Chicago’s public school system closed this week when the teachers’ union and the city clashed over in-person learning amid a spike in Omicron cases. The Gazette sought reaction from public health expert Joe Allen, an associate professor at the Harvard Chan School and director of the Healthy Buildings program, who believes the downsides of keeping children out of schools far outweigh the risks posed by COVID-19. The interview has been edited for clarity and length.

Q&A

Joe Allen

GAZETTE: Is it safe to sends kids back to school?

ALLEN: The argument for in-person schooling rests on to two pieces of evidence that we’ve had for a long time now: the risk to kids from this virus is low, and the costs of them being out of school is extraordinarily high. I want to be clear that by starting with kids, I’m not minimizing the adults in the school, teachers and staff. But this is not March 2020. We know a lot more; we have new tools at our disposal. The evidence on the low risk to kids has been consistent through each variant and each wave. The hospitalization rate has hovered at less than one per 100,000 through the Alpha wave, the Delta wave, and even the Omicron wave, and that’s important context because that level of risk is something we accept all the time.

The two most salient risk factors for this virus are age and vaccination status. And fortunately, kids have been low risk. If that doesn’t feel low risk enough, a safe and effective vaccine is available for all school-aged kids. It’s the same for adults ­— this vaccine is safe and effective. And even with Omicron and the higher risk of breakthrough infection, the protection against severe disease and death has stayed strong.

GAZETTE: What are the negative effects of not having kids in school?

ALLEN: The effects we’re seeing right now were predicted two years ago. We could start with learning loss. We see that students are four or five months behind in reading and math. We see even greater loss for Black or Hispanic students. And that’s the kids who were in school. Millions of kids are not — are missing from the system. Schools are the first place where we detect issues at home such as abuse, neglect, and maltreatment. And the idea that these short-term closures don’t have an impact is nonsense. In New York City, in just a few months there were thousands of cases of expected reports of child maltreatment that did not come in. I’ve written about the impacts on nutrition and kids, and food security, with Sara Bleich from the School of Public Health. We see the impact extend to women, working women in particular, who proportionately have the burden of childcare and homeschooling. So when we think about schools and risk, we can’t just think about the risk in the classroom, we have to think about what happens when you send these kids home. And I think there’s been a faulty assumption that if you close schools, that that protects everyone who would be at school. But that ignores the fact that social networks exist outside of school for kids and for adults, too. And we saw this when the winter break happened. Kids were not in school, teachers were not in school, and when they came back, even before they even entered school, some of the surveillance testing we’ve seen showed one-third of people were positive.

GAZETTE: Are teachers right to fear in-class teaching?

ALLEN: We need to reassure people that if you are vaccinated and boosted, you’re well protected. In addition, we’ve had the know-how, the guidance, and the money to put in effective controls in our schools for 18 months. From my understanding, they’ve done ventilation filtration upgrades in Chicago, they’re monitoring air quality in real time, they have vaccine clinics.

There has been this casualness about closing schools that I just don’t understand. When you match up the long list of harms when kids are out of schools against this idea that we’re just going to close for two days or a week or two weeks, which might turn into three weeks, who knows? I think that’s a mistake, and it ignores what we’ve learned over the past two years and all the new tools we have. Schools should not close.

GAZETTE: What are the best protections?

ALLEN: There’s been so much confusion over the past five months: Do vaccines work? What about a breakthrough case? Do those who are vaccinated transmit the same? What is the viral load? The higher order message that vaccines work got lost. You see it in the data everywhere. And we’ve seen it in the data since vaccines first came out. Vaccinated people are well protected from the most severe outcomes. Do breakthroughs happen that end up in hospitalizations? Yes. But they’re much less likely to occur for people who are vaccinated, and we’ve lost that message. I think that has fed into some of the concern around schools. It’s understandable that people are anxious, but they should be reassured that if they are vaccinated and boosted and again wearing a high-grade mask, then that’s excellent protection. So, the transmission is real, the breakthroughs are real. But I’m hoping that what people are starting to see, not just in the epidemiological data or the clinical data, but even their own personal anecdotal data, is that friends and relatives who are vaccinated and get this recover.

GAZETTE: What do you think about the test-to-stay approach that the CDC is has advised in order to help schools avoid online learning?

ALLEN: I fully support it. Quarantining is a blunt instrument that we used in the beginning of the pandemic when we didn’t know who was infectious. Now we can actually test to know who is infectious with good reliability, so you can keep kids in the classroom who may be in close contact with someone who has been infected but they aren’t infectious themselves. I also support test to return, which decreases the isolation period after you are infectious, and when you test negative you can come back. The challenge that the CDC has is that there’s just not enough testing around right now.

Scientists estimate that a one-year increase in alcohol consumption during the COVID-19 pandemic will result in 8,000 additional deaths from alcohol-related liver disease, 18,700 cases of liver failure, and 1,000 cases of liver cancer by 2040.

In the short term, alcohol consumption changes due to COVID-19 are expected to cause 100 additional deaths and 2,800 additional cases of liver failure by 2023.

The new research, published in Hepatology, was led by investigators at Harvard-affiliated Massachusetts General Hospital.

Using data from a national survey of U.S. adults on their drinking habits that found that excessive drinking (such as binge drinking) increased by 21 percent during the COVID-19 pandemic, investigators simulated the drinking trajectories and liver disease trends in all U.S. adults. The researchers noted that a sustained increase in alcohol consumption for more than one year could result in 19 to 35 percent additional mortality.

“Our findings highlight the need for individuals and policymakers to make informed decisions to mitigate the impact of high-risk alcohol drinking during the COVID-19 pandemic in the U.S.,” says senior author Jagpreet Chhatwal, associate director of MGH’s Institute for Technology Assessment and an assistant professor of radiology at Harvard Medical School.

“While we have projected the expected impact of societal drinking changes associated with the COVID-19 pandemic without any interventions, we hope that our research can help jumpstart needed conversations at every level of society about how we can respond to the many behavioral changes, coping mechanisms, and choices that have short- and long-term implications for the health of individuals, families and communities in America,” adds lead author Jovan Julien, a data analyst at the MGH Institute for Technology Assessment.

“The COVID-19 pandemic has had many unintended consequences with unknown long-term impact. Our modeling study provides a framework for quantifying the long-term impact of increased alcohol consumption associated with COVID-19 and initiating conversations for potential interventions,” notes co-author Turgay Ayer, the George Family Foundation Early Career Professor of Systems Engineering at Georgia Institute of Technology.

Co-authors include Elliot B. Tapper, Carolina Barbosa, and William Dowd.

Based on the quick rise and precipitous drop of Omicron in South Africa, Harvard experts are cautiously hopeful about a possible decline of the surging COVID variant in the very near future, even as they warn of dramatic case spikes, overloaded hospitals, and slowly rising deaths in the interim.

“In South Africa, the Omicron wave lasted on the order of weeks. I would imagine that this will be something that lasts similarly long, perhaps a bit longer in the U.S.,” said Jake Lemieux, an infectious diseases specialist at Massachusetts General Hospital, instructor in medicine at Harvard Medical School, and co-lead of the viral variants program at Massachusetts Consortium on Pathogen Readiness. “There’s a seasonal component to it — there was last season — so I think it’s going to be a difficult winter, and the maximal period seems like it’s about to unfold over the next few weeks.”

Lemieux and other coronavirus experts at MassCPR emphasized during a media call on Tuesday that important key questions remain unanswered and that the experience in South Africa — whose population is much younger than that of the U.S. — may not be mirrored here. Omicron peaked there weeks ago, followed by a rapid drop in cases, and the country has also seen proportionally lower levels of both hospitalizations and deaths.

“It’s very clear that there’s an astonishing number of cases, a moderate number of hospitalizations, and very low deaths,” said Dan Barouch, William Bosworth Castle Professor of Medicine at Harvard Medical School, director of Beth Israel Deaconess Medical Center’s Center for Virology and Vaccine Research, and co-lead of MassCPR’s vaccine research group.

Barouch also said that there is initial evidence in animal studies that the fast-spreading variant does indeed cause less severe disease, with infection concentrated in the upper airways and to a lesser extent in the lungs, where it can cause life-threatening pneumonia. “There is some emerging data in animal models … that infection of those animal models appears to result in robust upper-airway disease but less robust lower-airway disease and less severe pneumonias. That is certainly consistent with what we’re seeing clinically.”

Reports from the U.K., whose population more closely resembles the U.S. in age, indicate that cases have begun falling in London, though experts there questioned whether they might still plateau and warned that most of the decline has come in younger age groups.

The U.S. has seen no sign of an Omicron peak, however. Statistics from the Centers from Disease Control and Prevention show the seven-day moving average of new cases topping 491,000 on Jan. 3, nearly double last January’s pandemic peak of about 250,000. New daily hospital admissions, which typically trail cases by a few weeks, have risen as well, though, at 4.45 per 100,000 and have not yet topped last January’s Alpha variant-driven peak of 4.92.

Deaths, which trail hospitalizations, have surged since late November, but the seven-day average of 1,165 on Jan. 3 has not yet reached the levels seen during prior waves, including 2,299 during April 2020, when the original virus circulated, 3,421 in last January’s surge after Alpha had arrived on the scene, and 1,923 during this past September’s Delta wave.

Another result of Omicron’s rapid emergence in the U.S. has been rising numbers of children with COVID infections — 325,000 during the week ending Dec. 30 — though Katherine Luzuriaga, a pediatrician and vice provost for clinical and translational research at the University of Massachusetts Medical School, said they’re not seeing a significant increase in the rates of hospitalization or death due to the ailment.

“We’ve seen a huge surge in the number of children-reported cases of COVID infection,” Luzuriaga said, adding that some of those positives have come in youngsters admitted to hospitals for other conditions but tested for COVID. “Fortunately, to date we have not seen an increase in the rate of hospitalization due to COVID or in severity of disease due to COVID, and most of the severe cases that we are seeing in hospitals have primarily been in unvaccinated or under-vaccinated individuals.”

Despite those encouraging signs, the outlook for the immediate future remains perilous, with hospitals already operating at capacity and a recent survey of viral particles in Boston-area wastewater showing a massive spike in virus that so outstrips any point of the pandemic that Jeremy Luban, co-lead of MassCPR’s viral variants program, called it “absolutely terrifying.”

“We are, it is probably fair to say, engulfed in an Omicron wave right now, and the question is: How high does this wave go, and how severe is its impact going to be on patients, the health care system, and society?” said Lemieux. “We’re going to find out.”

Experts also pointed out that the U.S.’ size means it is likely that Omicron will play out — as did waves of other variants — at different times and in different manners in different parts of the country.

“The bottom line is that Omicron is going to visit every city and every town in the country and make its presence known,” said Luban, who is also a professor of molecular medicine, biochemistry, and molecular pharmacology at UMass Medical School. “I don’t think there’s any question about that.”

Though difficult weeks lie ahead, Barouch said that successive waves of infection and vaccination are shifting the landscape onto which new variants emerge to one where many potential hosts have some form of pre-existing immunity and some, having been vaccinated and infected, have several.

“I don’t think it’s a foregone conclusion that the next variant will necessarily be less pathogenic. That remains to be seen,” Barouch said about the odds of a new, less transmittable version. “But I do think that with each month that goes by, each variant that comes and goes, and each vaccine campaign, that we’re seeing a larger fraction of the U.S. population and also the global population with some level of immunity.”

Beliefs about which specific maternal behaviors or experiences have lasting effects on gestating offspring have shifted widely over time. In her new book, “The Maternal Imprint: The Contested Science of Maternal-Fetal Effects,” Sarah S. Richardson, professor of the history of science and of studies of women, gender, and sexuality, gives this rich history a clearer context in the discussion of reproductive responsibility. The Gazette spoke to Richardson, director of the Harvard GenderSci Lab, which studies biomedical research on sex and gender, about birth weight, bibliometrics, and her personal connection to histories of maternal stress. This interview was edited for clarity and length.

Q&A

Sarah S. Richardson

GAZETTE: “The Maternal Imprint” seems to intersect your professional and personal lives. Can you talk about why you wrote it?

RICHARDSON: My ear was turned by reading about studies of intergenerational Holocaust trauma at the level of the gene. This was around 2010, when a new field of science called epigenetics was emerging, claiming to solve a longstanding and problematic question in genetics, which is: How does the environment interact with our genes to change the way we grow and develop?

The hope was that these patterns of intergenerational transmission of trauma that had been explained narratively through stories could somehow be verified through empirical, material science. And I am the granddaughter of a Holocaust survivor. I am also the granddaughter of somebody who lived through the famed Dutch famine, which is another major study area in this field. So I couldn’t help but be riveted.

Furthermore, all of these claims were constructed through the matriline. I recognized as a historian of science that this new science was re-energizing a set of claims from the history of biology and genetics regarding the unique contribution of the mother to heredity. I saw it as deeply intertwined with a set of contestations about genetic determinism, and with conceptions of our bodies as both biological and social.

GAZETTE: Your research details a lot of eugenics history. What did this field have to offer you in the context of reproduction?

RICHARDSON: I was writing the chapter on prenatal culture when I was pregnant with my first child, and I actually found comfort in reading some of those funny ideas — for example, that you could do math equations while you’re pregnant to make a child who would be an accountant. It was sort of a beautiful thing. They were encouraging women to take control of their lives as pregnant women and suggesting that you could have some control over your future offspring, which in our current environment, where the risk discourse and the surveillance of pregnant people is incredibly intense, was such a different, almost magical space to step into.

I also think people will be surprised — and this is a well-known fact, though continuously underappreciated — that in the eugenic era, it wasn’t all about genetic determinism. It encompassed a wide range of prescriptions for health that included modes of behavior for before getting pregnant, while you are pregnant, and early development, that were laden with social values about the kinds of lives that were valuable.

GAZETTE: Maybe my favorite phrase in the book is “pop-science catnip,” which is what you call epigenetics. Can you explain?

RICHARDSON: Epigenetics has been cast in public conversation as something that allows you to shape your own potential and overcome hereditary limitations. This possibility of self-help, of plasticity, and of improvement and optimization walks right into our constantly contested ideas about our bodies, how we’re situated in generational time, and the degree to which outcomes are the result of nurture versus nature. And then you add the gender part, with women warned that if you eat a single potato chip you could be destining your child to a life of sloth and ADHD — definitely pop-science catnip.

We’re all very familiar with claims of the risks of fetal alcohol poisoning, or of not having enough folic acid in your diet when pregnant. This all comes from an earlier era of teratological research, which focused on an exposure to or deficit in a specific chemical agent or teratogen, imbibed by the mother, carried across the placenta, and impacting the fetus.

I am, in this book, talking about a different register of claims: this phenomenological thing called “maternal effects.” It’s something mediated by the mother’s body — her constitution, her condition, her environment. An obese mother would be an example of the prototypical exposure environment. The causes are very subtle exposures, and the effect sizes are small. We’re not talking about birth defects that are visible at birth that are extremely disabling. We’re talking about a couple of extra centimeters on the waist at age 59 after some exposure in the womb.

In short, this new field of science studies the coupling of small variations in the fetal environment with small variations in long-term health or development. It’s a different register of claims — and this is something I’m very interested to explore in the book, what I call crypticity, which characterizes the field’s knowledge landscape.

GAZETTE: You devote a chapter to birth weight, which has such an outsized reputation as a birth marker. Talk about your findings.

RICHARDSON: I could have written a whole book on birth weight, and maybe I should. It’s fascinating. Isn’t it incredible that we write on our birth announcements what the weight was?

The fascination with birth weight really developed in the ’60s and ’70s, a precursor to the same set of questions fascinating scientists today in the field of fetal epigenetic programming research. Could it be that the variation in fetal environment is a cryptic, as-yet-unappreciated cause of variation in life outcomes in the world? A whole body of scholarship — tens of thousands of papers — emerged correlating birth weights, which you can easily retrieve from birth certificates, with everything from health conditions and lung disorders to things like IQ, which I talk about in this chapter.

This research was racialized from its inception. It’s well known that there’s quite a racial disparity in birth weight in the United States, and that’s been quite persistent over time. I tell the story of scientists’ attempts to figure out why. The original theory was that it was all genetic, and there was just a different baseline for Black American babies [more of whom have low birth weights] compared to white American babies.

Two African American pediatricians, whose stories I was delighted to tell in this book, turned that theory around in the 1950s and ’60s by showing that birth weight cleanly correlates with income and access to prenatal care. This is the moment that maternal-effects science becomes entangled with a progressive biosocial science that has a vision of understanding how the social gets under our skin.

But as I show, the story turns out to be endlessly complex. Interpreting birth weight requires knowledge of the life history of how an individual became small as well as the context for how they became small. As a result, scientists eventually agree that birth weight is not a measure that is informative across populations for thinking about prenatal exposures. And that’s how we get to epigenetics.

GAZETTE: You said you could have written an entire book on birth weight. Were there other topics on which you found yourself deep in a rabbit hole that could have gone deeper?

RICHARDSON: Well, eugenics has been widely written about, so people think we have told its story. The literature is voluminous, encompassing nearly 50 years of production across the globe. My question was: What did these folks think about prenatal influences? That story had not been told. To get at this, I engaged in some mild empirical bibliometrics, which for me was new. I counted lines of text in dozens of formative eugenic books and made tables! After this work, it’s clear to me that we have so much more to understand about the full scope of eugenic ideas.

GAZETTE: Some pregnant people have access to so much information while others have not enough. What’s the lesson for researchers — or doctors, for that matter — in this book?

RICHARDSON: I would argue that in this moment we are at a high point for a highly medicalized approach to pregnancy combined with an expectation that pregnant people are aware of and following the most recent science, with genetics being our premier, elite paradigm for understanding risk. So, there is a priming of pregnant people to be very aware of every new piece of evidence and, in fact, to adapt their behavior in relation to it, combined with tremendous anxiety about optimizing birth outcomes.

Scientists in this field are incredibly passionate about bringing empirical science and novel tools like epigenetics to bear on questions on improving fetal outcomes. Regardless of their intentions, however, their work is received in a heightened risk discourse frame, where everything is positioned as either you are either hurting or helping your fetus. Under these conditions, parents and practitioners are not well-empowered by new epigenetic claims to make reasonable judgments about which risks to accept or not in the context of their own life.

A diagnostic blood test may provide early detection of lung cancer in asymptomatic patients, according to a new study.

Lung cancer, the leading cause of cancer death, is usually diagnosed at a late stage when the survival rate is extremely low. Early stage lung cancer is mostly asymptomatic, and low-dose spiral CT imaging, the current method for detecting early lung cancer lesions, isn’t feasible as a widespread screening test for the general population due to high cost and the radiation hazard of repeated screenings.

The study, published in Proceedings of the National Academy of Sciences provides proof-of-concept for the ability of a drop of blood to reveal lung cancer in asymptomatic patients. It was co-led by researchers at Harvard-affiliated Massachusetts General Hospital: Leo Cheng, associate biophysicist in pathology and radiology, Athinsula A. Martinos Center for Biomedical Imaging, and David Christiani, pulmonary and critical care physician.

“Our study demonstrates the potential for developing a sensitive screening tool for the early detection of lung cancer,” says Cheng. “The predictive model we constructed can identify which people may be harboring lung cancer. Individuals with suspicious findings would then be referred for further evaluation by imaging tests, such as low-dose CT, for a definitive diagnosis.”

Cheng, Christiani, and their co-investigators built a lung-cancer predictive model based on metabolomics profiles in blood. Metabolomics analyzes cellular metabolite flows to decipher healthy and pathological states by studying the metabolome — the dynamic biochemical suite found in all cells, fluids, and tissues of the body. The presence of lung cancer, with its altered physiology and pathology, can cause changes in the blood metabolites produced or consumed by cancer cells in the lungs. The researchers measured metabolomics profiles in blood using high-resolution magnetic resonance spectroscopy, a tool that can examine an array of compounds within living cells by measuring the collective reactions of metabolites.

The investigators screened tens of thousands of blood specimens stored in MGH’s biobank and others and found 25 patients with non-small cell lung cancer (NSCLC) with stored blood specimens obtained at the time of their diagnosis and at least six months prior to their diagnosis. They matched these patients with 25 healthy controls.

The researchers first trained their statistical model to recognize lung cancer by measuring metabolomic profile values in blood samples obtained from patients at the time of their diagnosis and comparing them to blood samples from the healthy controls. They then validated their model using blood samples from the same patients obtained prior to their lung cancer diagnosis. Here the predictive model yielded values between the healthy controls and the patients at the time of their diagnosis.

“This was very encouraging, because screening for early disease should detect changes in blood metabolomic profiles that are intermediate between healthy and disease states,” says Cheng.

The investigators then tested their model with a different group of 54 patients with NSCLC using blood samples obtained before their cancer diagnosis, which confirmed that the model’s predictions were accurate.

Values from the predictive model measured from prior-to-diagnosis blood samples could also predict five-year survival for patients, which may be useful in guiding clinical strategies and treatment decisions. A previous study by the investigators showed the potential for magnetic resonance spectroscopy-based metabolomics to differentiate cancer types and stages of diseases. Larger studies are needed to validate the use of blood metabolomics models as NSCLC early screening tools in clinical practice.

Next, the researchers will analyze metabolomic profiles of lung cancer’s clinical characteristics to understand the entire metabolic spectrum of the disease, which may be useful in choosing targeted therapies. They have also measured metabolomics profiles of more than 400 patients with prostate cancer to create a model that will distinguish between indolent cancer, which needs to be monitored, and more aggressive cancer that requires immediate treatment. The investigators also plan to use the same technology to screen for Alzheimer disease using blood samples and cerebrospinal fluid.

Cheng is associate professor of radiology at Harvard Medical School. Christiani is professor of medicine at HMS, and professor of environmental genetics at the Harvard T.H. Chan School of Public Health.

The National Cancer Institute funded this study.