SciencePodcast_210827

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0:00:05.7 Sarah Crespi: Welcome to The Science Podcast for August 27th, 2021, I'm Sarah
Crespi. Each week, we feature the most interesting news and research published in Science and the
Sister Journals. First up this week, News intern Rachel Fritts discusses a new way to think about
endometriosis. A painful condition in which tissue that normally lines the uterus grows outside the
uterus and it can bind to other organs. Next researcher Raphael Townshend talks about predicting
how RNA will fold into 3D shapes using deep learning. This is a machine learning approach that
relies on very few examples and limited data. Finally, in this month's edition of our limited series on
Race and Science, host Angela Saini is joined by author and Lundy Braun to discuss her book,
Breathing Race Into the Machine, The Surprising Career of the Spirometer from Plantation to
Genetics. Now we have News intern, Rachel Fritts, we're gonna talk about some new insights into
endometriosis. Hi, Rachel.

0:01:09.3 Rachel Fritts: Hi, how are you?

0:01:11.5 SC: I'm good. This is an interesting disorder, this is when the lining of the uterus, which
is shed during menstruation and then grows back, kind of cyclically, it also in endometriosis starts
to grow outside the uterus, which can create some painful problems, scar tissue build up, even
binding up of other internal organs. How common is endometriosis Rachel?

0:01:33.7 RF: Yeah, so it's a surprisingly common disease for one that I think a lot of people
haven't actually heard of. It impacts an estimated one in 10 women, which is equivalent to 190
million women globally. And it could be even as much as one in eight.

0:01:57.1 SC: What are the treatment options for endometriosis at this point?

0:02:00.5 RF: The treatment options at this point are not great. Basically, there are two major ways
that endometriosis can be treated. First is you can have a pretty invasive surgery to actually go in
and try to cut away this tissue that's built up kind of around the outside of your uterus and internal
organs to try to combat that build-up. But because it's cumulative, often just one surgery isn't going
to solve the problem. So, many people who suffer from endometriosis will have to undergo multiple
of these invasive surgeries. And then the second option is hormonal treatment. So that's just trying
to get at the fact that this tissue is trying to build up and shed during menstruation just like it would
within the uterus. And so, the hormone treatment is trying to disrupt the menstruation cycle. This
kind of treatment, it can have a lot of adverse side effects and different people may or may not
respond to different kinds of hormone treatment. So, they can be cycled through different ones, and
the process can take months and it can involve all of these really horrible side effects, and at the end
of the day, none of them might work. So, it can be a very frustrating thing to live with.

0:03:35.4 SC: Let's turn to the work that you talk about in this story. So, this actually started back
in the 90s.

0:03:42.9 RF: Yeah, this dates back to the 1990s when researchers really started to look into this
idea that endometriosis has at least partially this genetic basis. So, it's 50% heritable, which means

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that 50% of the risk of getting endometriosis is actually explained by genetics. But researchers had
to figure out if they could pinpoint which genes were actually involved.

0:04:14.8 SC: So, do they have to find family lineages where the women had endometriosis?

0:04:20.8 RF: There is this group of families where at least three of the women have endometriosis
and these families have been involved in research that goes back to the 1990s. And so, a lot of this
genetics research has been focused on these families, especially trying to dig into this heritable
component of endometriosis by comparing their genes to those of the general population. In the
end, this particular study sequenced the DNA of women in 32 different families. They also took this
more large scale, once they had narrowed down to a particular region of a particular chromosome,
where they went to the population level and actually looked at more than 3000 endometriosis
patients and compared their genes to roughly 7000 people who don't suffer from endometriosis and
tried to see where there might be variations.

0:05:28.7 SC: What did they find when they looked across all these genomes?

0:05:32.5 RF: They really narrowed down to this one particular gene called NPSR 1. And they
found that in populations with endometriosis, there were these variants that were just popping up
more. And NPSR 1 is actually a gene that's known to be involved in inflammation, just in general,
but it hadn't really been implicated in endometriosis in particular before. So, they decided to try to
see if they could inhibit the genes protein production and see if they could notice a difference.

0:06:15.9 SC: So they turned the gene off, I think in mice in the first case?

0:06:18.9 RF: Yeah, so they turned the gene off in mice. Mice don't menstruate but they can create
these mice in the labs that show similar symptoms to people with endometriosis. So, they did target
this particular gene in mice and they did find both a reduction in inflammation and a reduction in
pain, which is two of the major things that people who suffer from endometriosis would benefit the
most from.

0:06:48.2 SC: So, now we have some variants at hand that are associated with endometriosis and
we've seen some effects in these mouse models. What happens next?

0:06:55.8 RF: We're still a ways off having a drug that can target these genes and provide an
alternative to the hormonal drugs. But this is really one of the first times a research group has found
a potential gene target that could eventually pave the way to something that is a non-hormonal
treatment. So, the next steps for this particular gene are basically to study it more in non-human
primates like macaques and try to just kind of understand it more as a gene where it's expressed and
why it might play a role in endometriosis.

0:07:35.1 SC: Right, so does the protein have a role? Is the protein not being made correctly? All
those kinds of questions.

0:07:40.9 RF: Right.

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0:07:41.8 SC: Despite that this variant popped out from the study, it's not in every person who has
endometriosis, right?

0:07:47.9 RF: They really found this associated with what's called stage three or stage four
endometriosis, but definitely not everybody who had endometriosis in this study showed that they
have this variant, and also it could potentially pop up in people who don't have endometriosis.
Endometriosis is still a really complex and mysterious disease that researchers are really just
starting to dig into and learn about. So, this is one gene it's one piece of the puzzle but it's not the
whole picture yet.

0:08:30.0 SC: Thank you so much, Rachel.

0:08:31.8 RF: Yeah, thank you so much for having me.

0:08:34.1 SC: Rachel Fritts is a News intern for Science. You can find a link to the article we
discussed and a link to the related Science Translational Medicine paper at sciencemag.org/podcast.
Stay tuned for a chat with researcher Raphael Townshend about using deep learning to predict RNA
folding.

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0:09:00.0 SC: You may be familiar with protein folding. Proteins are made of chains of amino
acids and the sequence of these components affect how the chain folds, and once it does, you get a
working protein. You may not know that RNA can do the same thing. A lot like proteins, 3D folded
RNA has functions like catalyzing reactions or changing gene expression, even detecting small
molecules. But unlike proteins, RNA has fewer building blocks, just four basis versus 20 amino
acids. At the same time in the genome, there are a lot more RNAs coded for than proteins. Despite
it's importance, we know a lot less about how RNA folds into 3D structures. Raphael Townshend
and colleagues wrote about a machine learning approach to predict RNA folding this week in
Science. Hi Raphael?

0:09:50.5 Raphael Townshend: Hey Sarah, thanks for having me.

0:09:52.9 SC: Sure. So, why do we know so much more about protein folding than RNA folding?

0:09:57.1 RT: So, one simple answer to why we know so much more about protein folding really
than RNA folding is that the field as a whole has really focused a lot on the problem of protein
folding for a long time. There's been sort of this classical view that proteins are really the central
workhorse of the cell, which is definitely an accurate picture in many ways but only recently have
we really been starting to turn on to the fact that RNA does adopt well-defined 3D structures that
perform a wide range of interesting functions.

0:10:28.5 SC: And there's also this issue that proteins have relatives, I guess you would say, they
have sequence similarity across large classes?

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0:10:36.4 RT: Yes. So, there's definitely a lot of similarity between different kinds of proteins, and
there's a little bit of this sort of momentum effect going on as well, where once you get a few
protein structures you can use those to start modeling other protein structures through a process
known as homology modeling.

0:10:52.4 SC: In this paper, your team used a neural network for predicting RNA folding. And
instead of starting with a giant data set, tens of thousands of structures, you used 18 for input and
you didn't enter very many specifics about RNA structure as we know it. Why would you present so
little information? There is more out there, there are more structures out there, you could have said,
"Oh, if you see this sequence it forms a twist, if you see this sequence it's gonna have a hair pin."
Why did you withhold information as you were teaching this neural net how to make these
structures or how to predict these structures?

0:11:27.3 RT: Yeah, so there's really a sort of two parts to that answer. On the first hand, really
what we did is we sort of carefully selected the initial data set we trained on that contained various
common motifs seen within 3D RNA structure. So, there was a little bit of a careful amount of data
curation going on on the one end. The sort of other aspect of all of this is really this sort of key
assumption that ends up coming into play within various machine learning algorithms, which is
how many assumptions do you want to encode into your algorithm. Traditionally machine learning
when it is fairly data poor, when there aren't that many examples to train on, you wanna put a lot of
assumptions into the algorithm.

0:12:05.1 RT: So that essentially it can start making useful predictions without needing to look at
millions of examples. For example, for training self-driving cars, you need millions of images to
train an algorithm that can correctly detect pedestrians versus not. In this case, really, because the
data's fairly limited, you need to start being clever in terms of what assumptions you do build in, but
you don't wanna build in too many assumptions, because then you start sort of hampering the
algorithm really. And so, the assumptions that we did build in were sort of this knowledge of the
rules that physics obeys. A very simple one is really that if you rotate a molecule it's still the same
molecule, the laws of physics are invariant to rotations.

0:12:46.0 SC: You put in the atomic coordinates of all the atoms rather than... Then you didn't
actually say this is a base. Does that matter?

0:12:53.3 RT: That is a very interesting aspect. We definitely did not encode in the fact that we
were looking at specific bases, and really, this comes back to the fact that while the bases are
definitely a very useful unit of RNA structure to understand, at some high level really, you could
just instead have the algorithm re-derive which aspects of bases are important and which ones are
not relevant to the prediction of 3D RNA structure. And that's sort of the beauty of a lot of these
machine learning algorithms, is given enough data or the correct problem set up, it can re-derive
which pieces are important with RNA structure from scratch, in a way that if you direct the encoded
basis instead that certainly would be a useful piece of information, but it might not be exactly the
right piece of information.

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0:13:38.0 SC: Why is this called deep learning?

0:13:40.1 RT: So, that's really building off of the long history of machine learning at this point,
where early on there would be these machine learning algorithms such as support vector machines
or random forest or what have you with all sorts of fanciful names. Essentially, people would derive
high level features to represent their input data. For example, these bases or something like that, you
could imagine coming up with a bunch of individual pieces of RNA structure that you as an expert
in RNA structure might think are important, like base pairing, Watson-Crick base pairs versus non-
canonical base pairs, hydrogen bonding networks, all sorts of fun things and... Well, those things
are certainly useful, they essentially amount to educated guesses as to which things are really
driving RNA structure. Where deep learning comes into play is instead of deriving these high-level
features, you give it the most raw input possible, really just the atomic coordinates and then you
train multiple layers of a machine learning algorithm to drive on its own, which aspects of your
input data are the most relevant. And so that's really where the name deep learning comes from, is
you have this depth of machine learning being applied that can go from the rawest input data to the
final prediction you're interested in making all in one shot.

0:14:54.1 SC: How did these predictions fair? How did they compare with other approaches, either
the experimental approaches or with other computers or teams that have tried to predict RNA
structures?

0:15:06.5 RT: I wanna be very clear that the experimental methods are still the gold standard,
really. When you're evaluating on computational algorithm, you have to compare it's predictions to
something and these stated sort of like how well can you replicate the experimental data that you're
getting. Because if you can do that accurately, now you're talking about going from a year or a
month worth of a highly training graduate student's time to a couple hours or even less to predict a
single structure, which can be a real game changer if you get that correctly. In terms of being able to
compare to other computational methods, and this is part of what we're very excited about here, is
that we've seen that we're able to consistently outperform all other groups or teams working on this
problem on the prediction of RNA structure. And what's pretty exciting about this is we're sort of
seeing a similar trend to that that we've seen happen in the protein structure, protein folding land,
where there was sort of this slow gradual progress over the last several years based on the broader
academic community, but suddenly, once you started training the right sorts of machine learning
algorithms you have a bit of a breakthrough where suddenly you were getting double the
improvement that you expected over a year over your basis. And then a couple of years after that
the problem was essentially, depending on who you're talking to, could be considered solved at least
for single proteins.

0:16:25.6 SC: How would you say the status of the RNA folding prediction is now compared to
say, protein folding being almost solved we'll say?

0:16:35.2 RT: So, I definitely think that RNA structure prediction, RNA folding is further off than
protein structure prediction. The problem is most certainly not solved, and while our algorithm
definitely represents sort of a breakthrough in terms of the net change in ability to predict these
things, it's still far off from being able to always give you the correct answer. However, the part
that's pretty exciting about this is, I think this was a little bit what I was alluding to with the protein

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structure prediction problem, was that the progress in RNA structure prediction had been fairly
stagnant for the last decade or so. There was small improvements here and there, but what's sort of
interesting is some of our data that we're looking at is, it seems like we've had a little bit of a
breakthrough in terms of the net change in how well we're doing. And this was sort of similar to the
change that we saw in protein structure prediction two years ago, and so there's a sense that we
might be on the path to fully nailing this problem in fairly short order.

0:17:28.1 SC: There's also some additional gains in the machine learning side of things too, from
this research that you're talking about. If you're only doing atomic coordinates I can see it applying
to many different kinds of structures.

0:17:41.6 RT: Certainly, and that's definitely one of the aspects that we're very excited about. A
large part of the theme of my PhD was actually training machine learning methods that could be
applied to a wide range of different problems involving biomolecular structure. In fact, one line that
I've been saying for a long time sort of as an evangelist almost of this field, [chuckle] is machine
learning is classically succeeding computer vision where you have the Pixel. But it's also succeeded
in natural language processing where you have the character for things like Google Translator,
things like that. And really you should consider the atom as a sort of first class machine learning
data type, something that you can really train machine learning models on for a whole range of
different problems.

0:18:23.0 SC: Really interesting.

0:18:23.3 RT: The response that you could use it for screening new drugs, looking at DNA,
looking at interactions between different kinds of biomolecules, all sorts of things.

0:18:33.6 SC: Going back to RNA just for a moment here. What can we do with all this RNA
folding knowledge, say we get closer and closer to being able to predict them, we get tens of
thousands of new structures, how is that useful to the field?

0:18:47.6 RT: First of all, just from a fundamental biology perspective, our understanding of RNA
structure just generally is much less than that of protein. So, if you can fold many more RNA
structures or actually reason about the shapes they're taking on, that starts shining a lot more light
on the basic functioning of RNA. Another sort of direction that people have been excited about in
the last few years is that designing therapeutics that can target RNA directly, and this gives you a
way of tackling diseases that were previously un-drugable at the protein level.

0:19:23.5 SC: Are you able to learn more about how RNA folds -- the principles of it -- from this
process or are we kind of in the black-box phase right now?

0:19:31.9 RT: People have spent over a decade hand-designing energy functions for evaluating
RNA structure, and now we have this machine learning algorithm that's doing better. And so a very
natural question to ask is really, well, what is it learning. What is coming out of it. And so we
started doing some analysis in the paper where we see that certain very important aspects of RNA
structure sort of spontaneously emerging from what the algorithm has learned. You mentioned

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bases, that's something that is coming out of the algorithm, base pairing or hydrogen bonding or
things like that, these are all things that we are pretty excited to see, we're pretty naturally popping
out, the algorithm itself is just determining those were relevant. However, there's a sense that there
are things that are less classically well understood that the algorithm has learned, and we'd love to
be able to back out even more what those aspects are and potentially then go back and give the
RNA biologist fundamental insight into what drives RNA structure.

0:20:25.4 SC: Right? So finding motifs and then you can go all the way back to the DNA and see
them and then you can pick out other functions and where they are in the genome.

0:20:33.8 RT: Exactly.

0:20:34.5 SC: Very cool.

0:20:35.9 RT: Just as a point of clarification is definitely that's a very open area of research, how to
derive [chuckle] the principles from your learned algorithms. I like to refer back computer vision a
fair bit because it was sort of my home turf for a long time, but there's a sense that unlike in
computer vision where it's like you derive and then like, Okay, my algorithm has picked up...
There's cats in this YouTube video or something. If you can say, Oh, this specific motif in RNA
structure is really important. That's something that is just not known to us ahead of time, unlike the
fact that there's cats in YouTube videos.

0:21:09.7 SC: Yeah, it's pretty easy for you to double-check that they're seeing what you think
they're seeing rather than some invisible signature in the video file that the AI is clumping onto that
you are not aware of and is now somehow important to identifying cats.

0:21:26.3 RT: Exactly.

0:21:26.4 SC: Thank you, Raphael.

0:21:27.5 RT: Thank you so much for having me.

0:21:28.8 SC: Raphael Townshend has a PhD in Computer Science from Stanford University and is
founder and CEO of Atomic AI. You can find a link to the article we discussed at
sciencemag.org/podcast. Next, we have the latest in our series of book interviews on race and
science. This month, journalist and host, Angela Saini talks with author Lundy Braun about her
book on a medical device called The Spirometer.

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0:22:00.3 Angela Saini: Hello, I'm Angela Saini, science journalist and host of this series of books
podcast looking at science and race. This is Episode 2, and this month, I'm joined by Lundy Braun,
professor of medical science at Brown University. Her work focuses on the historical role of science
in the production of racial hierarchies. Her 2014 book, Breathing Race Into the Machine, explored
this question through the lens of a single medical apparatus. Still common today, the Spirometer,

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which is used to measure the movement of air into and out of the lungs, once described as a person's
vital capacity. On the surface, the Spirometer looks like a precision value-free device, it's just there
for taking measurements, but as Braun shows in certain hands from the 19th century onwards, it
also became a tool for reinforcing the myth that there were profound physical differences between
races on the inside. In fact, for decades, its data was used by scientists and physicians, mainly in the
US and South Africa, to claim that black patients had naturally weaker lung function.

0:23:13.3 AS: This led to what is known as race correction. Adjusting what is seen as biologically
normal for a patient depending on their race. The spirometer became one tool of this enterprise.
Braun writes, Race became invisibly entrenched in the hardware and software of the machine.
Lundy, thank you for being here. First of all, can you tell us a little about the history of the
spirometer and how it evolved into this gauge of human difference?

0:23:45.0 Lundy Braun: When I first read about the race correction of spirometry it was through
bio-medicine and it was in the newspaper. There was a big article in the Baltimore Sun and then it
was syndicated to my local paper. And I thought this was a little odd, but I had no context for
understanding it. There was a massive lawsuit going on and it was very, very contentious. So was
followed closely in the Baltimore Sun, the entire lawsuit for years and years and years. The lawsuit
was in general about compensation for all the damage that had been done to people mainly shipyard
workers around Baltimore, but not exclusively the damage to their lungs over their work life.

0:24:35.8 AS: So, Lundy just to fill listeners in here, in 1999, there was an American materials
company in Baltimore which had been accused of exposing workers to asbestos damaging their
lungs, and they brought race into this lawsuit. So as you explain in your book, the lawyers for this
company claimed that black workers should need a higher level of disability rating to qualify for a
claim because their lung function was naturally lower because of their race, and as you write, this
affected a lot of people.

0:25:05.7 LB: This one was, I think, 11,000 people were suing the industry. 1999 was the first time
that race correction was brought in to the debates.

0:25:17.3 AS: Why did that strike you as interesting, that race correction was being used in this
kind of way?

0:25:23.5 LB: Well it was really the language. I thought it was so weird, how could you correct for
race? I had no idea it had a history, none. And I went to a good friend who's an occupational
physician, he gave me a whole stack of papers all highlighted to look at, and he said, "Yeah, we
race correct." This was normal within the field with very varied level, only occasional contestation,
but the American Thoracic Society and the US government actually for cotton workers mandated
race correction.

0:26:00.8 AS: So this is a very real and relatively recent phenomenon that race correction meant
that workers who are being exposed to damaging chemicals like asbestos, were being denied the
same levels of compensation or even the possibility of compensation because they were seen to be
racially different. And in your book, what you do is you go into the history of this. So how did the

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spirometer then come into this picture?

0:26:27.0 LB: The appeal to the spirometer was that it gave numbers. And what I think it's actually
important to see is that this is the science. It's being used, absolutely, but the social is shaping the
science, which is what it always does. Scientists are part of the social world, and they're gonna
bring the social world with all the prejudices that exist into their science. I think what's interesting
about the spirometer and lung capacity is, why didn't it get questioned more. As I've written, the
only major people to question it was two leading black intellectuals WEB Du Bois from sociology,
but you couldn't pin him down in terms of his intellectual pursuits, and then Kelly Miller, who's a
mathematician, N.V Ball, a black physician in the 19th century, and then there was nothing.

0:27:32.0 AS: But among those people were, as you mentioned, the Howard University
mathematician, Kelly Miller. What were his arguments then? What argument did Miller make for
the differences that were being seen with the spirometer?

0:27:43.8 LB: So both Miller and Du Bois writing at the same time, made an argument for social
conditions to reduce it. Miller produced the pamphlet, and it was addressed specifically to Frederick
Hoffman's book, Race Traits and Tendencies of the American Negro, and it's a vicious, vicious
book. He was statistician for Prudential Life Insurance Company for decades. Both Du Bois and
Kelly Miller saw this book as important enough... Was reviewed in science, etcetera, to issue a very
transient critic. But to boil it down, they both argued in different ways that social conditions
produced poor lung capacity.

0:28:31.5 AS: And this is known these days in medicine as a social determinant of health. So how
you live, the job you do, the environment you live in, how you're treated, which as we are starting to
understand in medicine, can all have a very profound impact on individual health, particularly
among those from low socioeconomic groups, immigrants and minorities.

0:28:53.3 LB: I think this is an important moment. I think the questioning of algorithms as they get
introduced, they're questioned pretty quickly now. And there is a major social determinant
movement. I do think what we have to be careful of is to think that a determinant produces poor
lung capacity. So you see this in the literature, I use it myself a lot, but we have to think about how
conditions are not necessarily measurable. So we wanna be attuned to both what's measurable and
measure it and demonstrate that. But I think the real challenge is how to keep our minds focused on
what's not measurable. And that's what carried me through the project is because I reviewed all the
scientific evidence and produced a paper on that. Only 17% of the papers I reviewed defined race,
and I've had scientists say, "Well, you just know it when you see it," or when I would question in a
clinic, "How did you know what race somebody was?" The response was uncomfortable, but said,
"I just eyeball it." So I guess I would say there's more discomfort whether we're gonna really be
able to shake the conceptual foundations is what's important right now.

0:30:19.8 AS: So scientists and physicians have for so long been observing differences, ascribing
them to race, but then not recognizing that race is not a biological grouping. They're not looking to
complex social factors to explain these gaps. Why do you think it has been so important to them to
believe that these differences must be innate, that people are born with them. Why have they clung
to this idea?

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0:30:44.8 LB: I think scientists were people of their time. In the 19th century, they certainly were
very involved in categorizing or producing the category of "Mulatto". They were heavily involved
in census categories, etcetera. So I think the question is, why couldn't scientists see through this?
But we're reproducing it over and over. I'm sure you know there's a lot of debate about race
correction to kidney function, race correction of fetal growth factors, concussion, etcetera. It just is
on and on. Some of it is under the rubric of social justice.

0:31:29.8 AS: Yeah. But there is that argument there that I have seen, ethnic minority and black
physicians make that we need to understand the differences in order to help people in different
ways. And why do you think that's a dangerous road to go down?

0:31:44.3 LB: First of all, assumes difference, and the difference is often based on really small
sample sizes; we see this with COVID, things are in the newspaper with the sample sizes of the
eight, it's certainly incredible. And that is true historically, but what's problematic for me is that they
view difference as innate. So if you view black difference and white difference as biological, then
you're not gonna look at the environment, and I think for lung capacity, what's been overlooked
profoundly, is pollution. Even though we have lots of evidence about pollution, we know where
minority populations live in the US, and this is true worldwide. I have more exposure to pollution,
and yet those two aren't brought together, and I think in the idea of innate difference that we have
now measured for centuries is hard to overcome.

0:32:48.3 AS: So even to this day?

0:32:50.4 LB: Even to this day.

0:32:51.8 AS: It is still routine for medical researchers and physicians to use these kind of race
corrections or to assume innate differences. We know what was motivating scientists in the 19th
century, which is the kind of politics of slavery and segregation at the time. What is motivating
them now?

0:33:09.4 LB: I mean, many people will say social justice. I think one point I wanna make is "race
correction" or adjusting for race looks different now than it did in 1974 when the correction factor
was introduced. Now, people are using population standards, but if you take those population
averages and look at them, they're basically... They're hierarchical with white people on top. So you
still have white people having the best lung capacity and the idea of innate difference has not been
jettisoned at this point. The 'why' is an important question to keep pushing on, and I have thought
about it for years and years, and I think it's very hard for scientists to get out of the society in which
they live, and you wouldn't see it popping up everywhere; algorithms with racial difference
embedded in them, if there wasn't an idea that racial difference was deep, biological, and
measurable.

0:34:19.0 AS: Really at the heart of your book is this idea that just because something can be
measured, that doesn't mean observations are purely objective or value-free or free of politics. What
are the lessons in that history for modern day researchers then?

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0:34:36.4 LB: One of the important lessons I would take from this work... So I had been trained in
science, I had also been trained in Humanities, and then did a fellowship with NSF that allowed me
to take a year off and actually look into this from other perspectives. I think my interdisciplinary
background was extraordinarily helpful, and I do think that we need to build interdisciplinary
thinking into the sciences, not just some quick and dirty science, but something that looks at the
debates that have gone on in science, what is at stake in those debates, and that is what held my
interest for about 14 years or more.

0:35:26.0 AS: Thank you, Lundy Braun for your time, and thank you a time for listening. I'm
Angela Saini, and I hope you'll join me for the next episode in the series in which I'll be
interviewing Alondra Nelson, author of "The Social Life of DNA", that'll be one month from now.

0:35:43.7 SC: And that concludes this edition of the Science Podcast. If you have any comments or
suggestions for the show, write to us at sciencepodcast@aaas.org. You can listen to the show on the
science website at sciencemag.org/podcast. On the site, you'll find links to the research and news
discussed in the episode. And of course, you can subscribe anywhere you get your podcast. The
show was edited and produced by Sarah Crespi with production help from Podigy, Meagan
Cantwell and Joel Goldberg. Transcripts are by Scribie, and Jeffrey Cook composed the music. On
behalf of Science Magazine and its publisher, AAAS, thanks for joining us.

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