Cutting-edge work on molecular mechanisms involved in the cellular response to stress was the focus at the 18th annual John B. Little Symposium, held October 23-24, 2015 at Harvard T.H. Chan School of Public Health.
The symposium is hosted each year by the John B. Little (JBL) Center for Radiation Sciences. Both the symposium and the center are named for John B. Little, James Steven Simmons Professor of Radiobiology Emeritus, one of the first scholars to characterize problems in public health associated with radiation exposure.
Attendees packed the School’s Snyder auditorium to hear experts in the field discuss topics related to oxidative stress, which is caused by high levels of chemically reactive molecules containing oxygen (called reactive oxygen species, or ROS). Oxidative stress can cause damage to DNA, protein, and lipids, leading to myriad pathologies such as type 2 diabetes, Alzheimer’s disease, atherosclerosis, and cancer. Some speakers focused on mitochondria, the cell components that convert food and oxygen into energy and power metabolic activities. Mitochondria also generate ROS, and may overproduce it if their function is deregulated.
Work in this area provides important evidence toward advancing the JBL Center’s research mission in radiation sciences, said Director Zhi-Min Yuan, professor of radiobiology. One of the ways that oxidative stress is induced is through ionizing radiation from environmental sources or medical procedures such as CT scans. Elucidating this process will help researchers understand mechanisms underlying the cellular response to ionizing radiation and how the biological system adapts, he said.
In his opening remarks, Acting Dean David Hunter observed that some attendees may be wondering why this event was being held at a school of public health. A quarter of the School’s faculty identifies as laboratory scientists, Hunter said, and the School has “a deep commitment to analyzing problems from the cell level to the community level.”
Hunter and other speakers acknowledged the support that the Morningside Foundation, established by the family of the late T. H. Chan, has provided to the JBL Center and the symposium. The foundation also supported the establishment in 2012 of the Morningside Professorship in Radiobiology, in honor of Little. Gerald Chan, SM ’75, SD ’79, director of the foundation, was a student of Little’s.
Presenting during the symposium’s opening session, Tobias Walther, professor of genetics and complex diseases, discussed new advances in understanding the complex biology of lipid droplets—organelles that store energy for cells and interact with mitochondria. Walther’s research partner Robert Farese, professor of genetics and complex diseases, moderated the session, which also included Amy Wagers of Harvard Medical School. She described her lab’s work identifying a protein that seems to reverse age-related muscle mass decline in mice. Read more about Walther and Farese’s work.
— Amy Roeder
Photos: Emily Cuccarese
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Last month, the public health community marked one of the most significant biomedical milestones in the fight against malaria in nearly half a century: European regulators authorized the world’s most advanced malaria vaccine candidate — more than three decades in the making — and paved the way for subsequent review by the World Health Organization. Now, as this historic vaccine, known as RTS,S/AS01 (RTS,S), prepares for its next major step, critical new insights into how it fends off malaria are coming to light.
In a technological tour de force, an international research team has harnessed sophisticated molecular tools and analysis methods to probe the underlying biology of RTS,S, helping to explain how it protects against a disease that kills roughly half a million people each year, mostly infants and young children in Africa. The work, led by the Harvard T. H. Chan School of Public Health, the Broad Institute, the Fred Hutchinson Cancer Research Center, the University of Washington, and other leading institutions, was published online October 21, 2015 in the The New England Journal of Medicine. Read the article.
“Through this broad, multinational collaboration, we have brought the power of genomic tools to bear on a disease that poses one of the most significant threats to global public health,” said senior author Dyann Wirth, the Richard Pearson Strong Professor of Infectious Diseases and chair of the Department of Immunology and Infectious Diseases at the Harvard T. H. Chan School of Public Health. Wirth led the NEJM study together with Peter Gilbert of the Fred Hutchinson Cancer Research Center.
Malaria is caused by the Plasmodium parasite, a single-celled organism that is transmitted to humans by mosquitoes. The disease is prevalent in tropical and sub-tropical areas, especially countries in sub-Saharan Africa, and jeopardizes the health of more than half of the world’s population. Efforts to control and hopefully eradicate this global health threat require multiple defensive measures, including effective anti-malaria drugs, insecticide-treated bed nets and other efforts aimed at insect vector control. Another key component is a robust vaccine, which can provide long-term protection against the disease.
Recognizing this need, scientists at GlaxoSmithKline (GSK) embarked on the design of RTS,S in the late 1980’s. Following its early development, GSK and PATH, an international non-profit focused on global health innovation, launched a public-private partnership to further develop the vaccine. Roughly four years ago, as RTS,S progressed through clinical testing, the data revealed a sobering reality: The vaccine was effective in young children, but its protection was not absolute — it offered only partial protection against malaria, and that protection waned over time.
Wirth and her colleagues set out to understand the basis of this partial efficacy. They knew the vaccine was engineered to target a specific protein that sits on the surface of the parasite, called CS (short for circumsporozoite), and that CS was highly variable among parasites. They wondered if the effectiveness of RTS,S might vary according to the genetic makeup of CS, similar to the way the seasonal flu vaccine works. For example, some flu vaccines are better at fighting disease because they are more closely matched to the genes of the influenza viruses that predominate in a given year. (Unlike the flu vaccine, however, the composition of RTS,S is stable, and does not shift from year to year.)
To explore this question, the team harnessed advanced genomic technologies and statistical methods to understand how genetic variation in CS influences the vaccine’s ability to ward off malaria in young children. The work, made possible by a scientific collaboration spanning more than 15 countries and over 25 institutions, was conducted as part of a phase 3 trial of RTS,S/AS01 that ran from 2009 to 2013. The trial included 11 study sites in Africa and involved over 15,000 children.
The research team was given special access, through a collaboration with the vaccine division of the healthcare company GlaxoSmithKline, to blood samples from over 5,000 trial participants. By isolating and sequencing parasite DNA from these samples (which include samples from both vaccinated and unvaccinated children), the team was able to determine whether certain versions (or “alleles”) of CS are linked with better vaccine protection. Earlier efforts, which involved fewer patient samples and cruder methods, failed to detect such an association.
“This uniquely valuable data set posed some challenges to data analysis. The statistical team extended methods previously developed for HIV to provide interpretable answers about differential vaccine efficacy by malaria genetics,” said Peter Gilbert, director of the statistical center for the HIV Vaccine Trials Network at the Fred Hutchinson Cancer Research Center.
Through their deep survey of genetic variability in CS, the researchers made a crucial discovery: The vaccine is significantly more effective at preventing malaria in children infected with parasites that match the vaccine’s version of CS (so-called “matched” alleles) than in those who harbor mismatched parasite alleles. In the case of matched alleles, vaccine efficacy is 50% (measured over one year); with mismatched alleles, it is 33%. (The same effect was not noted in infants.) Moreover, Wirth and her colleagues found that the vaccine was most effective shortly after the final dose.
“This is the first study that was big enough and used a methodology that was sufficiently sensitive to detect this phenomenon. Now that we know that it exists, it contributes to our understanding of how RTS,S confers protection and informs future vaccine development efforts,” said Dan Neafsey, associate director of the Genomic Center for Infectious Diseases at the Broad Institute and co-first author of the NEJM paper.
The researchers’ findings also uncover fundamental aspects of the anti-malaria immunity conferred by RTS,S. These include a non-specific component that offers protection regardless of the parasite strain and a second, strain-specific component that provides additional protection if there is an identical match between the parasite’s CS and the one used in the vaccine.
“Expanding scientific knowledge and innovation is of paramount importance in global efforts to control malaria,” said Pedro Alonso, Director of the WHO Global Malaria Program. “The results of this new genomic study will give us a better understanding of how the RTS,S malaria vaccine works and how it might be improved. This, in turn, could have long-term implications for future vaccine development.”
While the NEJM study offers important insights into the RTS,S vaccine and suggests a path forward for its deployment, it also offers a model for tackling other major infectious diseases that involve highly variable vaccine targets. The approach is already being applied in HIV vaccine trials, and Wirth and her colleagues plan to apply it to future malaria vaccine trials.
Moreover, the work underscores how a full and comprehensive catalogue of the genetic diversity of key pathogens could inform the design of robust, effective vaccines. Indeed, the development of RTS,S began more than thirty years ago — when the scientific tools for probing microbial genomes where just in their infancy. Now the biomedical arsenal has advanced considerably, transformed by the growth of modern, genome-scale tools.
“The tools and methods needed to fully characterize the genomes of major pathogens are now well within our grasp,” said Wirth. “We have an unprecedented opportunity — and an obligation — to apply them in novel ways that will benefit public health across the globe.”
— Nicole Davis
To see the original article, please click here.
Two faculty members from Harvard T.H. Chan School of Public Health—Xihong Lin and Brendan Manning—will receive prestigious National Cancer Institute Outstanding Investigator Awards (OIA). These multimillion-dollar seven-year awards, providing extended funding stability, are aimed at giving promising and productive investigators enough time and money to continue or embark on projects of unusual potential in cancer research—and to take greater risks in their work.
Lin, Henry Pickering Walcott Professor of Biostatistics and chair of the Department of Biostatistics, is globally recognized for her leadership and expertise in statistical genetics and genomics. She will receive $6.6 million to develop and apply innovative statistical and computational methods for analyzing massive genetic and genomic data in cancer epidemiology and clinical science. This work will aid in the development of cutting-edge methods for discovering genetic and environmental factors of cancer; provide a better understanding of cancer progression; and inform new approaches to studying cancer progression and new treatment strategies.
“I am very much flattered by this enabling award,” said Lin. “The award gives me plenty of flexibility and freedom to explore cutting-edge data science research in cancer.”
Manning, professor of genetics and complex diseases, has led seminal research over the past decade that has shaped understanding of the mechanisms and potential therapeutic targets for the treatment of human diseases, with a core focus on genetic tumor syndromes and sporadic cancers. His highly innovative approach integrates biochemistry, cell biology, genetics, genomics, proteomics, metabolomics, bioinformatics, and animal models. He will receive $5.3 million for efforts to define the wiring and functions of a signaling network—the PI3K-mTOR network—that is aberrantly regulated at a high frequency across a wide spectrum of human cancers. Manning will examine the critical role of this network in influencing the sensitivity and resistance of tumors to targeted cancer therapies and in tumor cell metabolism.
“I am honored to receive this award on behalf of the members of my laboratory, both past and present, who made the foundational discoveries on which our future research is grounded,” said Manning. “This seven-year grant, its substantial resources and the freedom of its structure will allow us to explore some of the most difficult, but critically important, aspects of tumor biology.”
— Karen Feldscher
photo: Emily Cuccarese
To see the original article, please click here.
A Special Report by Amy Gutman, Boston-based writer,
and Madeline Drexler, editor, Harvard Public Health
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The Gray Wave. The Silver Tsunami. The Agequake.
Aging societies have been on the horizon for decades, not just in the United States but also around the world. The driving forces are well-established: falling fertility rates (by far, the most important factor), longer life expectancy, and the maturing of large cohorts such as the baby boomers in the U.S.
But what demographers once thought would be the passage of a single large generation—like the postwar boomers—through the age brackets is now predicted to be a permanent fixture of many developed societies. Age distributions in many countries once formed a pyramid—with billions of young people filling out the bottom and dwindling numbers of older survivors at the apex. Soon, however, this distribution may more nearly resemble a square, with roughly equal numbers of people in each age group.
Imagining what this “new normal” will mean for developed and developing societies alike raises profound questions. How will societies age successfully? Will most people live longer lives but be sicker for more years than in prior generations?
How should work be organized when a society has more people over 65 than under 5? As people live longer, when will they want or need to retire because of cognitive or physical aging? Will growing economies slow or even reverse their trajectories as older cohorts leave the workforce?
What can people do to increase the number of years of healthy, joyful senior living? Will people in their 80s, 90s, or older need as much help with aspects of daily living in the future as they did 20 years ago, or will they be more self-sufficient longer? Will “dying with dignity” be possible in a culture driven by technologically advanced health systems and nursing homes focused more on protecting the frail elderly than on empowering them?
This issue of Harvard Public Health examines how individuals and societies will navigate the previously uncharted waters of rapidly aging societies. Among the experts interviewed are faculty from the Harvard T. H. Chan School of Public Health, in fields ranging from social epidemiology to health policy to biochemistry. Here are their thoughts on what lies ahead.
1. What Is “Successful Aging”?
The MacArthur Foundation Research Network on an Aging Society has defined successful aging by three criteria: avoidance of disease and disability; maintenance of high cognitive and physical function; and engagement with life.
By these standards, the U.S. has generally done well. As life expectancy has improved overall (though some sections of the country have seen declines), more older people have managed to stay healthy or disability-free. This scenario—higher life expectancy and lower incidence of disease and disability—has led to what public health researchers call a “compression of morbidity”: more years spent in good health and fewer lived in poor health.
In the future, will people enjoy a “compression of morbidity”—living both longer lives and fewer years in poor health? Or will those extra years be spent paying the price of unhealthy lifestyles—in poor health due to heart disease, diabetes, and other chronic conditions?
But according to Lisa Berkman, Thomas D. Cabot Professor of Public Policy and of Epidemiology at the Harvard T.H. Chan School of Public Health and director of the Harvard Center for Population and Development Studies, this promising trend may have stalled in recent years. “There is evidence from national studies that people who are now in their 30s and 40s may actually be in worse shape than people that age were a generation ago—an increase in diabetes, obesity, and other chronic conditions,” she says.
“This virtuous cycle, where people are living not only longer but healthier, may not continue.” Moreover, says Berkman, there are substantial social and economic gaps in healthy life expectancy, with those who are poorer or who have less education facing much worse outcomes. And racial and ethnic disparities in healthy aging reflect a historical legacy of disadvantage.
WILL AGING SLOW THE ECONOMY?
An older population with chronic diseases bodes ill not only for public health but also for the economy. “Nations with swiftly aging populations may find themselves with a growing disease burden on their hands: nearly one-quarter of the world’s burden of disease is attributable to illness in adults aged sixty and over,” notes an article in the Spring 2015 issue of Daedalus written by David Bloom, Clarence James Gamble Professor of Economics and Demography in the Harvard Chan Department of Global Health and Population; David Canning, Richard Saltonstall Professor of Population Sciences and professor of economics and international health; and research assistant Alyssa Lubet. “In turn, the majority (nearly 70 percent) of the older-adult disease burden is due to noncommunicable diseases (NCDs) such as heart disease, cancer, chronic respiratory disease, musculoskeletal conditions, and mental disorders such as Alzheimer’s and dementia.”
As a result, population aging may slow economic growth, strain existing pension and health care systems, and weigh down younger generations. “One dire prediction,” the authors warn, “is that population aging will slow or perhaps even reverse the engines of national economic growth.”
ORGANIZING WORK REQUIRES NEW ASSUMPTIONS
“Until now, everybody had been looking at what makes individuals age successfully. But nobody asked: How do societies age successfully?” observes Berkman. “What happens to a country when there are more people over 65 than there are under 5? The fundamental issues are not how are we going to pay for Social Security or Medicare, although those are not trivial issues. The deeper issues are how should work be organized? What will happen to people with disabilities? How do different life trajectories lead to different health outcomes? In dealing with these issues, you can’t reorganize a little bit—you have to reorganize dramatically. To do this well, you have to rethink a lot of assumptions as a society.”
DOES AGE NO LONGER MATTER?
One of the fundamental assumptions that may change is that all older people need help. In economics, the oft-cited Old Age Dependency Ratio—or ratio of individuals ages 65 and older (presumably “dependent”) to those ages 18–65 (in the labor force)—bears this out. But in 2014, Dana Goldman of the University of Southern California and colleagues published in the Journal of Gerontology a study of older Americans that contradicts this model. The researchers found that among individuals ages 85 and older, 28 percent had excellent or very good self-reported health and 56 percent reported no health-based limitations in work or housework. As the study’s authors ask, “When does age no longer matter?”
THIS IS NO DEMOGRAPHIC GLITCH
“Originally, we thought the aging society would look like the boa constrictor in The Little Prince,” says Harvard Chan’s Lisa Berkman. “The boa constrictor swallows an animal, and you see the animal move all the way through the snake. But that’s not how this demographic shift is going to happen. The structure will probably be with us forever.”
At the beginning of the 20th century, the distribution of the U.S. population looked like a pyramid. Only 4.1 percent of the population was age 65 and older; today, that figure is 14 percent, and the classic pyramid is morphing.
By 2050, the senior cohort will rise to more than 20 percent, and the age structure in the U.S. and all other developed nations will have at least as many people alive at older ages as at younger ages. The global number of people ages 100 and older will likely more than double by 2030, with projections of nearly 3.4 million by 2050. “Never before in history have countries had their population age to this extent and as rapidly,” adds David Bloom, Clarence James Gamble Professor of Economics and Demography in the Harvard Chan Department of Global Health and Population. “These are uncharted waters.”
2. Sowing Healthy Habits
Don’t smoke. Exercise regularly. Eat a healthy diet filled with plenty of fruits and vegetables, replace saturated fats with plant oils, and limit sugar-sweetened beverages. Drink moderate amounts of alcohol.
Those are the pillars of healthy aging, according to Walter Willett, Fredrick John Stare Professor of Epidemiology and Nutrition and chair of the Department of Nutrition at the Harvard Chan School. And a mountain of public health research backs up his advice—including the Nurses’ Health Study (NHS), established in 1976 by the Harvard Chan School’s Frank Speizer, now professor of environmental science, with funding from the National Institutes of Health.
This ongoing investigation, which began with some 121,000 middle-aged women, “shows the flip side of the coin,” explains Willett—revealing not only the conditions that elevate the risk for disease but also those that help prevent potentially fatal conditions, from breast cancer and atherosclerosis to diabetes and dementia.
The Nurses’ Health Study defines healthy aging as survival past age 70 without any major chronic diseases or major impairments in memory, mental health, or physical abilities. In 2011, all of the women in the original NHS were 65 or older. Here are the study’s key findings about their healthy aging:
BODY MASS INDEX (BMI)
Of the women who survived until at least age 70, those who had a higher BMI at midlife were less likely to survive to a healthy old age. Obese women (with BMI of 30 or greater) had an 80 percent lower chance of healthy survival compared with their leaner counterparts (with BMI between 18.5 and 22.9). And the more weight a woman gained from age 18 until midlife, the lower her chance for healthy survival after age 70.
Higher physical activity levels at midlife predicted healthier survival. Better yet, the chance of healthy aging markedly improved even at modest activity levels: Women who jogged or cycled about five hours per week almost doubled their chance of healthy aging. Two or more hours per week of brisk walking also upped the chances of a healthy old age. Perhaps most encouraging: Regardless of whether a woman was lean or over-weight, being physically active increased her odds of optimal health.
MEDITERRANEAN DIET AND TELOMERES
The Mediterranean diet appeared to increase telomere length, a key biomarker of aging. Likened to the plastic tips on the ends of shoelaces, telomeres are stretches of DNA at the ends of chromosomes that protect genetic data. Shorter telomeres are associated with decreased life expectancy and increased rates of age-related chronic diseases.
FLAVONOIDS AT MIDLIFE
A midlife diet rich in flavonoids improved the odds of healthy aging. Bioactive compounds in plant foods, flavonoids have been linked to lower risks of fatal or nonfatal cardiovascular disease, hypertension, stroke, cancer, diabetes, and neurodegenerative diseases. High-flavonoid foods include oranges, berries, onions, and apples.
VITAMIN D AND COGNITION
Among women ages 60 to 70, lower levels of vitamin D in the blood of were associated with significantly worse cognitive function—such as memorization of words and numbers. The finding bolsters the theory that vitamin D, which is critically important for bone and muscle health and the prevention of falls, may also play a role in brain function.
3. Rethinking Work
When Social Security was established in 1935, most other government benefits kicked in at age 65. To put that in context, life expectancy for American men at the time was only about 60 years. Today, however, according to the Social Security Administration, men who retire at age 65 can expect to live for an additional 19 years; women, an additional 21 years. Should retirement therefore be postponed?
In general, being employed is positively associated with health, says Lisa Berkman. Partly that’s because healthy people are more likely to be able to work. But employment itself also appears to bring both physical and mental health benefits. Having a job boosts social engagement, keeps up intellectual and interpersonal skills, and staves off the time when one must draw on savings and pensions. “One of the good parts of working longer is the maintenance of cognitive functioning,” says Berkman. “In societies where retirement age is early, such as France and Italy, cognition falls more as people age.”
That fact argues for delayed retirement. But not everyone is able or willing to stay in the workforce, in part because people hold onto their health or lose it at vastly different rates—and government policies must acknowledge this heterogeneity. According to Berkman, certain segments of the population—such as people whose health has been worn down by physically arduous jobs—need the option to take an early path to retirement. And as David Bloom notes, people who are more educated and who earn more tend to live longer—which raises questions of fairness in retirement policies. “If some people will have much longer lives and some people will have just modestly longer lives, but you raise the retirement age for everybody, there’s an ethical issue,” he said in a recent interview.
BENEFITS OF VOLUNTEERING
Perhaps the most convincing argument for encouraging people to keep busy and engaged after 65—whether or not in the formal workforce—is a raft of research showing that senior volunteering has been tied to reduced risk of hypertension, improved self-reported health and well-being, delayed physical disability, enhanced cognition, and lower risk of death. And research shows that while members of lower socioeconomic groups are less likely to volunteer, they will reap disproportionately greater benefits.
“One of the good things about eternally volunteering is that it embeds people in social networks,” explains Berkman. “They are engaged, they work with others, they collaborate with people of all ages. They’re not receiving support, they’re giving support—and giving support turns out to be really important. One of the best things we can do is to keep people naturally embedded in communities that are cohesive and enduring.”
Employment can yield both physical and mental health benefits as one ages – a potent argument for raising the retirement age. But for those whose jobs have worn them down physically or emotionally, the discussion about raising the retirement age raises important ethical and practical issues.
In the U.S., the most robustly studied volunteer program is Experience Corps, which invites volunteers ages 55 and older into public elementary schools several times a week (for at least 12 hours total) to tutor children at risk of reading failure. A 2010 study in Social Science & Medicine by S.I. Hong of the National University of Singapore and Nancy Morrow-Howell of Washington University compared changes in health outcomes over two years between Experience Corps volunteers and a matched sample of older adults who were not engaged in high-commitment volunteering. The study found that the Experience Corps group reported fewer depressive symptoms and fewer functional constraints in such activities as walking, running, or climbing stairs, while the comparison group showed an increase in these measures.
REMOVING THE COBWEBS
A 2009 study in the Journal of Gerontology by Michelle Carlson of the Mailman School of Public Health at Columbia University and colleagues explored in finer detail the cognitive gains among Experience Corps volunteers. This small study involved African-American women in Baltimore. All were all low-income and low-education and therefore faced a statistically greater risk for cognitive impairment. The researchers used fMRI scans, which measure blood flow, to trace the biological underpinnings of brain plasticity. After their stints as volunteers, the women demonstrated increases in activity in several key areas of the brain, compared with those in the control group. They also had better scores in standard tests of visual function and concentration. As one woman said of her time at Experience Corps, “It removed the cobwebs from my brain.”
“[T]hese activities are generative in giving meaning and purpose to one’s life … which may make them more rewarding and personally enriching than highly stimulating activities performed alone,” the researchers wrote. “As a result, individuals may place more value on these activities beyond their immediate personal benefit and may sustain interest longer.”
Just as compelling, the program’s dividends were truly multigenerational, reaching far beyond the volunteers themselves. Compared with students in the control schools, the kindergarten-to-third-grade students in the Experience Corps schools had improved standardized reading scores and markedly fewer referrals for behavioral problems.
THE “LUMP OF LABOR” FALLACY
Some say that older people who feel healthy and prefer to stay in the workforce should be encouraged to do so. Others argue that the senior cohort will steal jobs from younger people.
But according to Harvard Chan’s Lisa Berkman, the latter assumption is plain wrong. Indeed, its wrongness has a catchy name in the economics literature: the “lump-of-labor fallacy.” Writing in Daedalus in 2015, Berkman and her co- authors explain: “For many years, common sense suggested that the number of jobs in the economy is finite, and that a new population entering the labor force would therefore push other workers out. This so-called lump-of-labor fallacy has been invoked at moments in history when women’s labor-force participation increased, because it was thought that they would take ‘good jobs’ away from men. Immigrants to the United States continue to be accused of stealing jobs from other, native lower-wage workers. Likewise, many older people who wish to continue working today are accused of taking jobs from younger workers, creating intergenerational conflict.
“The lump-of-labor fallacy is one of the most dangerous myths in economics. … This is shown most clearly in the United States, where the sharp increase in female labor force participation not only did not cause mass unemployment for men, but actually correlated with a rise in male employment rates. More specifically, recent findings from cross-national comparisons show that higher employment of older individuals is actually positively correlated with higher employment of the young; that is, countries with a high prevalence of early retirement tend to have higher unemployment rates and lower employment of the young.”
As Berkman says, “If older people are working, they’re earning, they’re spending. They don’t draw on Social Security as much. They contribute productively. Overall, that’s good for growth.”
4. Breakthroughs in Biology
Imagine old age without heart disease, cancer, or dementia. Imagine a long life of physical and mental vigor, capped by a brief period of decline before death. Imagine being able to achieve this ideal through a pill or simple changes in diet.
That’s exactly what Harvard Chan School scientists in the Department of Genetics and Complex Diseases are imagining in their quest to understand the biology of senescence and the secrets of what has come to be known as “healthy aging.”
JUNKING THE “RUST” METAPHOR
Until recently, bodily decline was considered to be the inevitable outcome of tiny corrosive hits to the system: genetic, cellular, metabolic, environmental, stress-induced. The reigning metaphor was the body as rusting car, with each failing part the final stage of a distinct chain of biological events.
Today, however, researchers suspect there is a fundamental cause behind all these seemingly separate breakdowns. “As humans grow older, they don’t get just one aging-related disorder—they suffer a spectrum of disorders,” says associate professor James “Jay” Mitchell. “The new thinking is that these disorders are mechanistically linked to the aging process itself—whatever that process is.”
According to assistant professor William Mair, the key questions in this new paradigm are: “Why are we more likely to get diseases when we’re old than when we’re young? And how can we shift that risk of frailty?”
CLUES IN THE LAB
The idea that aging is driven by a biological mainspring is buttressed by epidemiological studies of centenarians. These resilient human survivors of 100-plus years tend to die
not from cardiovascular disease or malignancies or neurodegeneration, but rather from the complications of overall deterioration and the body’s inability to maintain homeostasis and rebound from injury or infection. Centenarians usually succumb swiftly at the end—to a broken hip, say, or a short bout of pneumonia. Put another way, they enjoy a longer “health span.”
Can centenarians’ hardy biology be replicated? Mitchell and Mair believe it can.
Animal research has proven that dietary restriction—whether cutting total calories, reducing specific dietary constituents such as proteins, or placing animals on various fasting regimens—extends life span and decreases age-related debility. So dramatic is this biological benefit, Mitchell describes its inverse—today’s human epidemic of obesity-related metabolic disorders—as a wave of “premature aging.”
Elaborating on these findings, Mitchell has shown that lowering quantities of certain amino acids in the diet causes mice to increase cellular production of the gas hydrogen sulfide, which in turn protects the animals against tissue damage after minor surgery. He has also found that increased production of the gas extends life span in worms, flies, and yeast—along the same biological pathways conserved in Homo sapiens.
Research in the lab suggests that dietary restriction— cutting calories or reducing certain items in the diet—extends lifespan and decreases age-related debility. In that context, today’s human epidemic of obesity-related diseases could be seen as a wave of “premature aging.”
Mair, meanwhile, has demonstrated that nematode worms that express an active form of a protein called AMPK—a kind of molecular fuel gauge—were likewise long-lived, despite eating normally. The implication is that tweaking cellular mechanisms in the nervous system that sense energy generated by nutrients could confer the same propensity for healthy aging as do low-calorie diets, without the need to alter food intake.
Both Mitchell and Mair foresee a day when their kind of basic research finds its way into human clinical medicine.
Mitchell predicts that doctors may someday prescribe certain kinds of fasts before surgery or chemotherapy to boost the body’s resilience and improve outcomes. Mair hopes to find molecular targets that could pave the way to therapeutic drugs; if taken in old age—when one was about to encounter risk factors for certain diseases or suffer early symptoms—the medications could prevent the afflictions or at least reduce their spread or severity.
The goal, the scientists agree, is not a fountain of youth but rather golden years that are relatively robust and independent. As Mitchell sees it, “Aging is a public health problem—and basic biology is the answer.”
INVESTMENT IN DELAYED-AGING RESEARCH COULD HAVE LARGE PAYOFF
Aging is a primary risk factor for numerous deadly and debilitating conditions, but research to date has largely focused on treating the conditions commonly linked to aging today—such as cancer and heart disease—rather than on addressing the biological processes at the root of aging.
Slowing the biological aging process—what scientists call “delayed aging”—may offer substantial health and economic returns. A 2013 study in Health Affairs estimated that delayed aging could increase healthy, nondisabled life expectancy in the U.S. by an additional 2.2 years. Researchers calculated the economic value of this gain to be $7.1 trillion over 50 years, using a standard formula in which a healthy year of life is valued at $100,000.
5. Connecting With Others
Good advice on lifestyle and successful aging is one thing— following it is another. “Many investments have to be made throughout the life course, in terms of health habits like exercise and diet,” says Ichiro Kawachi, John L. Loeb and Frances Lehman Loeb Professor of Social Epidemiology and chair of the Department of Social and Behavioral Sciences at the Harvard Chan School. “But I’m also interested in what you can do once you do reach old age and you haven’t made those investments. Can you still make a difference?”
Kawachi’s answer: a resounding “yes.”
“One of the most important things that you can do individually, if you retire, is to maintain social connections,” he says. “Connecting with other people is as important as diet and exercise. It’s not too late, even at age 60, to overcome some of the health problems you may have encountered earlier in life.
“When you socialize and converse with friends, you’re exercising all your facilities and improving blood flow to the brain, which helps maintain cognitive function,” says Kawachi. “There’s exchange of information of different kinds, such as learning about the latest health tips or getting advice. And you receive affirmative messages and emotional support.”
Socializing with friends after retirement is as important as diet and exercise. It improves blood flow to the brain, maintains cognitive function, promotes the exchange of useful information, and elicits emotional support.
SURPRISES FROM JAPAN’S “SPORTS CLUBS”
Japan’s population is aging at the fastest pace of anywhere in the world. The proportion of its population over the age of 60 is projected to rise to an astounding 42 percent by 2050. To minimize the impact of this trend on health care costs, Japan’s government has focused on preventing long-term care as much as possible—using social participation approaches.
One of Kawachi’s intriguing studies, published in PLOS One in 2012, looked at the effect of membership in Japan’s “sports clubs”— organizations that offer mini-golf, walking clubs, lawn tennis, croquet, and other activities shared with friends. He divided his subjects, who were 65 and older, into four groups: those who were physically active and belonged to a sports club; those who were physically active but exercised alone; those who were not physically active but still belonged to a sports club (doing administrative or other work); and those who were not physically active and did not belong to a sports club.
As predicted, people who actively exercised and belonged to sports clubs enjoyed the best health. But those who belonged to sports clubs and didn’t exercise came in a very close second—their functional disability rate was virtually the same as the avid sports club exercisers. Those who exercised alone actually fared worse than the sports club sedentarians. And the stay-at-home couch potatoes, not surprisingly, came in last.
“In other words, the exercise didn’t add to the benefits of participating,” says Kawachi. “It was the belonging that prevented disability.”
IKIGAI: A LIFE WORTH LIVING
In a 12-year study of more than 30,000 men and women published in 2009 in the Journal of Psychosomatic Research, a Japanese team of researchers explored the effect of Japan’s powerful—but, to Westerners, perhaps ineffable—concept of ikigai, which the Japanese believe to be an important factor for achieving health and a fulfilling life. Ikigai is variously defined as something to live for, the joy and goal of living, a life worth living, or “the reason to get out of bed.” It includes not only pleasure and happiness but also meaning and self-realization. As a baseline measure at the beginning of the study, the researchers simply asked participants: “Do you have ikigai in your life?”
In Japan, people who said they had ikigai—pleasure and happiness, a life of meaning—12 years later had lower risk of death from all causes.
A dozen years later, the middle- aged and elderly men and women who answered “yes” had less risk of death from all causes, including external causes such as injury. Death from stroke and coronary heart disease was also lower among men and women with ikigai than among those without it.
6. Preserving Purpose
In 1991, a family practice physician named Bill Thomas conducted a radical experiment: He brought life to a place where death had prevailed.
A PARAKEET OR A PLANT
The medical director of Chase Memorial Nursing Home in the upstate New York town of New Berlin, Thomas was struck by the sterility and despair that pervaded every room. So he issued an almost unfathomable order: to move 106 additional residents into the facility, pretty much all in one day. The newcomers included two dogs, four cats, and 100 parakeets. They were soon followed by a colony of rabbits, a flock of laying hens, and hundreds of indoor plants. Each of the nursing home’s human residents was soon taking care of his or her own parakeet or plant.
ABOLISHING NURSING HOME PLAGUES
Thomas calls himself a “nursing home abolitionist.” He sees his mission as eradicating what he calls the three plagues in modern nursing homes: boredom, loneliness, and helplessness. And he is one of Atul Gawande’s heroes. In his new book Being Mortal: Medicine and What Matters in the End, Gawande, a surgeon, professor in the Department of Health Policy and Management at the Harvard Chan School, and director of Ariadne Labs, explores the “medicalization of mortality”: the myopic focus on disease instead of goals when caring for patients at the end of life.
“When we don’t know what people’s priorities are, their care is often out of alignment with some of their most important goals,” Gawande said in a recent interview. “You really see it when you visit people who end up requiring residential care—assisted living or full-scale nursing homes. The facilities look more and more like hospitals. They’re built around nursing stations. The rules are focused on safety.”
On the one hand, it seems prudent to put safety first in nursing homes. But the upshot is that other goals of life may matter more to people, Gawande says. “People are forbidden from having a drink if they want to. Alzheimer’s patients on medically ordered puréed diets get caught sneaking cookies. You could have a roommate imposed upon you with no choice whatsoever. No regard for privacy. These are incredibly important concerns.”
Gawande’s prescription for this devastating mismatch of intent and results includes a list of clarifying questions that should be asked when a person has a serious or life-threatening illness, such as cancer, congestive heart failure, chronic obstructive pulmonary disease, or end-stage renal disease.
CONVERSATIONS IMPROVE OUTCOMES
“We measure the wrong things,” he says. “Less than a third of the time do people who arrive at the end of life have any conversation about what their goals and priorities are for the time they have left. When they have those conversations, they have markedly better outcomes, including reduced suffering, spending more time at home, and also living at least as long as they otherwise would—in many cases, longer. And better outcomes means that they’re less likely to get unwanted care. They have more peacefulness at the end of their lives.”
Serious Illness Conversation Guide for Doctors and Patients
1. How much information about what is likely to be ahead with your illness would you like from me?
2. What is your understanding now of where you are with your illness?
3. If your health situation worsens, what are your most important goals?
4. What are your biggest fears and worries about the future with your health?
5. What abilities are so critical to your life that you can’t imagine living without them?
6. If you become sicker, how much are you willing to go through for the possibility of gaining more time?
7. How much does your family know about your priorities and wishes?
AUTONOMY, NOT JUST SAFETY
Gawande adds that Bill Thomas’ innovative experiment and similar interventions have demonstrated that people with the opportunity for purpose—even caring for a bird—at the end of life can bring meaning and joy to one’s final days, even for people with severe disabilities.
But to get there, society must overturn its conventional thinking about old age. “There are sometimes regulations that stand in the way, but most of the obstacles are cultural,” Gawande says. Medical care professionals frequently focus on giving patients the longest possible life, regardless of the quality. What a patient with a terminal disease may actually be looking for is “a few good days,” Gawande notes. As one nursing home administrator told him, “Safety is what we want for those we love; autonomy is what we want for ourselves.”
The roots of the current Syrian crisis may be found in the massive drought that afflicted the country between 2006 and 2009 and precipitated a migration of more than 1 million people from rural to urban areas. According to Harvard T.H. Chan School of Public Health researchers speaking at an event during the inaugural HUBweek, the drought was likely caused by climate change — and the world should have predicted the conflict that followed.
HUBweek, a series of events celebrating “big ideas and bold solutions,” was held throughout Boston and Cambridge October 3–10, 2015. It is a first of its kind civic collaboration between The Boston Globe, MIT, Massachusetts General Hospital and Harvard University. Harvard Chan School hosted a series of panels on October 5 at the Joseph B. Martin Conference Center highlighting four major global health threats: infectious diseases, harmful environments, humanitarian crises, and failing health systems.
Acting Dean David Hunter set the stage for the day’s panels by inviting the audience to imagine a world where AIDS is prevented by a vaccine, air pollution is less prevalent, humanitarian responders can do their jobs more safely, and disparities in health care based on income and race are eliminated. These are not dreams, he said, but rather are among the many efforts underway at the School to make the world a healthier place.
Flaminia Catteruccia, associate professor of immunology and infectious diseases, opened the first panel by highlighting the threat posed by a pest often underestimated in the Western world: the mosquito. While mosquito-borne diseases such as malaria don’t tend to grab international headlines, they have killed 12 million people since 2000, she said, and simply relying on bed nets and other methods to prevent stings is not enough. Catteruccia’s lab is studying mosquitoes’ biology, working toward the day when the insects can be genetically engineered to not pass on diseases to humans.
Success in the field of infectious diseases has the potential to save millions of lives, observed moderator Dyann Wirth, Richard Pearson Strong Professor of Infectious Diseases and chair of the Department of Immunology and Infectious Diseases. Ric Marlink, Bruce A. Beal, Robert L. Beal, and Alexander S. Beal Professor of the Practice of Public Health, said that success requires the ability to move beyond assumptions of what is possible —from “We can’t do that” to “What will it take?” Marlink recalled sceptics who believed that efforts to scale up AIDS treatment in Africa would be futile.
The day’s second panel, which focused on harmful environments, presented the environment as a complex web of influences that act on people’s biological processes and personal choices, from poor air quality to cigarettes sold at the corner store. Panelist Aaron Bernstein, associate director of the Center for Health and the Global Environment, said that climate change has the potential to affect all aspects of health, citing examples including the drought in Syria and Boston’s precarious position if sea levels rise. Actions taken to combat climate change, such as reducing carbon emissions and red meat consumption, will also make us healthier, he said.
Jennifer Leaning, François-Xavier Bagnoud Professor of the Practice of Health and Human Rights, spoke on the third panel about the need for the humanitarian community to get out in front of crises before they blow up. Panelist Jacqueline Bhabha, a professor at the FXB Center for Health and Human Rights, discussed the current Syrian migration to Europe and some of the challenges, including political opposition in some Western countries to accepting the refugees.
Researchers on the final panel stressed that health systems around the world are doing better than ever, although there remain significant failures. While Obamacare has improved access to care in the U.S., success can’t be sustained without improving quality, panelists said.
— Amy Roeder
Photos: Emily Cuccarese
To see the original article please click here.
Public health practitioners, policy makers, and industry representatives from China and the U.S. gathered September 28–29, 2015, to share experiences and ideas around health system reform. The 5th U.S.–China Summit, hosted by Harvard T.H. Chan School of Public Health at the Joseph B. Martin Conference Center, included for the first time a forum and innovation competition for young public health leaders. This year’s Summit speakers touched on topics such as linking health information systems across institutions and increasing the number of primary care doctors in both countries.
The Summit grew out of the School’s China Initiative, and has been held alternately at Harvard Chan School and in China since 2011.
The year’s event highlighted China as one of the success stories of the United Nations’ Millennium Development Goals, which expire this year. The country reached 95% health insurance coverage, and has reduced under-five mortality by at least two-thirds and maternal mortality by three-quarters.
Acting Dean David Hunter and other speakers observed that attendees from China and the U.S. were coming together just days after the U.N. adopted the Sustainable Development Goals, which aim to foster international cooperation and knowledge sharing to address pressing challenges including achieving universal coverage and improving health.
Sun Zhigang, vice minister of China’s National Health and Family Planning Commission, and director of the State Council Office of Health Reform, highlighted the need to improve access to safe and affordable drugs. He also pledged that by 2020 every Chinese family would be registered with a general practitioner — and that efforts would be stepped up to ensure that there are enough primary care physicians to make this goal possible.
Kelly Cronin, director of the U.S. Office of Care Transformation in the Office of the National Coordinator for Health Information Technology, described efforts to move the health care system toward paying providers based on the quality, rather than the quantity, of care they give patients. The Department of Health and Human Services has set a series of goals and a timeline, which includes moving 50% of Medicare payments to these models by the end of 2018.
In remarks on U.S. health care reform under the Affordable Care Act (ACA), John McDonough, professor of the practice of public health said, “Debates about health care reform in all countries are not about data; they are about core values in societies.” He and other speakers said that although the U.S. and China are very different societies, they share the same challenge in bringing good and affordable health care to all of their citizens.
William Hsiao, K.T. Li Research Professor of Economics, observed that health care in China remains in conflict between economic interests and the public good, and called on its government to do more to improve quality and reduce corruption in its public hospitals. Hsiao has played a role in health care reform in China. He piloted a subsidized, community-governed basic health care system in two provinces that has helped shape the national plan.
Ashish Jha, K.T. Li Professor of International Health, said that whether or not the ACA is seen as a success remains a deeply partisan issue. For his own report card, Jha gave it an A on improving access to care, a C on controlling costs, and an incomplete on improving health care quality.
Other Harvard Chan speakers at the Summit included Katherine Baicker, C. Boyden Gray Professor of Health Economics; Barry Bloom, Harvard University Distinguished Service Professor and Joan L. and Julius H. Jacobson Professor of Public Health; David Christiani, Elkan Blout Professor of Environmental Genetics; China Initiative Founding Director Yuanli Liu, dean of the Peking Union School of Public Health and senior lecturer on global health at Harvard Chan; and John Quelch, professor in the Department of Health Policy and Management.
First prize in the inaugural innovation competition was awarded to the team Cocoon Biotech, which has developed a drug delivery platform using biocompatible silk protein to treat osteoarthritis. The competition encourages students, researchers, physicians, and entrepreneurs ages 45 and under to develop innovative healthcare solutions. Out of 81 proposals, 27 teams were invited to present at earlier events held in Boston and Beijing. Seven finalists were chosen to pitch their ideas to a panel of judges at the Summit.
— Amy Roeder
Photos: Emily Cuccarese
To see the original article, please click here.
If you’re looking for a miracle drug that cuts heart attack and diabetes risk by 80 and 90 percent, respectively, and also reduces the danger of cancer, stroke, and late-life cognitive decline, just close the medicine cabinet door.
Look in the mirror instead.
Despite recent headlines on potentially revolutionary cholesterol-lowering drugs, panelists in a recent forum at the Harvard T.H. Chan School of Public Health said that the most dramatic health effects will continue to come from the lifestyle choices we make every day.
Eat a healthy diet, don’t pack on the pounds, get regular exercise, and don’t smoke. That recipe for the medical miracle is reliable enough that the panelists said it should be taught in grade school and through health-education campaigns. And research, they suggested, should be directed toward figuring out how to deliver that message in ways that get more people to pay attention.
“The evidence is quite strong that lifestyle factors will go a long way, but we don’t know how to promote a healthy lifestyle, how to get people to do it,” said JoAnn Manson, the Michael and Lee Bell Professor of Women’s Health at Harvard Medical School (HMS). “We need some creative solutions, we need more research to understand how to engage healthy lifestyles in the population.”
Frank Sacks, a professor of cardiovascular disease prevention at the Harvard Chan School and Harvard-affiliated Brigham and Women’s Hospital, agreed with Manson, saying that a 75-year-old who adheres to recommended lifestyle measures — getting enough exercise, eating a healthy diet, and maintaining a normal body weight — will likely experience no cognitive decline for at least the next 10 years.
“We have a very optimistic message,” Sacks said, “we just have to deliver it.”
Panelists also included Patrick O’Gara, a professor of medicine at HMS and the Brigham and past president of the American College of Cardiology, and Paul Ridker, a professor of medicine and director of the Brigham’s Center for Cardiovascular Disease Prevention. The event, “Rethinking Cholesterol: Drug Developments and Lifestyle Choices,” was co-sponsored by Reuters and Harvard Health Publications and moderated by Reuters correspondent Bill Berkrot.
While lifestyle choices remain paramount as a foundation for good health, the panelists agreed that statins have been beneficial in lowering cholesterol for millions of patients. The Food and Drug Administration last summer approved the new drugs — called PCSK9 inhibitors — for those with ultra-high cholesterol because of genetic reasons, for those who have already had a heart attack or stroke, and for those for whom statins are ineffective or cause intolerable side effects.
The jury is still out, however, on whether those lower levels might help the millions of people in the broader population who routinely take statins. The new drugs reduce LDL, or “bad cholesterol,” beyond what is possible with statins. Their potential health effects — in reduced heart attacks and strokes — are being examined in an ongoing study of 60,000 people.
Even if the study does find salutary effects, questions about cost and benefit will remain, panelists said. The new drugs are expensive — $14,000 per year for a normal regimen — and, in an era of steadily rising medical costs, will likely come under scrutiny if they are recommended for a large number of people currently on statins.
Manson worried that relying on drugs to treat the nation’s health problems could encourage a scenario in which children too regularly use statins, blood pressure medicine, and diabetes drugs. Aside from the unknown effects of taking such drugs for a lifetime, the illness and cognitive decline linked to unhealthy living would continue.
“The medicines are terrific for high-risk, targeted population groups, but not the ultimate solution to the [problem of] chronic disease throughout the world,” Manson said.
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When Robert Farese and Tobias Walther were negotiating to join Harvard T.H. Chan School of Public Health last year as professors of genetics and complex diseases, they proposed a twist to their appointments—a joint laboratory run as an equal partnership. Although they were working in different institutions and came from different disciplines—Farese from physiology and biomedicine, Walther from cell biology and biochemistry —they had been collaborating remotely for a decade, finding fertile ground in their shared research interests, scientific values, and wide-ranging curiosity.
With research largely focused on how cells store and synthesize fat—a principle applicable to understanding obesity and its related diseases—they were keen to join a department well-known for its metabolism research. But their unusual lab arrangement might have been a hard sell in some quarters. Fortunately, Genetics and Complex Diseases Chair Gökhan Hotamisligil got it, Farese said. “He was very enthusiastic.”
At the School, the two scientists have combined their areas of expertise to give the lab the capability to “bridge anything from physics to human genetics and everything in between,” Walther said. Both contribute ideas and act as each other’s sounding board. “If I can’t convince my best science friend that something is important and should be done, then there is a serious problem with it,” said Walther. “If we’re both excited about an idea, and we’re still excited a month later, it’s probably a better idea.”
Working together, they have identified more than 200 genes that regulate storage of lipids (fatty acids and oils that store energy and provide materials needed to build and maintain cell membranes). Lipids are stored in organelles known as droplets that play an important role in metabolic function. Walther and Farese have published a growing body of work unravelling the complex biology of lipid droplets, including a paper published August 10, 2015 in Developmental Cell, which explains a principle behind the composition of proteins on the surface of the organelles.
Their efforts received a significant endorsement in May when Walther was named a Howard Hughes Medical Institute Investigator. The prestigious five-year appointment provides each investigator with his or her full salary, benefits, and a research budget. Although the award is in his name, Walther is quick to include Farese in the honor.
A fruitful meeting
Their collaboration goes back to 2005 when Farese, then a professor of medicine, and biochemistry and biophysics at the Gladstone Institutes at the University of California, San Francisco (UCSF), decided to take a sabbatical year in his colleague Peter Walter’s lab to learn about cell biology. “I wanted to learn about how to think about problems differently,” Farese said. “I got really lucky because I sat down next to Tobi.”
Walther, then a postdoctoral researcher, was equally inspired by Farese. “I was on the trajectory of being a biochemist and cell biologist,” he said. “Then this sabbatical professor showed up who came from a different discipline and started talking about all these problems that had a strong overlap with my interests.”
Ten years later, they both agree that the collaboration has likely changed how they approach their research and what they produce. “It would be like if he wrote a song and I wrote a song and then we wrote one together,” said Farese. “All three would be completely different.”
Among the shared scientific values that bring them together is an emphasis on working towards a legacy focused on training the next generation of researchers and translating scientific contributions into clinical practice and public health.
Walther said, “We want to explain fundamental mechanisms and how they impact human health and disease. We’re not satisfied with scratching on the surface, and we will challenge each other and our lab members on clarity. I think we both have a pretty high allergy against intellectual mud.”
In addition to their work on metabolism research, Walther and Farese are working on understanding the mechanisms underlying neurological and neurodegenerative diseases. When asked where they hope to be in five years, Walther leaves the door open for the serendipity of discovery.
“The world is full of wonders,” Walther said, quoting Walter. “Every time you turn over a stone, there is something amazing lurking under it.”
— Amy Roeder
Photo: Kent Dayton
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The Harvard Integrated Life Sciences (HILS) Program warmly invites you to attend the HILS 10th Anniversary Gathering: “Celebrating a Decade of Creativity, Collaboration, and Connection” on Thursday, October 8, 2015 from 1:00 p.m. – 5:00 p.m.
Featuring a keynote address by David Altshuler MD/PhD ’90 (Executive Vice-President, Global Research and Chief Scientific Officer, Vertex Pharmaceuticals), an alumni career panel, reception, and poster presentations will also be featured.
Find the full schedule and register for the event here
Don’t miss this opportunity to connect with HILS students, faculty, and alumni to celebrate Harvard’s life sciences achievements!