In this episode of the COVID, Quickly podcast, we talk about why we’ve had years shaved off our average collective life since 2020. Also, we talk about “mabs” and why you might want to know what they are.
How the Pandemic Shortened Life Expectancy and New Drugs on the Horizon: COVID, Quickly, Episode 40
Tanya Lewis: Hi, and welcome to COVID, Quickly, a Scientific American podcast series!
Josh Fischman: This is your fast-track update on the COVID pandemic. We bring you up to speed on the science behind the most urgent questions about the virus and the disease. We demystify the research, and help you understand what it really means.
Lewis: I’m Tanya Lewis.
Fischman: I’m Josh Fischman.
Lewis: And we’re Scientific American’s senior health editors. Today we’re going to talk about how COVID has driven a notable decline in U.S. life expectancy …
Fischman: … and some new monoclonal antibodies that could protect us from variants.
Fischman: People in the U.S. have been living longer and longer during most of the past century. Then COVID hit. And all of a sudden we’re going backwards. Why are we losing years of our lives?
Lewis: Life expectancy has only declined a few times in recent memory: during the 1918 pandemic, during World War II, and during the HIV/AIDS crisis. But over the last two years, it’s declined by almost three years. That’s equivalent to the U.S. life expectancy in 1996.
Fischman: That’s pretty astounding.
Lewis: It is. But while almost every demographic saw a drop, some groups lost more years of life than others.
Fischman: Which groups had the biggest declines?
Lewis: Native American and Alaska Native populations’ lost a total of 6.6 years from 2019 to 2021. The Hispanic population lost 4.2 years. The non-Hispanic Black population lost four years. The white population lost 2.4 years. And the Asian population lost 2.1 years.
The data come from the CDC’s National Center for Health Statistics, which recently published provisional data for 2021. Elizabeth Arias and her NCHS colleagues calculated something called a life table. It basically takes a hypothetical group of infants born in 2021, and applied the real-world death rates of every age group to those infants across their whole lives. The result is an estimate of the total population’s life expectancy.
Fischman: So, what are the reasons for all the lost years?
Lewis: Well, COVID was the primary cause—more than a million people in the U.S. have died from the disease. But unintentional injuries—mostly drug overdoses—were also a big reason for the decline.
Deaths from heart disease, chronic liver disease and suicide also contributed to the decline in life expectancy over the past year. Economists Anne Case and Angus Deaton first brought attention to these “deaths of despair”—deaths from overdoses, alcoholism and suicide. They were already rising before the pandemic, which just accelerated the trend.
Fischman: In other words, COVID pushed people who were already struggling over the edge.
Lewis: Most likely. And this was especially true for the Native American population. Native American people have some of the poorest levels of housing, education and health care. And a lot of this stems from the U.S. government’s colonialist policies, Crystal Lee, an assistant professor at the University of New Mexico’s College of Population Health, told me.
Lee is Dine’—a member of the Navajo Nation—and is also CEO of the nonprofit organization United Natives and the company Indigenous Health. “We need to hold the U.S. government accountable, by honoring the existent treaties,” Lee says.
Fischman: Those treaties would improve healthcare, among other things.
Lewis: Exactly. I think the biggest take home message here is really that we weren’t prepared for this pandemic, and that we really need to revamp our health care system and make it work for everyone in this country if we want to stop this backsliding and live longer, healthier lives.
Lewis: Josh, we’ve both talked about the several hundred people who are getting severely sick and dying from COVID every day. And some of the medicines developed to treat sick people don’t work well against the new variants. You’ve been hearing about some drugs that might work better, though, right?
Fischman: I have. The new drugs are variants themselves, versions of older medicines called monoclonal antibodies. They’ve usually got long, difficult names, but they typically end in “mab,” so that’s the giveaway.
Lewis: For COVID, those have been around for a year or so, haven’t they?
Fischman: Yep. They were developed to glom onto the early 2020 form of the virus, and prevent it from penetrating into a cell. And originally they did a pretty good job.
Lewis: But recently, not so much, right? I saw a study in which scientists tested 21 different “mabs” against the BA.4 and 5 variants, and only one was able to neutralize them.
Fischman: And that’s precisely the problem. These mabs were configured to fit that early virus, like a key fitting into a lock. But now there are 5 or so newer variants making the rounds—BA.5 is still the dominant one—and those have mutations that essentially change the shape of the lock. So most of the mabs don’t fit anymore. One, called bebtelovimab, still does a pretty good job, but most of the others that have been authorized by the FDA do not.
Lewis: So what’s the solution?
Fischman: Go broad. Scientists used to pick these mabs based on how strongly they attached to a particular virus. But now they are looking for antibodies that are “broadly neutralizing.” They grab onto a wider range of variants, not just one.
I’ve been talking about this with Bill Haseltine, the molecular biologist who worked on some of the original AIDS therapies. He thinks this approach is very promising. Mab developers are picking antibodies that take aim at what scientists call “highly conserved” regions of the virus. In plain English that means spots that don’t mutate from variant to variant, so the mabs can still lock on.
Lewis: Can people use these now?
Fischman: Not yet. There are about 10 of these mabs in various stages of testing. Some are now being tried on people, and some are still in animal tests.
Lewis: But don’t a lot of drugs that work well in animals actually fail when they get to humans?
Fischman: Not mabs, in general. The antibodies are often developed in mice that have been genetically modified to have human-like immune systems—a technique that goes back to the days of AIDS drug development. Because of that, they generally translate well to people, Haseltine says.
Another advantage mabs have is they can be used to prevent infection in people who are in high-risk situations. Some may be immunocompromised and don’t get much benefit from vaccines, mabs can play a prevention role for them. Others may work in nursing homes, which have had high rates of outbreaks.
Lewis: I can see that. Look, I don’t want to keep tossing out problems, but mabs aren’t a pill like Paxlovid. They have to be infused, or at least injected. That creates an accessibility problem.
Fischman: You’re right. It’s not like you can easily use them at home. But the injection technology is getting easier. And, just for instance, plenty of people with diabetes have learned to inject themselves with insulin.
Cost will be an issue, too. Mab manufacturers can charge just over $2000 per dose. Right now the government picks up the tab for COVID patients. It turns out, though, that mabs are actually cheap to produce these days, just one or two hundred bucks a pop.
So there’s a chance we’ll be seeing new and affordable therapies, able to handle the range of variants that COVID keeps tossing at us.
Lewis: Now you’re up to speed. Thanks for joining us. Our show is edited by Jeff DelViscio and Tulika Bose.
Fischman: Come back in two weeks for the next episode of COVID, Quickly. And check out sciam.com for updated and in-depth COVID news.
[The above text is a transcript of this podcast.]