative implications for society. "What would we do with all these people who are living so long?" he asks. "Would we stop having children? Would we never retire?"</p>
<blockquote>Adding 2.2 healthy years to the U.S. life by delaying aging could benefit the economy by $7.1 trillion over 50 years.</blockquote>
<p>If people keep working well past their 60s, that could mean there would be fewer jobs available for younger people, says Maxwell Mehlman, professor of bioethics at Case Western Reserve University's School of Law in Ohio. Mehlman says society may have to rethink age discrimination laws, which bar firing or refusing to hire people over a certain age, to make room for younger workers. On the other hand, those who choose to retire and live another two or three decades could strain pension and entitlement systems.</p><p>But a longer healthspan could reduce costs in the healthcare system, which now are driven disproportionately by older people. Jay Olshansky, an epidemiologist at the University of Illinois at Chicago School of Public Health, has estimated that adding 2.2 healthy years to the U.S. life by delaying aging would benefit the economy by $7.1 trillion over 50 years, as spending on illnesses such as cancer and heart disease drop.</p><p>For his part, Robbins says that the scientific conferences in the anti-aging field, which tend to focus on the technical research, should hold more sessions on social and economic impacts. If anti-aging therapies start extending healthy lifespans, as he and other researchers hope they will within a decade or so, society will need to adjust.</p><p>Ultimately, it's an extension of health, not just of longevity, that will benefit us. Extra decades of senescence do nobody any good. As Green says, "Nobody wants to live in a nursing home for 1000 years."</p>
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Neil Savage writes about science and technology from Lowell, Massachusetts. His work has appeared in Nature, Discover, Scientific American, Cell, IEEE Spectrum, and Chemical & Engineering News, among others. A former newspaper reporter, he received an MS in Science Journalism from Boston University.neilsavagewrite
February 25 | 2021
A Doctor Who Treated His Own Rare Disease Is Tracking COVID-19 Treatments Hiding In Plain Sight
Dr. David Fajgenbaum looking through a microscope at his lab.
Courtesy of Fajgenbaum
In late March, just as the COVID-19 pandemic was ramping up in the United States, David Fajgenbaum, a physician-scientist at the University of Pennsylvania, devised a 10-day challenge for his lab: they would sift through 1,000 recently published scientific papers documenting cases of the deadly virus from around the world, pluck out the names of any drugs used in an attempt to cure patients, and track the treatments and their outcomes in a database.
Before late 2019, no one had ever had to treat this exact disease before, which meant all treatments would be trial and error. Fajgenbaum, a pioneering researcher in the field of drug repurposing—which prioritizes finding novel uses for existing drugs, rather than arduously and expensively developing new ones for each new disease—knew that physicians around the world would be embarking on an experimental journey, the scale of which would be unprecedented. His intention was to briefly document the early days of this potentially illuminating free-for-all, as a sidebar to his primary field of research on a group of lymph node disorders called Castleman disease. But now, 11 months and 29,000 scientific papers later, he and his team of 22 are still going strong.
<p>They're running a publicly accessible database called the <a href="https://cdcn.org/corona/" target="_blank" rel="noopener noreferrer"><u>CORONA Project</u></a> (COvid19 Registry of Off-label & New Agents) that to date tracks 400 different COVID-19 treatments that have been tried somewhere in the world, along with the frequency of their use, and the outcomes.</p><p>"There's so many drugs being used all over the place, in different ways, with different outcomes," says Fajgenbaum. "We're trying to add some order to the madness."</p><p>20,000 people have accessed the registry—other physicians and researchers, those in the pharmaceutical industry , and even curious lay people—and the data are now being shared with the U.S. Food and Drug Administration in the hopes of launching large-scale trials that would lead to approving a constellation of treatment options for COVID-19 faster than any new drugs could come online. </p><p>"What David's group has done with the CORONA Project is on a scale that I don't think has ever been seen before," says Heather Stone, a health science policy analyst at the FDA who specializes in drug repurposing. She was not involved in establishing the project, but is now working with its data. "To collect and collate that information and make it openly accessible is a massive feat, and a huge benefit to the medical community," she says. </p>
On a Personal Mission
<p>In the science and medical world, Fajgenbaum lives a dual existence: he is both researcher and subject, physician and patient. In July 2010, when he was a healthy and physically fit 25-year-old finishing medical school, he began living through what would become a recurring, unprovoked, and overzealous immune response that repeatedly almost killed him.</p><p>His lymph nodes were inflamed; his liver, kidneys, and bone marrow were faltering; and he was dead tired all the time. At first his doctors mistook his mysterious illness for lymphoma, but his inflamed lymph nodes were merely a red herring. A month after his initial hospitalization, pathologists at Mayo Clinic finally diagnosed him with idiopathic multicentric Castleman disease—a particularly ruthless form of a class of lymph node disorders that doesn't just attack one part of the body, but many, and has no known cause. It's a rare diagnosis within an already rare set of disorders. Only about 1,500 Americans a year receive the same diagnosis. </p><p>Without many options for treatment, Fajgenbaum underwent recurring rounds of chemotherapy. Each time, the treatment would offer temporary respite from Castleman symptoms, but bring the full spate of chemotherapy side effects. And it wasn't a sustainable treatment for the long haul. Regularly dousing a person's cells in unmitigated toxicity was about as elegant a solution to Fajgenbaum's disease as bulldozing a house in response to a toaster fire. The fire might go out (though not necessarily), but the house would be destroyed.</p><p>A swirl of exasperation and doggedness finally propelled Fajgenbaum to take on a crucial question himself: Among all of the already FDA-approved drugs on the market, was there something out there, labeled for another use, that could beat back Castleman disease and that he could tolerate long-term? After months of research, he discovered the answer: sirolimus, a drug normally prescribed to patients receiving a kidney transplant, could be used to suppress his overactive immune system with few known side effects to boot.</p><p>Fajgenbaum became hellbent on devoting his practice and research to making similar breakthroughs for others. He founded the Castleman Disease Collaborative Network, to coordinate the research of others studying this bewildering disease, and directs a laboratory consumed with studying cytokine storms—out-of-control immune responses characterized by the body's release of cytokines, proteins that the immune system secretes and uses to communicate with and direct other cells. </p><p>In the spring of 2020, when cytokine storms emerged as a hallmark of the most severe and deadly cases of COVID-19, Fajgenbaum's ears perked up. Although SARS-CoV-2 itself was novel, Fajgenbaum already had almost a decade of experience battling the most severe biological forces it brought. Only this time, he thought, it might actually be easier to pinpoint a treatment—unlike Castleman disease, which has no known cause, at least here a virus was clearly the instigator. </p><blockquote>"Because [a drug] looks promising, we need to do a well-designed, large randomized controlled trial to really investigate whether this drug works or not ... We don't use that to say, 'You should take it.'"</blockquote>
Thinking Beyond COVID
<p>The week of March 13, when the World Health Organization declared COVID-19 a pandemic, Fajgenbaum found himself hoping that someone would make the same connection and apply the research to COVID. "Then like a minute later I was like, 'Why am I hoping that someone, somewhere, either follows our footsteps, or has a similar background to us? Maybe we just need to do it," he says. And the CORONA Project was born—first as a 10-day exercise, and later as the robust, interactive tool it now is. </p><p>All of the 400 treatments in the CORONA database are examples of repurposed drugs, or off-label uses: physicians are prescribing drugs to treat COVID that have been approved for a different disease. There are no bonafide COVID treatments, only inferences. The goal for people like Fajgenbaum and Stone is to identify potential treatments for further study and eventual official approval, so that physicians can treat the disease with a playbook in hand. When it works, drug repurposing opens up a way to move quickly: A range of treatments could be available to patients within just a few years of a totally new virus entering our reality compared with the 12 - 19 years new drug development takes.</p><p>"Companies for many decades have explored the use of their products for not just a single indication but often for many indications," says Stone. "'Supplemental approvals' are all essentially examples of drug repurposing, we just didn't call it that. The challenge, I think, is to explore those opportunities more comprehensively and systematically to really try to understand the full breadth of potential activity of any drug or molecule."</p><img lazy-loadable="true" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNTY4Njk0MC9vcmlnaW4ucG5nIiwiZXhwaXJlc19hdCI6MTY3NDk0ODk1NH0.gXwUKS-odLep_tIfSrCZE6Qw-7DHezUEBywEykMTqaI/img.png?width=980" id="451c9" class="rm-shortcode" data-rm-shortcode-id="9f95fcbeb11a6ac2cd08a8c91ec75539" data-rm-shortcode-name="rebelmouse-image" data-width="1700" data-height="1064" />
The left column shows the path of a repurposed drug, and on the right is the path of a newly discovered and developed drug.
Cures Within Reach
<p>In Fajgenbaum's primary work, promising drugs stand out easily. For a disease like Castleman, where improvement almost never occurs on its own, any improvement that follows a treatment can pretty clearly be attributed to that treatment. But Fajgenbaum says tracking COVID outcomes is less straightforward since "the vast majority of people will get better, whether they take steroids or they take Skittles." That's why the intent of the database is to identify promising treatments only to generate hypotheses and fruitful clinical trials, not to offer full-throated treatment recommendations. Within the registry, Fajgenbaum considers a drug promising if it's being used in humans, not just in lab animals, and a significant proportion of cases report patient improvement.</p><p>"It's that sort of combination of rock-solid randomized controlled trial data, plus anecdotal retrospective data, that we combine to say, 'Wow, this drug looks more promising than another,'" says Fajgenbaum. "Because it looks promising, we need to do a well-designed, large randomized controlled trial to really investigate whether this drug works or not ... We don't use that to say, 'You should take it.'"</p><p>Experts say that the search for repurposed drugs to treat COVID could have implications for rare diseases in general. Rare diseases, of which Castleman is one, affect <a href="https://globalgenes.org/rare-facts/" target="_blank" rel="noopener noreferrer"><u>400 million people</u></a> around the world. 95% of them don't have a tailor-made, FDA-approved drug treatment. Developing one is a lengthy and often prohibitively expensive process. If only a dozen people will benefit from and buy a drug, it's not often worth it to pharmaceutical companies to spend millions of dollars making them. On occasion when they do, however, that overhead shows up in the price tag: <a href="https://www.medscape.com/viewarticle/879422" target="_blank" rel="noopener noreferrer"><u>the top 10 most expensive drugs</u></a> in the world are all for rare diseases, often making them inaccessible to patients. Identifying new clinical uses for drugs that already exist is critical for opening a trap door out of a cycle that prioritizes profits over health outcomes.</p><p>"COVID is an interesting case where it's demonstrated that when the scientific and medical community really focuses all of its efforts and talents on a single problem, a solution can be identified and in a much faster time period than has ever historically been the case," says Stone. "I certainly wish it hadn't taken a pandemic to do that, but I think it does have lessons for the future in terms of our ability to accomplish things that we might have previously not thought were possible"—for example, mainstreaming the idea of drug repurposing as a treatment tool, even long after the pandemic subsides.</p>
A Confounding Virus
<p>The FDA declined to comment on what drugs it was fast-tracking for trials, but Fajgenbaum says that based on the CORONA Project's data, which includes data from smaller trials that have already taken place, he feels there are three drugs that seem the most clearly and broadly promising for large-scale studies. Among them are <a href="https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30503-8/fulltext" target="_blank" rel="noopener noreferrer"><u>dexamethasone</u></a>, which is a steroid with anti-inflammatory effects, and <a href="https://www.fda.gov/news-events/press-announcements/coronavirus-covid-19-update-fda-authorizes-drug-combination-treatment-covid-19" target="_blank" rel="noopener noreferrer"><u>baricitinib</u></a>, a rheumatoid arthritis drug, both of which have enabled the sickest COVID-19 patients to bounce back by suppressing their immune systems. The third most clearly promising drug is <a href="https://www.nih.gov/news-events/news-releases/full-dose-blood-thinners-decreased-need-life-support-improved-outcome-hospitalized-covid-19-patients" target="_blank" rel="noopener noreferrer"><u>heparin</u></a>, a blood thinner, which a recent trial showed to be most helpful when administered at a full dose, more so than at a small, preventative dose. (On the flipside, Fajgenbaum says "it's a little sad" that in the database you can see hydroxychloroquine is still the most-prescribed drug being tried as a COVID treatment around the world, despite over the summer being <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2021801" target="_blank" rel="noopener noreferrer"><u>debunked</u></a> widely as an effective treatment, and continuously since then.)</p><p>One of the confounding attributes of SARS-CoV-2 is its ability to cause such a huge spectrum of outcomes. It's unlikely a silver bullet treatment will emerge under that reality, so the database also helps surface drugs that seem most promising for a specific population. <a href="https://jamanetwork.com/journals/jama/fullarticle/2773108" target="_blank" rel="noopener noreferrer"><u>Fluvoxamine</u></a>, a selective serotonin reuptake inhibitor used to treat obsessive compulsive disorder, showed promise in the recovery of outpatients—those who were sick, but not severely enough to be hospitalized. <a href="https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2772185" target="_blank" rel="noopener noreferrer"><u>Tocilizumab</u></a>, which was actually developed for Castleman disease, the disease Fajgenbaum is managing, was initially written off as a COVID treatment because it failed to benefit large portions of hospitalized patients, but now seems to be effective if used on intensive care unit patients within 24 hours of admission—these are some of the sickest patients with the highest risk of dying. </p><p>Other than fluvoxamine, most of the drugs labeled as promising do skew toward targeting hospitalized patients, more than outpatients. One reason, Fajgenbaum says, is that "if you're in a hospital it's very easy to give you a drug and to track you, and there are very objective measurements as to whether you die, you progress to a ventilator, etc." Tracking outpatients is far more difficult, especially when folks have been routinely asked to stay home, quarantine, and free up hospital resources if they're experiencing only mild symptoms. </p><p>But the other reason for the skew is because COVID is very unlike most other diseases in terms of the human immune response the virus triggers. For example, if oncology treatments show some benefit to people with the highest risk of dying, then they usually work extremely well if administered in the earlier stages of a cancer diagnosis. Across many diseases, this dialing backward is a standard approach to identifying promising treatments. With COVID, all of that reasoning has proven moot. </p><p>As we've seen over the last year, COVID cases often start as asymptomatic, and remain that way for days, indicating the body is mounting an incredibly weak immune response initially. Then, between days five and 14, as if trying to make up for lost time, the immune system overcompensates by launching a major inflammatory response, which in the sickest patient can lead to the type of cytokine storms that helped Fajgenbaum realize his years of Castleman research might be useful during this public health crisis. Because of this phased response, you can't apply the same treatment logic to all cases.</p><p>"In COVID, drugs that work late tend to not work if given early, and drugs that work early tend to not work if given late," says Fajgenbaum. "Generally this … is not a commonplace thing for a virus." </p><blockquote>"There are drugs that are literally sitting in every single hospital pharmacy in the country that, if a study shows it's effective, can be deployed that evening to patients on a massive scale."</blockquote>
<p>This see-sawing necessitates tracking a constellation of drugs that might work for different stages of the disease as a patient moves from the weak immune response stage into the overzealous immune response.</p><p>"COVID is difficult, compared to other diseases, because there are so many different levels of disease severity, and recovery at different rates," says Stone, the FDA researcher. "That makes it hard to see the patterns or signals and it makes it very important to collect very, very large numbers of cases in order to really reliably identify signals."</p><p>This particular moment in the pandemic feels like a massive tipping point, or the instant a tiny pinprick of light finally appeared at the end of the tunnel: several vaccines are already here, with more on the way imminently. In the U.S., more than 65 million doses of the vaccine have been administered, and positive COVID cases are finally falling back to levels not seen since October. On the hopeful surface, it might seem a strange moment to be preparing to launch trials that will validate treatments for a virus it seems the U.S. may finally be beating back. But at best, Americans are still months away from reaching herd immunity through vaccination, and new circulating variants may threaten to upend our fragile progress. </p><p>"In the meantime, there are drugs that are literally sitting in every single hospital pharmacy in the country that, if a study shows it's effective, can be deployed that evening to patients on a massive scale. It wouldn't have to be newly produced, it wouldn't have to be shipped, it's literally there already," says Fajgenbaum. "The idea that you can save a lot of lives by finding things that are just already there I think is really compelling, given how many people are going to die over these next few months." </p><p>Even after that, not everyone can or will be vaccinated, and, as the <a href="https://www.wsj.com/articles/as-vaccines-raise-hope-cold-reality-dawns-covid-19-is-likely-here-to-stay-11612693803" target="_blank" rel="noopener noreferrer"><u><em>Wall Street Journal</em></u></a> recently reported, "The pathogen will circulate for years, or even decades, leaving society to coexist with Covid-19 much as it does with other endemic diseases like flu, measles, and HIV." Neither vaccines, personal behavior, or treatments alone is a panacea against the virus, but together they might be. </p><p>"It's important to explore all avenues in this public health emergency, and drug repurposing can continue to play a role as the pandemic continues and evolves," says Stone. "I think COVID variants in particular are a big concern at the moment, and therefore continuing to investigate new therapeutics, even as the vaccines roll out, will continue to be a priority."</p>
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Julia Sklar is a Boston-based independent journalist who covers science, health, and technology. You can follow her on Twitter at @jfsklar.
February 22 | 2021
Announcing March Event: "COVID Vaccines and the Return to Life: Part 1"
Leading medical and scientific experts will discuss the latest developments around the COVID-19 vaccines at our March 11th event.
Photo by Daniel Schludi on Unsplash
EVENT INFORMATION
DATE:
Thursday, March 11th, 2021 at 12:30pm - 1:45pm EST
On the one-year anniversary of the global declaration of the pandemic, this virtual event will convene leading scientific and medical experts to discuss the most pressing questions around the COVID-19 vaccines. Planned topics include the effect of the new circulating variants on the vaccines, what we know so far about transmission dynamics post-vaccination, how individuals can behave post-vaccination, the myths of "good" and "bad" vaccines as more alternatives come on board, and more. A public Q&A will follow the expert discussion.
<p><strong>CONTACT:</strong></p><p>kira@goodinc.com</p><p><strong>LOCATION:</strong></p><p>Zoom webinar</p>
SPEAKERS:
<img lazy-loadable="true" data-runner-src="https://leaps.org/media-library/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNTY3Mzc4NS9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTY0NjYwNjU4NX0.Tdrh5pze5P4XxgiJK3J4JFrsrijfabIzNJz-AATghDE/image.jpg?width=534&coordinates=365%2C3%2C299%2C559&height=462" id="87554" class="rm-shortcode" data-rm-shortcode-id="b6c7311be7aec25807f9af19b683bf1d" data-rm-shortcode-name="rebelmouse-image" data-width="534" data-height="462" />Dr. Paul Offit speaking at Communicating Vaccine Science.
commons.wikimedia.org<p><strong><a href="https://www.research.chop.edu/people/paul-a-offit" target="_blank" rel="noopener noreferrer">Dr. Paul Offit, M.D.</a>, is the director of the Vaccine Education Center and an attending physician in infectious diseases at the Children's Hospital of Philadelphia. He is a co-inventor of the rotavirus vaccine for infants, and he has lent his expertise to the advisory committees that review data on new vaccines for the CDC and FDA.</strong></p>
<img lazy-loadable="true" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNTY5MDQyOS9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTY1MDQwODAyM30.iyeh3Ew-xzU7pxxe20y1zV7zgX0MBIRh5UO-oc4h_00/img.jpg?width=980" id="d9258" class="rm-shortcode" data-rm-shortcode-id="06314b30d800d4c12690d36233020fa9" data-rm-shortcode-name="rebelmouse-image" data-width="640" data-height="640" />
Dr. Monica Gandhi
UCSF Health
<p><a href="https://profiles.ucsf.edu/monica.gandhi"></a><strong><a href="https://profiles.ucsf.edu/monica.gandhi" target="_blank">Dr. Monica Gandhi, M.D., MPH,</a> is Professor of Medicine and Associate Division Chief (Clinical Operations/ Education) of the Division of HIV, Infectious Diseases, and Global Medicine at UCSF/ San Francisco General Hospital.</strong></p><img lazy-loadable="true" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNTY3Mzc5NC9vcmlnaW4uanBnIiwiZXhwaXJlc19hdCI6MTY3MzUyODMzOX0.ThfzyknBvgG1QOwTWgEdmUtKlyYh9nQ5b7pSZ4KIYbU/img.jpg?width=980" id="34f7d" class="rm-shortcode" data-rm-shortcode-id="ce09faedd068e87cdf23498da32dd6c1" data-rm-shortcode-name="rebelmouse-image" data-width="3600" data-height="2880" />
Dr. Onyema Ogbuagu, MBBCh, FACP, FIDSA
Yale Medicine
<p><strong><a href="https://medicine.yale.edu/profile/onyema_ogbuagu/" target="_blank" rel="noopener noreferrer">Dr. Onyema Ogbuagu, MBBCh</a>, is an infectious disease physician at Yale Medicine who treats COVID-19 patients and leads Yale's clinical studies around COVID-19. He ran Yale's trial of the Pfizer/BioNTech vaccine.</strong></p><img lazy-loadable="true" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNTY3MzgyOC9vcmlnaW4ucG5nIiwiZXhwaXJlc19hdCI6MTYzNTYxMTA3MH0.mYcKGJi-GCL92TjgboHxD4DLg1PpQINl9yFyB8w7D4g/img.png?width=980" id="e0874" class="rm-shortcode" data-rm-shortcode-id="5f4bf126d15abcdf722486c3d3dad03e" data-rm-shortcode-name="rebelmouse-image" data-width="512" data-height="512" />
Dr. Eric Topol
Dr. Topol's Twitter
<p><strong><a href="https://www.scripps.edu/faculty/topol/" target="_blank" rel="noopener noreferrer">Dr. Eric Topol, M.D.</a>, is a cardiologist, scientist, professor of molecular medicine, and the director and founder of Scripps Research Translational Institute. He has led clinical trials in over 40 countries with over 200,000 patients and pioneered the development of many routinely used medications.</strong></p>REGISTER NOW
<p>This event is the first of a four-part series co-hosted by <a href="https://leaps.org/" target="_self" rel="noopener">LeapsMag</a>, the <a href="https://www.aspeninstitute.org/programs/science-society/" target="_blank" rel="noopener noreferrer">Aspen Institute Science & Society Program</a>, and the <a href="https://www.aspeninstitute.org/programs/health-medicine-and-society-program/the-sabin-aspen-vaccine-science-policy-group-2/" target="_blank" rel="noopener noreferrer">Sabin–Aspen Vaccine Science & Policy Group</a>, with generous support from the <a href="https://www.moore.org/" target="_blank" rel="noopener noreferrer">Gordon and Betty Moore Foundation</a> and the <a href="https://www.hhmi.org/" target="_blank" rel="noopener noreferrer">Howard Hughes Medical Institute</a>.</p><p><img src="https://aspeninst.zoom.us/w_p/93233317073/121cb7d4-3b73-48cc-a193-2962dae5ac3c.png" alt="Webinar logo"></p>
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Kira Peikoff is a journalist whose work has appeared in The New York Times, Newsweek, Nautilus, Popular Mechanics, The New York Academy of Sciences, and other outlets. She is also the author of four suspense novels that explore controversial issues arising from scientific innovation: Living Proof, No Time to Die, Die Again Tomorrow, and Mother Knows Best. Peikoff holds a B.A. in Journalism from New York University and an M.S. in Bioethics from Columbia University. She lives in New Jersey with her husband and son.