Issue 104

Immunity vigilantes, lagging vaccination rates, and an effective double-masking strategy

Hello friend! Welcome to Scrap Facts.

I'm a reporter covering health and science with insatiable curiosity. I love everything I learn, not all of which gets its own story. Each issue, I'll bring you some of my favorite facts that I picked up on the job or while out living life.

Love Scrap Facts? Consider hitting the “like” button, or tell your friends to sign up!

B-cells break all the rules in biology.

Found while reporting this obsession email on the immune system.

Generally speaking, pathogens like viruses and bacteria can evolve a lot faster than we do. They’re constantly reproducing, which gives them a chance to introduce mutations which may make them better at infecting us.

We, of course, evolve very slowly. Ordinarily, this would mean that we wouldn’t have time to evolve new defenses against these pathogens. But, we’ve got a trick up our sleeves (er, in our bloodstreams): Vigilante adaptive immune cells.

B-cells, which produce antibodies that glob onto pathogens to prevent them from invading our cells, break all the rules of biology to keep pace with pathogens. Usually, the last thing you want to do as a cell is mutate or break your double-stranded DNA on purpose. That can cause cancer down the line.

But B-cells do just that to avoid an even more dangerous, imminent threat of an infectious disease. It’s “basically an accelerated evolutionary process, or like natural selection happening in miniature,” Kevin Bonham, a researcher with a doctorate in immunology, who studies microbiology at Wellesley College, told me. When threats are that big, there are no rules.

A breakdown of who’s getting vaccinated in the US by race/ethnicity.

Found while reporting: Why many US Latinos aren’t getting Covid-19 vaccines.

In the first month that Covid-19 vaccines were available in the US, it was mostly non-Hispanic White people getting the shots.

These data only represent about half of all vaccinations during that time period; healthcare providers didn’t always collect demographic information.

But it speaks to a much larger problem at hand: Minorities, who have been most harmed by the Covid-19 pandemic, are getting protection from it the slowest. It’s not only an issue of access—though that’s a clear part of it. And there’s not one solution to public health experts can point to.

It’s going to take a nuanced approach to reach minorities at the community level. The first step is understanding broadly why these disparities exist. I took a look into the historical and present circumstances that are affecting Latino populations in the US.

First, there’s a history of neglect by the US government, which often left some people out of benefits they were entitled to. Second, the Trump administration intimidated documented and undocumented immigrants to the point where they felt severe distrust of any governmental figures. And third, misinformation on encrypted social media like WhatsApp runs wild in limited-English proficiency circles.

Building trust in any community takes time, but public health officials have to start somewhere. It’s not just for the sake of this pandemic on our hands; it’s any future public health crisis that comes our way, too.

Bonus: Vaccines won’t eradicate the pandemic—and that’s okay. Science journalists (myself included) and healthcare providers have been writing all kinds of warnings about the dangers of assuming that vaccines will fix everything. It’s understandably made a lot of readers frustrated; this was the thing we were holding out

PSA: More masks isn’t always better.

Found while reporting: Why don’t we have an ideal mask yet?

As SARS-CoV-2 variants continue to spread, it’s not a bad idea to increase the filtration your mask provides. In fact, shortly after I wrote the above article, the US Centers for Disease Control and Prevention updated their guidelines to recommend wearing two masks.

There’s one catch, though: both your masks, whatever they’re made of, should still be breathable when over your nose and mouth.

If they aren’t, that means that air and water droplets aren’t actually being filtered through them, which is the whole purpose of wearing a mask in the first place. Instead, the air you’re taking in comes from gaps around the bridge of your nose or under your cheeks.

One quick way to check if your double masks are too thick is to go outside with glasses or sunglasses on. Some fogging from escaped air is inevitable, but your glasses shouldn’t steam up entirely. If they are, it’s a sign that a lot of air is coming out from gaps over your nose, which can be addressed with a mask that has a metal band on the top.

✨ Do you have Covid-19 vaccine questions that are still unanswered? I got ya—tune in at 11 am US eastern on Wednesday, March 3 to hear a conversation with me and Panagis Galiatsatos, a critical care pulmonologist at Johns Hopkins Bayview Medical Center. It’s free! Register here:

Other stuff you may have missed:

Pfizer took a big bet on their six-dose vaccine vials. Without the right syringes, though, most healthcare providers won’t be able to extract all the doses possible.

In addition to the above story, I talked about it with Arirang News in South Korea.

All you need to know about the SARS-CoV-2 variants. In case you weren’t sold on double masking before.

Johnson & Johnson’s Covid-19 vaccine prevents severe Covid-19 cases, even if it doesn’t block illness entirely—and that’s a key way to end the pandemic. This story was written before the single-dose jab got authorized on Saturday night, and carries even more relevance now.

The tech and ethics behind the fertility business: Watch the recap of the Kavli Conversation with MIT Tech Review’s Antonio Regalado and Dr. Norbert Gleicher.

I hope you enjoy these screenshots; I think they are very funny.

That’s all for now—stay curious, friend ❤️

If you love Scrap Facts, consider hitting the “like” button at the bottom of this page, or sending it to a friend. You can also send your own scrap facts to scrapfacts@gmail.com to be featured in future editions. Wanna keep in touch outside of this newsletter? Follow me on Twitter and Instagram.

Top image by Rachel Couch; headshot by Matt Anzur.

Kavli Conversation: Biotechnology, journalism, and the future of fertility

A FREE live (on the internet) event, Wednesday, Feb. 25 at 6:30 ET

Hello friend! Welcome to Scrap Facts.

I'm a reporter covering health and science with insatiable curiosity. I love everything I learn, not all of which gets its own story. Each issue, I'll bring you some of my favorite facts that I picked up on the job or while out living life.

Love Scrap Facts? Consider hitting the “like” button, or tell your friends to sign up!

Let’s talk about talking about biotech businesses.

There are a lot of important questions for journalists to ask when writing about science—and even more when there’s major money to be made.

On Thursday, Feb. 25, at 6:30 pm ET, I’ll be moderating a conversation with Antonio Regalado, MIT Tech Review’s senior biomedicine editor, and Norbert Gleicher, a reproductive endocrinologist and pioneering scientist in fertility medicine. We’ll be looking at the fertility industry as a case study of when science and medicine meets business, and talking about how the media covers it.

This event is FREE, and open to anyone. Sign up here! I’ll be facilitating audience questions.

If you like this conversation, be sure to check out other Kavli Conversations, happening online later this spring, as well as an archive of previous conversations. These are all sponsored by Sponsored by the Kavli Foundation and the Science, Health and Environmental Reporting Program at New York University (my alma mater).

That’s all for now—stay curious, friend ❤️

If you love Scrap Facts, consider hitting the “like” button at the bottom of this page, or sending it to a friend. You can also send your own scrap facts to scrapfacts@gmail.com to be featured in future editions. Wanna keep in touch outside of this newsletter? Follow me on Twitter and Instagram.

Top image by E. Y. Smith; headshot by Matt Anzur.

Age: Issue 2

Coral: passing down genetic life lessons

Feb. 14, 2021

Hello friend! Welcome to Age, a bi-weekly special edition of Scrap Facts.

Every issue, I’ll be exploring how different kinds of life experience time, based on an interview with a researcher in the field. Got a question about aging you’d like answered? Reply to this email and you may see it in a future edition.

Love Scrap Facts? Consider hitting the “like” button, or tell your friends to sign up!

Coral: passing down genetic life lessons

In conversation with Iliana Baums, a molecular ecologist at Penn State University.

The first thing to know about coral is that they’re relatives of jellyfish.

While jellyfish expand and contract their bell-like bodies to float around and drag their tentacles with them, “corals lay down on the bell side,” says Baums. Slowly, over decades, they painstakingly construct calcium carbonate skeletons to protect their fragile polyps, and dangle their tentacles outside to munch on drifting plankton.

Coral and their skeletons provide the backbone for entire reef ecosystems. Their skeletons are homes to algae, with whom coral swap carbon dioxide for sugar. Coral polyps and tentacles secrete a thick, nutrient-rich mucus—which happen to be the favorite food of bacteria. Bacteria, in turn, happen to be the favorite food of plankton, which happen to be the favorite food of the corals themselves, as well as the tiny fish and crustaceans who seek refuge in the nooks and crannies of corals’ skeletons. These small fish are the favorite food of larger fish, who are the favorite food larger fish, and so on and so on. It’s a beautiful, snot-based economy, says Baums.

A coral reef with a school of fish swimming nearby. Image credit: NOAA.

The second thing to know about coral is that they’re uniquely able to pass down survival tips through their genes to their offspring. Scientists call this having “an un-sequestered germ line.” What this means is that mutations coral pick up over the course of their lifetimes get passed down to their offspring. Though it’s common in plants, it’s rare in the animal kingdom, and it helps make coral masters of immortality.

Let’s dive into that more:

Like kelp, coral are stuck where they settled as larvae; they’re at the mercy of their environment, says Baums. This means that if coral hope to survive, they better find ways to constantly adapt. One way to do so is to collect beneficial mutations over time.

For us, mutations are generally a bad thing. They’re an unfortunate byproduct of staying alive: The longer we live, the more copying mistakes our cells make over time. Some of these mistakes are random, and some are the result of external exposures, like UV rays or chemicals.

The more copying mistakes, the greater the likelihood that one of them will lead to cancer other diseases. We have some internal anti-cancer protection: The DNA in our cells are equipped with telomeres, which shorten with every division. wWhen telomeres get to a critical length, they forbid the cell from dividing anymore because the risk of developing a cancerous mutation is too high. As a result, the cells senesce and eventually self-destruct—that’s a big part of aging for us.

We keep our gametes (eggs and sperm) separate from the rest of our cells that pick up these mutations over time. That’s why a person who develops an injury, like a burn, or an illness, like cancer,* won’t pass it down to their kids. For example, I have numerous scars on my knees from falling and scraping the skin; if I ever had children, they wouldn’t be born with scar tissue on their knees. They’d have smooth skin, like mine was before I picked up trail running.

(*Cancer can be the result of an environmental exposures, like smoking, drinking alcohol, or certain chemicals. People who develop cancers related to one of these exposures may not pass it on to their children. But sometimes, cancer is the result of a combination of genes and environment; it’s an incredibly complex disease. Some of these genes could get passed onto children, even if they didn’t guarantee that child would develop cancer.)

But coral are different. Coral reproduce sexually and asexually. The giant colonies of corals, like the one pictured above, are the result of hundreds of thousands of rounds of asexual reproduction.

Asexual reproduction is essentially cloning. It doesn’t always go perfectly; sometimes, a clone may have a genetic mistake that leads the offspring polyp to die. But, because there are hundreds of thousands of successful clones, the colony as a whole survives.

When a colony’s environment changes, like if the water gets warmer or more more acidic, coral have to adapt. While much of it may die off, some of its polyp clones will have mutations help them survive in this new environment. Those polyps have got a positive mutation on its hands (tentacles)! Polyps with this beneficial mutation can clone itself again and again, and the colony survives.

But then it’s coral’s turn to ~sexually~ reproduce. This mixing of genes across gametes is critical for the survival of the species, and not just the immediate colony. It happens just once a year. For Caribbean corals, it’s like clockwork “three nights after the August full moon between 10pm and 11pm,” according to Baums. Corals release their egg and sperm into the water column and hope they meet up to form a zygote that can float and finds a suitable surface to latch onto to build a colony of its own.

Coral gametes, however, collect the mutations of their parents. Theoretically, this means they have all the genetic life lessons of their parents: How to survive in warmer water, how to survive in more acidic water, and maybe even how to survive with a little less food available. And while that inheritance could be dangerous for us humans, for coral, it could be the key to survival.

It also brings up an unusual question about a coral’s age, which Baums and her team are studying: Because scientists can count the rate mutations in coral over time, like rings on a tree, they can figure out how old its parent coral was when it sexually reproduced to start a new colony, at least roughly. It’s usually give or take a few hundred years, Baum says. And then, based on the size of the colony itself, you can figure how long ago that was.

Theoretically, if all coral keep adapting over time, which allows them to grow their individual colonies until it’s time for sexual reproduction, coral would be live forever. We know that coral dies, though, when its environment changes too quickly for it to adapt. Being immortal doesn’t mean evading death entirely; it just means you don’t age into death. And coral, it seems, may have cracked the code for a form of immortality—at least for a creature remains forever in its place.

That’s all for now—stay curious, friend ❤️

If you love Scrap Facts, consider hitting the “like” button at the bottom of this page, or sending it to a friend. You can also send your own scrap facts to scrapfacts@gmail.com to be featured in future editions. Wanna keep in touch outside of this newsletter? Follow me on Twitter and Instagram.

Top image by Rachel Couch; headshot by Matt Anzur.

Issue 103

Immunology in your mucosal membranes, falling life expectancy, and a glob of amino acids.

Hello friend! Welcome to Scrap Facts.

I'm a reporter covering health and science with insatiable curiosity. I love everything I learn, not all of which gets its own story. Each issue, I'll bring you some of my favorite facts that I picked up on the job or while out living life.

Love Scrap Facts? Consider hitting the “like” button, or tell your friends to sign up!

Mucosal immunology is “ridiculously complicated.”

Found while reporting: Can you spread Covid-19 if you get the vaccine?

Our protective immune system is not universal across our bodies. The immune cells that patrol our innards—places like our blood vessels, muscle tissue, and organs, which have no contact with the outside world—are aggressive: They see an intruder and hit hard and fast by producing antibodies called immunoglobulin G (IgG). And for good reason! Infections in those areas are brutally hard to treat and especially dangerous.

IgG antibodies are the kind we happen to make when getting vaccines that are jabs in our upper arms…like, say Covid-19 vaccines. Our arm muscles end up doing the majority of the legwork (heh) of making an immune response against Covid-19. And they work well at preventing Covid-19 cases, based on the data vaccine manufacturers have presented to regulatory authorities across the globe.

Interestingly, though, IgG antibodies aren’t the ones that would necessarily stop Covid-19 transmission. SARS-CoV-2, the virus that causes Covid-19, spreads through the parts of our bodies that interact with the outside world: our respiratory pathways, which include our noses and mouths. These areas are called mucosal surfaces, and they basically line everywhere on our bodies that aren’t covered with skin. (Skin, by the way, is first and foremost a part of our immune systems we don’t consider—it’s an ideal physical barrier to the outside world! And the biggest organ you’ve got. In addition to being the most aesthetically pleasing.)

The immune cells that patrol these pathways are a lot chiller than than the immune cells in our blood streams. They produce immunoglobulin A (IgA) antibodies, and they only attack things they know for sure can hurt us. And again, for good reason: If they set off an immune response every time a foreign object entered our systems, we’d be sick all the time. We’re never not exposed to foreign entities. How these immune cells make their selection is a field called mucosal immunology, and it has entire journals dedicated to it because it’s so complex and opaque (for now).

So IgA antibodies are the ones that can stop SARS-CoV-2 on our mucosal surfaces—and vaccines don’t necessarily generate those kinds of antibodies. Which sounds bad! But, we know that vaccines still prevent a lot of Covid-19 cases, which means at the very least that the virus isn’t getting a chance to replicate a lot. Less replication means less of a chance to spread it to others. How much so? Unclear—but promising! We’ll know more the more people get vaccinated by looking at how case counts decrease.

If you’ve been lucky enough to get vaccinated, congrats!! You’re at a much lower risk of getting sick with Covid-19, and spreading it to others. But just in case, you should still be wearing a mask. It won’t be forever.

US life expectancy is about to take its biggest downturn in years—particularly among marginalized groups.

Found while reporting: What Covid-19 is doing to life expectancies for Black and Latino Americans.

This chart should speak for itself.

Black and Latino populations have been hit exceptionally hard by the Covid-19 pandemic—and it’ll likely have a long-term effect on their life expectancies from birth.

There is still time to reverse, or even flatline these trends—but it’ll take continued protective measures and an effective vaccine distributions among these populations. This is going to be made even harder by the distrust many people in these groups feel after the present and historical neglected or abused by the US medical system. Effectively reaching these groups will require a lot work, which at the moment seems to be shouldered by unpaid or underpaid community leaders and physicians of color.

PS. The US hasn’t been great at collecting its non-White populations, which is why the Hispanic life expectancies on the chart above don’t start until 2006. Hispanic here also means “Hispanic or Latino”—there’s a slight difference in the two words, which you can read about here.

The Covid-19 spike protein isn’t a “spike” so much as its a massive amino acid glob.

Found while reporting: Will the Covid-19 vaccine work on the new variants?

I’ve written in the past about how the SARS-CoV-2 spike protein works like a key to the ACE2 receptor in our cells. It’s a good analogy! But perhaps misleading in the kind of shape we’re working with.

The spike proteins on the SARS-CoV-2 virus actually line the sphere. They’re a mix of some ~1,300 amino acids (think LEGO bricks for proteins), with some sugar molecules on there. They’re also not stagnant, and can shape-shift to be either stickier on the surface of our cells, or sneakier getting into our cells into our cells. Because the spike protein has such an integral role in infection, all the vaccines available so far target it.

A lot of the mutations you’ve probably heard about with SARS-CoV-2 represent slight changes to the spike protein. Variant B.1.1.7, for example, has swapped out a dozen or so amino acids on the protein for another on spike proteins, which happen to provide an extra opportunity for the virus to infect our own cells. This makes it about 50% more infectious.

While scientists are studying whether these mutations can help the virus evade antibodies from a vaccine (an idea which sounds terrifying) it’s important to remember just how big spike proteins are: The fact that they’re made up of over 1,000 amino acids means that swapping a few out here and there won’t matter too much in the long run.

Even some of the vaccine trails that have shown less efficacy against some mutations, some priming to our immune system by a vaccine is better than none. Our immune system learns over time, and adapts to new circumstances (much like we do, dear reader). If the immune response a vaccine generates aren’t a perfect defense to a new spike protein, it’ll change.

That change in response may take some time—which is why it’s still as important as ever to try not to get sick, as much as possible. But all hope is not yet lost.

Other work you may have missed:

Why has vaccine rollout has taken so long? For Aspen Ideas, I spoke with virologist and vaccinologist Florian Krammer from the Icahn School of Medicine to answer some of these questions.

Pet food suffers the same marketing gimmicks as people food. Without the invention of pet food, we’d never have pets! But we now also have a highly competitive market, desperate to pull in health-conscious pet owners.

PCR testing won’t help reopen your workplace. Look to antigen testing instead—it’s cheaper and produces faster results, even if it’s not your lab gold-standard.

Some workplaces are paying employees to get vaccinated. Dollar General was one of the first to announce such an incentive.

Biden’s pick to head Operation Warp Speed is an anomaly among FDA commissioners. David Kessler one of the few to have minimal ties to Big Pharma. This pick goes in line with Biden’s generally scientific approach to stopping the pandemic.

Don’t stress if you get your second Covid-19 shot later than you meant to. More time for your immune system to learn is generally a good thing.

Drug companies are teaming up with competitors to mass-manufacture vaccines. It’s a first in Big Pharma’s history.

And finally, everything we know about the only one-jab vaccine in late-stage clinical trials.

That’s all for now—stay curious, friend ❤️

If you love Scrap Facts, consider hitting the “like” button at the bottom of this page, or sending it to a friend. You can also send your own scrap facts to scrapfacts@gmail.com to be featured in future editions. Wanna keep in touch outside of this newsletter? Follow me on Twitter and Instagram.

Top image by Rachel Couch; headshot by Matt Anzur.

Age: Issue 1

The advanced life cycles of kelp

Jan. 17, 2021

Hello friend! Welcome to Age, a bi-weekly special edition of Scrap Facts.

Every issue, I’ll be exploring how different kinds of life experiences time, based on an interview with a researcher in the field. Got a question about aging you’d like answered? Reply to this email and you may see it in a future edition.

Love Scrap Facts? Consider hitting the “like” button, or tell your friends to sign up!

Kelp and its advanced life cycle.

In conversation with Sean Grace, a marine ecologist at Southern Connecticut State University.

We humans busy ourselves with a variety of personal and professional pursuits, but most of life just has a single goal: reproduction. The majority of creatures on Earth expire shortly after they reach sexual maturity. For some species, their final days are quite dramatic; salmon, for instance, die shortly after making a mad dash upriver to spawn. Wheat are the same way, albeit there’s no death march involved. (This is called semelparity) Most of life gets the chance to reproduce a handful of times—called iteroparity—but still, their days after reaching sexual maturity are numbered.

Kelp are a semelparous algae. On the east coast of the US in the Atlantic Ocean, they live for just one year; in the colder months in the northern hemisphere (so, now), their spores are settling and finding rocks to cling to. Over the summer, they grow at a truly alarming rate to the tune of 20 inches (50 cm) in per day as they get to their reproductive stage.

"Kelp is interesting because it has what’s known as an alteration of generation,” says Grace. Although kelp reproduce sexually—meaning, with male and female gametes, just like us—not all kelp do.

Some kelp grow up to be sporophytes. This means that they produce spores that can go on and become other other kelp. This is a version of asexual reproduction. There’s no gene combination between parents; it’s essentially cloning a parent.

Kelp spores, however, go on to produce another stage of kelp, called gametophytes. These kelp produce the sperm and egg cells that go on to mix to form a little kelp zygote somewhere in the water column—nearby, or as far as 200 miles away. This is a version of sexual reproduction, which makes sure that kelp mix up their gene pools to stay healthy as a species.

If you were to meander into a kelp forest in the shallow ocean waters, however, you wouldn’t be able to the difference between the sporophytes and gametophytes. “They look exactly the same,” says Grace.

It may seem like a ridiculous extra step to grow a whole other algae to create future generations of kelp, but it’s a survival mechanism. “It ensures reproduction.” If marine animals were to eat kelp to survive (as they tend to do), or if a kelp’s thallus (main leafy-looking body) were damaged in any way, it wouldn’t matter if it were a sporophyte or gametophyte—there would always be backup.

After they release their spores or gametes, kelp die. Their cells senesce, just like ours, which is when they essentially stop trying to multiple and repair their DNA. Instead, they realize their time has come, and they die—settling to the bottom of the sea floor to become sediment. (They bring all their carbon with them—another massive form of carbon storage we probably take for granted.)

But having this advanced life cycle—breaking up reproduction, in other words, “is a form of fitness,” Grace says. Kelp are a brown algae that have an advanced life cycle; many species of red algae do the same. Generally, the more ways a species can reproduce, the better for the survival of the species.

Other species with advanced life cycles don’t experience time the way we do. Although kelp age and die, just like we do, there are some other creatures with advanced life cycles, like some coral, that don’t. As long as they have a stable environment and food, they simply forget to age. Some of them have spent thousands of years on Earth. This feat that is tied to all the ways they can reproduce, which we’ll get into next issue.

In addition to teaching us about advanced life cycles, kelp can also teach us a thing or two about living in times of uncertainty. Read my story for Quartz here.

That’s all for now—stay curious, friend ❤️

If you love Scrap Facts, consider hitting the “like” button at the bottom of this page, or sending it to a friend. You can also send your own scrap facts to scrapfacts@gmail.com to be featured in future editions. Wanna keep in touch outside of this newsletter? Follow me on Twitter and Instagram.

Top image by Rachel Couch; headshot by Matt Anzur.

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