SciencePodcast_210730

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0:00:05.5 Sarah Crespi: Welcome to the Science Podcast for July 30th, 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, staff writer Jennifer Couzin-Frankel discusses ongoing research into the
paradox of so-called healthy obesity. Next, researcher Colin Dayan talks about approaches to
slowing and maybe one day preventing type 1 diabetes in children. Finally, in the first installment
of our series of monthly book segments on science and race, author Samuel Redman discusses his
book Bone Rooms: From Scientific Racism to Human Prehistory with guest host Angela Saini.

0:00:49.8 SC: Now we have staff writer Jennifer Couzin-Frankel. She wrote a feature story this
week on the complex relationship between obesity and health. Hi, Jennifer.

0:00:58.8 Jennifer Couzin-Frankel: Hi, thanks for having me.

0:01:01.4 SC: I'm happy to have you and I'm going to try to be very careful about how I describe
what's going on here. This is a very tricky topic. Was this difficult in general to research and write
about?

0:01:11.5 JC: It was. I think the language we use is very important and very weighted, no pun
intended...

0:01:19.3 SC: Oh, boy.

0:01:20.1 JC: Here, and there's really kind of a push and pull from both ends of the spectrum. So
there are people who would say that obesity is generally unhealthy, and then there are other people
who would say, that's really not true, we've kind of adopted that idea, but it's not correct. So my
story is trying to walk the line here and do what I always try to do, which is to look at the evidence
as best I can.

0:01:44.0 SC: And the first piece of evidence you present in your story is a really great opener.
These are the most overweight mice that have ever been bred, I guess. They aren't necessarily
metabolically unhealthy.

0:01:57.8 JC: Yeah, so these were mice created by a researcher who normally studies diabetes at
the University of Texas Southwestern Medical Center, and he created these mice. There was one set
of parents who lacked the hormone leptin. Leptin is a hormone that's an appetite suppressant that
essentially signals to us when it's time to stop eating when we feel full, and the other parents of
these mice over-produced another hormone called adiponectin, which is churned out by fat cells and
is thought to support metabolic health, protecting against certain diseases like type 2 diabetes.

0:02:34.3 JC: So essentially, these mice didn't have leptin, they didn't know when to stop eating,
but then they did make this other beneficial hormone adiponectin, and the mouse pups kind of
combined the traits of their parents, they ate non-stop, but unlike other leptin-deficient mice, and
also people, there are people who cannot make leptin, they did not have metabolic abnormalities,

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they had normal cholesterol, they had healthy blood glucose, they didn't end up with type 2
diabetes.

0:03:00.0 SC: But they were over 100 grams.

0:03:03.0 JC: Yes, so these mice weighed about 130 grams, which doesn't sound like a whole lot,
but for a mouse, that's the equivalent of about 600 pounds in a person, so they were really, really
obese.

0:03:16.3 SC: This is where we start to get to this idea of metabolically healthy obesity. The mice
are large, they were eating out of control, but some of these markers for issues with cholesterol and
glucose, they were within healthy ranges.

0:03:30.4 JC: Yeah, they really didn't have the risk factors that obesity is thought to increase risk of
getting.

0:03:38.0 SC: And the story here is not just, oh, well, if you have that hormone that's protective,
that's associated with that, then you're all good. The researchers that you talk about are really trying
to figure out what uncouples weight and health status, what are some of these differentiating
factors. Can you give some examples of what they're looking at?

0:03:57.1 JC: Yeah, and so first, you know, I'd say it's really important to mention that just as with
any other biologic difference or condition, there's a lot of variability here. So we know that there are
people who are overweight or obese, obese is defined as having a body mass index above 30 and
overweight is 25 to 30. So there are people who are... Particularly, who are obese and who do look
metabolically healthy, and then there might be somebody who's lean who is not metabolically
healthy. Obviously, there are a lot of individual differences, but when we talk about obesity, as one
researcher said to me, there are different subtypes of obesity, and some of them we kinda
understand and some of them we don't.

0:04:33.5 JC: So one of the differences is how one carries one's fat. There are a couple of different
places where fat can be stored in the body, and one is subcutaneous, meaning under the skin, so
there you would have fat under the kind of like the thighs, the upper arms, the back side, and the
other area's visceral, which is kind of behind the muscles in the abdomen. You might see someone
with a bigger belly and that person might have excess visceral fat. And what scientists know from
having studied this is that visceral fat tends to be associated with a much higher risk of different
metabolic conditions or markers that aren't healthy than subcutaneous fat. And subcutaneous fat can
be healthy too, we need fat, so if you don't have fat, you've got a problem, and storing it
subcutaneously is considered healthy. That's a good storage space for fat.

0:05:25.8 SC: One of the debates that you touch on in your story is this definition, if we were going
to make one, of someone who has metabolically healthy obesity, what are the different camps, how
might this be staked out?

0:05:40.9 JC: Yeah, so of course, if we want to study something and also use it in the clinic, we

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need to have a definition. And right now, there is not a definition that's universal or universally
agreed upon for metabolically healthy obesity. One definition that's been not uncommon is
essentially the absence of obvious metabolic concerns, in particular, the absence of something
called metabolic syndrome, which is a constellation of risk factors that increases one's risk of
cardiovascular disease and diabetes.

0:06:10.0 JC: And lean people can have metabolic syndrome, people who are obese can have it,
and some people say, if you don't have metabolic syndrome and you are obese, you're metabolically
healthy. Other people may question that because they say, well, you can not have metabolic
syndrome, but you can still have markers of ill health.

0:06:29.9 SC: You can still check some of the boxes, but not all the boxes.

0:06:33.7 JC: So you could have high blood sugar, for example, but not have metabolic syndrome.
Another question is, what's the goal here? Is the goal to say that somebody who's metabolically
healthy and who is obese doesn't die any sooner than somebody who is metabolically healthy and
lean? There was another definition recently proposed that looked really just at mortality across
different weight classes, and proposed another definition of metabolically healthy obesity based on
that, saying that this is what we care about. And so let's define it on that basis.

0:07:05.4 SC: Well, the first two you talked about, whether or not metabolic syndrome is present or
whether one or two parts of that are present, they create a much different landscape of obesity. So
for example, in the United States, where 40% of adults are considered obese, what percentage of
them would be metabolically healthy depends on which definition, and it's a very big difference.

0:07:27.0 JC: Yeah, it's a huge range. And depending on your definition, and there have been a lot
of different studies on this, I would say anywhere from about 5% to more than half of people with
obesity would be considered metabolically healthy. So that's such a difference.

0:07:41.0 SC: Another quote that you have in the article says, "Maybe metabolically healthy
obesity exists, but it could just be a stop along the way to having problems later."

0:07:52.5 JC: Yeah. And that was something that I think researchers struggle with how to think
about that. So there are a few features that make one more likely to be metabolically healthy if one
has obesity. One is being a woman. It's more common in women to be metabolically healthy if
obese. Another is being younger. The third is having a BMI under 35. But the piece about being
younger is really important. So if you look at cohorts of adults of different ages, you might see that
a higher percentage who are younger are metabolically healthy, if they are obese, or if they're lean,
for that matter. All of us are more likely to develop metabolic issues as we get older.

0:08:31.0 JC: So researchers might say well, maybe you're metabolically healthy now at 40 with a
BMI of 35. But what's going to happen to you at 60? Are you going to be metabolically unhealthy?
But someone else might say well, but if you have an extra 20 years of not being metabolically
unhealthy, that's pretty beneficial, versus somebody who has, say, type 2 diabetes when they're 40.
That's a big difference. So there's a debate there. But I think there is agreement to some extent that

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if you're metabolically healthy right now, that is important.

0:09:01.8 SC: Right. There are a lot of problems for people carrying excess weight outside of
metabolism, like cancer or joint pain, things like that.

0:09:09.9 JC: My story is really focused on metabolic health. And I think it is important to
remember that there are other health concerns associated with obesity. Sleep apnea's another one
that's pretty common, particularly in people who really struggle with obesity. But yes, there's a
higher risk of cancer, there's a higher risk of osteoarthritis and so on. So metabolism doctors and
researchers will say that's not the only concern. But it's a big one.

0:09:35.0 SC: Despite obesity's links with metabolic issues and other health concerns, focusing on
weight loss as treatment might not be the best idea.

0:09:44.1 JC: Well, I think there's disagreement in this field, and there is disagreement among
advocates who worry about discrimination and other concerns, and then researchers and doctors.
One thing that people really do agree on is that we do not do a good job in general of helping people
who have obesity. And studies have shown that it's really tough to keep off weight that's lost.
Weight can be lost. But then over one year, two years, five years, not necessarily all of that weight,
but a lot of that weight is likely to be regained just statistically, if you're looking across a
population.

0:10:18.7 JC: Physicians I've talked to said they have seen so many people really struggle with this
and lose and regain. And it's just so, so difficult in so many ways, and it's not really medically
helpful. So one question is, do we need to recalibrate or reframe how we treat people with obesity in
a medical setting? Right now, we look at someone and we see their weight. And of course that's
true, whether it's in medicine or just in general. But we don't see what's happening inside their body.
So we might see somebody who is carrying what looks like a lot of extra weight, but they might
have great cholesterol and great blood glucose and no type 2 diabetes.

0:10:55.1 JC: Then there might be someone who is not as overweight but does have those
problems. And so if we're talking about weight loss, and people might want to lose weight for all
sorts of reasons. But if we're talking about weight loss, we might want to consider success based on
metrics beyond just the number of pounds lost or the percentage of body weight lost. You know,
with somebody who's starting with high blood glucose, improving that by losing some weight. And
that can be, I think, really helpful.

0:11:23.0 SC: Right. So if the focus of metabolic health are these biomarkers, then should those
biomarkers be the focus of treatment or someone's plan to get healthier?

0:11:33.9 JC: Yeah, definitely. And I think some physicians probably do that already. And then
others don't. I wouldn't say nobody is focused on that. But there is some question about does this
need to permeate medical care a little more, and could that be helpful in a number of different ways.

0:11:49.8 SC: There's also some problems where if a person goes to the doctor and they have a

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health complaint, a lot of doctors focus on weight loss and forget about the health complaint that
got them there in the first place.

0:12:01.3 JC: That's something that I heard about in reporting this story. They may forget the
health complaint, or they may say that the only way to solve the health complaint is by losing
weight. And that may be possibly one way to find improvement, but it may not be the only way.
And then there are people who have obesity who may just not go to the doctor because they know
that this is what's going to happen, and they don't want to deal with that. So I think it is a real
problem right now.

0:12:27.2 SC: As scientists tease apart the mechanisms at work here, what are doctors supposed to
do today when the patient comes in and yes, they want to be healthy?

0:12:35.9 JC: One point that several people I spoke with made to me, and they treat patients
themselves, is the importance of exercise, or movement as some like to call it, 'cause exercise can
sound a little intimidating. And really moving around more, going for hikes or walks, doing yoga,
swimming, any number of different forms of movement or exercise can be hugely beneficial
metabolically. It can improve the body's response to insulin, it can help clear fat from the liver, and
that can happen even without someone losing much weight.

0:13:06.6 JC: So a number of people I spoke with felt that that's something they advise, and they
also feel like it's more attainable, doable for a lot of people, if we think of ways to make it fit what
they are comfortable with, and medically it can be really beneficial and psychologically beneficial
potentially, too, for all of us, not just for people with obesity.

0:13:25.3 SC: Thank you, Jennifer.

0:13:27.1 JC: Thank you.

0:13:28.2 SC: Jennifer Couzin-Frankel is a staff writer for Science. You can find a link to the news
story we discussed at sciencemag.org/podcast. Stay tuned for a chat with researcher Colin Diane
about preventing type 1 diabetes in childhood.

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0:13:48.1 SC: This year marks the hundredth anniversary of the discovery of insulin. Up until
1921, a type 1 diabetes diagnosis was a death sentence. By the beginning of 1922, insulin was being
administered, this time to a 14-year-old boy in Canada. Today, T1D has become a chronic disease.
This week, as part of a package on type 1 diabetes, Colin Dayan and colleagues write a review on
preventing type 1 diabetes in childhood. Hi, Colin.

0:14:15.5 Colin Dayan: Hi.

0:14:17.1 SC: Type 1 diabetes is an autoimmune disease. Can you describe how we get from
autoimmune disease to not enough insulin to diabetes?

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0:14:26.7 CD: An autoimmune disease means that the immune process is attacking parts of our
own body, and a very specific part, because in type 1 diabetes, the only cell that's targeted is the
beta cell that makes insulin. It attacks the beta cells, there are antibodies, but actually the damage to
the beta cells is probably predominantly due to T lymphocytes or white blood cells that crawl into
the islet and then kill the beta cell.

0:14:54.0 SC: Now, in the past, the detection of this disease came at a point when many of the beta
cells had already been lost, typically you write about 12 years of age. But there is a way to detect it
earlier. What are some of the ways that researchers are looking to detect type 1 diabetes before it's
progressed so far?

0:15:15.5 CD: So we seem to be able to lose about 80% of our ability to make insulin before the
glucose level goes up, but we can detect the autoimmune process, and the most sensitive way we do
that now is with detecting antibodies to the beta cells, so proteins within the beta cell. So these are
all molecules, proteins that are present only in the beta cell or almost only in the beta cell. So the
presence of high titers of these antibodies suggest that you do have an autoimmune process going.
There are other approaches you can take. Do you remember that the T cell response is what actually
damages the cells. That's very tricky to measure, and people have tried a long time to measure T
cell responses in the blood. But a third approach is to look at genetics, because we can identify
people at high risk. That doesn't say you've got the disease, but it helps us to focus on the people
who are likely to get it.

0:16:05.8 SC: How early would it be possible to, say, find an antibody to one of the proteins that
would indicate that beta cells are going to be under attack at some point?

0:16:15.6 CD: You can potentially in the first year, probably the best time if you wanted to catch as
many people as possible is around the age of 3 years.

0:16:22.9 SC: Now, does it make sense to incorporate something like this into these population-
wide screens that we do of infants?

0:16:30.5 CD: So it does make sense, but it's a moving target. So if you were to measure it, for
example, in the UK, we think of this pre-school vaccination that's around the age of three-and-a-
half, if we do that, we will catch about 50% of all the children who are going to get type 1 diabetes
during childhood. We'll have missed the ones that are going to be diagnosed at the age of 1 or 2 or
3, and we'll miss some who haven't gotten their antibodies yet, so that's what I mean by a moving
target. You may have to do it at more than one time point.

0:17:01.9 SC: What are the benefits of knowing that type 1 diabetes is coming down the pike for a
kid?

0:17:08.2 CD: We realized that there are benefits in several different ways. So the first is to do with
the advantages of knowing early, and most children, and adults, actually, when they're diagnosed
with type 1 diabetes, are diagnosed pretty late, which means they have lost quite a lot of their

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insulin and they're beginning to get sick. And when you lose that last part of insulin, the blood
sugars go up pretty quickly, and then very soon you develop ketoacidosis, which is when there's so
little insulin around that it's not switching off the ketone-generating process. And then you could
become very acidotic, end up in intensive care, and in the UK, at least one child every year or every
two years dies in ketoacidosis at the first diagnosis because it was picked up too late.

0:17:49.4 SC: Wow.

0:17:50.0 CD: So this is a dangerous game to play. If you pick it up early before the blood sugars
have begun to rise, those people don't get ketoacidosis, and instead of a rate of around 30% of
ketoacidosis of presentation, it drops to less than 5%. But I think there's a second really important
advantage that maybe people who haven't dealt at lot with type 1 diabetes don't quite get. So when
you're diagnosed with type 1 diabetes, it means you're going to take insulin for the rest of your life.
This is not just a tablet you have to swallow every day. Insulin is a drug you have to change every
day, according to exercise, according to your carbohydrate intake, according to other stresses that
are happening. You have to monitor your sugar many times a day and make those adjustments.

0:18:30.3 CD: It is the most difficult drug we ask people to take, and there's a huge amount to
learn. We often have courses lasting five days to teach people how to adjust their insulin. Now,
imagine trying to learn that when you're in intensive care, when you've just had this shock of a
diagnosis.

0:18:47.3 SC: Or when you're 8.

0:18:48.6 CD: Or when you're 8 years old, exactly. Whereas if you're told a couple of years before
it's coming, we know that when you're one year out we'll be able to pick that up and we can start
having classes, you can start talking to other people, you can start beginning to think about it. But
what that does is you get over the shock of the diagnosis and you come to a calmer place where you
can take all of this on board in a much more relaxed way. And we believe that actually sets you up
for the disease better for the rest of your life.

0:19:16.0 SC: There's also the idea of putting off the destruction, slowing things down through
treatments. Can you talk about some of the approaches where you interfere with this progression of
the autoimmune part of this disease?

0:19:31.4 CD: So getting screened is good. But once you have been screened, I've mentioned the
advantages of knowing early, but you obviously would prefer to have an intervention. So in 2019
was the first report of a monoclonal antibody against T cells called teplizumab, that transiently
depleted T cells and then allowed them to repopulate and, remarkably, that resulted in a delay in
onset of type 1 diabetes by two, in fact, three years on average. And some of those people haven't
even got known diabetes yet. Clearly, that tells us that the immune system is the key player here,
and targeting the immune system is going to be beneficial.

0:20:09.7 CD: And almost queueing up behind it, like planes trying to land on a runway, are
several other immune interventions, which have already shown benefit. Now, when I say they've

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shown benefit, they were generally tested in new onset cases. So we've mentioned that when you're
newly diagnosed, you have about 20% of your beta cells left, you can give immune interventions at
that point and show that the remaining part of your insulin is lost more slowly. And there's, I'd say,
at least six treatments that have shown benefits at that time.

0:20:39.2 SC: We're talking about delaying onset, but not necessarily completely averting the
onset. That's why you say preventing childhood type 1 diabetes.

0:20:49.2 CD: Correct. And we're trying to think of a staged approach into this. So many of the
other autoimmune diseases routinely use immune therapies, and I should just say we're not talking
about the kind of a immune therapy that's used in transplantation, this is not destructive therapy that
completely disables your immune system, it's the kind that's used routinely in inflammatory bowel
disease, Crohn's disease, rheumatoid arthritis, juvenile, idiopathic arthritis from age of 2 years old,
in psoriasis, so skin disease. These have been used for over 10 years, in the case of rheumatoid
arthritis for 20 years.

0:21:22.0 CD: And what they've learnt in rheumatoid arthritis is that one drug works for a while
and then maybe it doesn't work, so now you need to switch to another and then another and another,
and doing this, what they've found is that you don't get the long-term destruction that people used to
see of joints. And we can do the same thing in type 1 diabetes. By just knowing where you are, we
can keep putting off the time that you need insulin.

0:21:47.3 SC: Right. And there are a lot of benefits in the long term to putting off that time to when
you need insulin.

0:21:53.0 CD: Yeah, absolutely. With insulin comes hypoglycemia, with insulin comes all the
carbohydrate counting, all the drug adjustment. If you don't need insulin, that means that your
sugars are controlled by your own body. So here's the advantages, you don't need to think about
insulin, don't need to take it, you have pretty much normal blood sugar control with no effort. And
the longer that you have good blood sugars, the more you reduce the risk of the long-term
complications of diabetes, so blindness, kidney failure, foot problems and so on. And we do know
that early control is money in the bank, so it's actually better to have good control at the beginning
than after 30 years, because it gives you advantages that last 20 or 30 years beyond that.

0:22:37.8 SC: The wild swings in sugar is bad for you, especially early.

0:22:41.4 CD: Yes. The reason that this is such a challenge is that insulin is such a dynamic
hormone that we cannot mimic it, even with the advanced close-loop therapies. They try, but they
don't quite manage what the body can do. Currently, less than 30% of people manage to control
their blood sugar to target levels, and that doesn't mean completely normal, that's to the target that's
been set. And even those who do, it's a huge effort for them and a worry about hypoglycemia day
in, day out. So removing a lot of that. And particularly, if you think about childhood, if you think
about a child of 8, 9, 10 years old, they just want to go to school, they want to play, they want to run
around, they want to do exercise, they don't want to be thinking about oh, they have to have a jab
here and a glucose check over there.

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0:23:26.5 CD: And their parents also don't want to be worrying about hypoglycemia in the night
and are they missing something, what's happening when they go to camp. All of that gets swept
away for the period that you don't need insulin.

0:23:36.5 SC: And the next step that might be on the map here would be to avert this altogether, to
do those early detections and to stop the disease in its tracks. It's further away, but can you talk
about some of the options that are being considered for that approach?

0:23:51.8 CD: The drugs that I've talked about that are widely used are selective, but they're not
absolutely beta cell-specific, and what you'd ideally want is just to affect the immune response to
those beta cells, the bad one, and leave the whole of the rest of the immune system, that would be
the dream. So one way of thinking about it is that we do know that there are regulatory T cells. So
as well as bad guys, destructive cytotoxic T cells, there are also ones that protect us. And they're
present in everybody, and that's how you stop autoimmune diseases. So if you could give what I
sometimes call an un-vaccine, you could give a protein from the beta cell in such a way that you
expand the regulatory cells, not the way we normally do, which is to expand the destructive cells
against the foreign microbe or infection, then that would be it, that would protect you, you could
have booster jabs, the kind of thing we do for COVID-19, then that would keep things going
without negative impact on the rest of your immune system.

0:24:50.0 SC: Kind of saying, here is a piece of yourself, instead of saying here's a foreign invader
you should attack.

0:24:54.7 CD: Correct. We don't know how that platform would look, but there's a lot of people
working in that technology. And those of us who work in the immune system know that it's actually
much tougher to stop an immune process than to prevent it happening in the first place. So that once
the immune system gets its teeth into things, it's got strong memory and it keeps trying to go back to
that, that's how vaccination works so effectively. So why can't we avert it in the first place. And to
give you a sense of why that might work in identical twins, there's a concordance for about 50%.
That means that in 50% of cases, the identical twin never get type 1 diabetes, even though they're
genetically identical.

0:25:36.7 CD: So all of these things are telling us that there are things in the environment that are
beyond genetics that influence whether you go from that stack of genetic risk into actually getting
autoimmunity ever, and that's what we want to try and target, and the belief is that the microbiome
plays a large part there.

0:25:54.8 SC: Yeah, I was really surprised to read, especially at the end of the review, that we're
suddenly talking about the microbiome. How could that be involved in the development of type 1
diabetes?

0:26:05.1 CD: From the moment that you are born, your body is colonized, in the gut, from the
skin, and so many parts of your body have microbes that live day in, day out. And you can't spend
all your time trying to destroy them, they're part of you. The immune system has to learn to deal

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with that. And so you can imagine, they shape your immune system, they punch holes in the
immune system by identifying things that you should not respond to, that you then begin to treat
almost as self. And that can make you vulnerable, but it can also affect what happens in terms of
autoimmunity, if you're responding to bugs that look a little bit like your beta cell. So that's where
the idea emerged, there's absolutely no doubt that your microbiome affects the development of your
immune system.

0:26:51.8 SC: What's the evidence that this is linked with T1D?

0:26:56.4 CD: So what we do know is that there are certain bacteria, bifidobacteria, it's a peak that
happens between about 6 and 12 months of age, and that peak seems to be associated with a higher
risk of people going on to get the autoantibodies and then go on to developing type 1 diabetes. So
the idea is that if we could actually change how that microbiome is developed, particularly avoid
the peak that some people seem to get of a particular bug, that actually that might shape the immune
system, get it into much better shape in a form that it will resist any attempts of the environment to
try and induce autoimmunity to the beta cells.

0:27:34.2 SC: In the far off distant future, we'll be shaping the immune systems of infants through
the bacteria that live in their gut and on their skin.

0:27:41.7 CD: Exactly right. People are getting more and more scientific about this and identifying
particular probiotics, particular mixtures of bacteria that live in your gut that you could populate.
And the thought is that if you do it pretty much from birth, you can establish a stable, different
microbiome, and that that would then set you up to avoid things in the future. Now, you could do
that to every child, but we have ways of identifying the people particularly at risk, and so we can
start the probiotic from birth, particularly covering a period probably in the first 12 months when it's
critical how the microbiome is formed, and thereby reduce substantially their chance of getting type
1 diabetes.

0:28:25.9 CD: So you can start with the microbiome, and if that reduces incidence by 50%, that's a
good thing, and then as they seroconvert, that's a point at which we can think about, maybe there's
antigen-specific interventions, and then later on we can think about teplizumab, those drugs that are
around now. And then, we might have to give a few people insulin at the end of the day, but I often
say to my medical students, I'd like it to be that when we see a diagnosis of type 1 diabetes in
childhood it's a real rarity, the doctors gather around, they go, "Look at this, that is so unusual."
That's what I'd like to see.

0:28:58.5 SC: That would be amazing. Alright, thank you so much, Colin.

0:29:03.8 CD: Great.

0:29:03.9 SC: Colin Dayan is a Professor of Clinical Diabetes and Metabolism at Cardiff
University and Senior Clinical Researcher at the Wellcome Centre For Human Genetics at the
University of Oxford. You can find a link to the review we discussed and the rest of the special
issue on type 1 diabetes at sciencemag.org/podcast.

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0:29:21.1 SC: Don't miss the first in our series of six book segments on the intersection of science
and race. This month, host Angela Saini talks with Samuel Redman about his book, Bone Rooms:
From Scientific Racism to Human Prehistory.

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0:29:40.4 Angela Saini: Hello and welcome. I'm Angela Saini, science journalist, author and host
of this series of books podcasts. This is the first of six monthly episodes, each looking at a different
book, exploring facets of the fraught subject of science and race.

0:29:57.1 AS: Today, I'm joined by Samuel Redman, Associate Professor of History at the
University of Massachusetts Amherst. Before graduate school, Redman worked at the Field
Museum of Natural History, among others, and it was during this time that he became interested in
the collection and interpretation of human remains. In 2016, he published Bone Rooms: From
Scientific Racism to Human Prehistory in Museums, looking at the work of American museums,
including the Smithsonian, to tell the human story through skeletons.

0:30:30.7 AS: In the book, he writes: "The act of organizing bones on museum shelves represented
something of a physical articulation of attempts to create a science to classifying humankind." As
he shows, having something to measure and quantify doesn't mean that your research is apolitical.

0:30:50.2 AS: So Samuel, thanks so much for joining me. First of all, for those not familiar with
this concept, what are these bone rooms that you mention in the title of your book?

0:31:00.7 Samuel Redman: When I was a new intern looking around for missing collections, I first
heard the term bone rooms, and I really didn't know what that was or what that meant. But it turns
out there are these designated rooms or spaces within museum collections that hold hundreds and in
many cases thousands of human remains that represent the legacy of collecting and science around
the human body at natural history museums and museums of anthropology. If we go back to the
19th century, the world of research was quite a bit different than it was today. Colleges and
universities, at least in the United States at that time, were still pretty sleepy places where people
were doing things like memorizing, rote learning of Greek and Latin, training how to be priests and
things of that nature.

0:31:48.2 SR: Museums, on the other hand, were some of the most cutting edge research spaces in
the world. When James Smithson gave his gift of his inheritance to the young United States, there
was a huge debate about what should be done with that money. Should they create a national
university? Should they create an astrological research institute or study astronomy? And what they
landed on was a museum, because museums in that era were considered some of the most important
research engines. So if we're thinking about the construction of ideas about race and humanity and
human anatomy, it became really interesting to me not just to look at some of these intellectual texts
or these sort of treatises that people would put out, but to think about the physical evidence that they
were trying to gather to match those things or to support the different ideas that they had. And
ultimately many of these things ended up in spaces like bone rooms.

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0:32:44.6 AS: What I found fascinating about your book is just how central these skeletons became
to the scientific understanding of race. And it wasn't as though the skeletons came first, and then the
idea of race emerged. The idea of race was there, and then the skeletons kind of reinforced it. Can
you explain how that happened?

0:33:02.6 SR: So understanding those ideas, common ideas that were emergent in the 19th century,
and in some ways connected to things like debates about slavery and justifications for enslavement
of human beings from Africa and elsewhere around the world, it became this really complicated
project that was multi-faceted. People disagreed about the nature of these things. But importantly,
and I think that this speaks to your question, bones were seen as a fairly stable data point, or a way
to render these questions with some stability. So, measuring people out in the field, it proves
cumbersome and unwieldy. Human bones are actually pretty stable, in that you can take a human
skull and if kept under the right conditions, will more or less look like the same human skull 50 or
100 years later.

0:33:53.1 SR: That became a really important tool for people who were utilizing the science of the
era to try to unpack ideas about racial difference. This is deeply imbued with what we now rightly
consider racist science. I also think that there are some interesting fundamental questions that are
still pertinent and relevant to us today, that if we try to look without these horrible racist actions and
connections to scientific racism, we still wonder why people look different from different
continents. We still wonder what potentially are there differences between the sexes, and ideas
about gender are really hotly contested in our public discourse today.

0:34:38.0 SR: All of those ideas in some ways had some connection back to the legacy of building
these massive bone rooms. It wasn't just this esoteric thing that people were doing on the side. I
argue that it becomes really central to all of these debates, and if you look at newspapers and
magazines and major exhibitions, not just museum records, you can see how this was popularly
debated and thought about and attractive in some ways to people in the United States.

0:35:08.3 AS: You could say that it would have been possible for people to look at skeletons and
study human difference, or you can study the idea of race in a neutral way, but embedded within all
of this was not just classification, there was also hierarchy, wasn't there?

0:35:23.5 SR: Without a doubt. One of the major scientists right off the bat that I quote says
something like, "I think that American Indians should be ascribed a lower place on human hierarchy
than Euro-Americans." Another collector that I look at, Aleš Hrdlička, who's a complicated, nasty
guy, he says at one point that African-Americans, in his view, are capable of 80% of what the
typical Euro-American is capable of. It is intensely linked up to racialist and indeed racist ideas of
the era that were quite common. But in some meaningful ways, those ideas motivated the actions of
collecting.

0:36:08.5 AS: I was just going to say, these people that you mention are not marginal figures either.
They are central to science and museums.

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0:36:16.0 SR: Without a doubt. I think there are two things happening there that I became really
interested in bone rooms. But one of the things I became interested in, and this is a problem I argue
with a lot of history of science, is that sometimes we could latch on to these major figures in the
story and think about individuals that listeners may have heard of, like Samuel George Morton, who
was called by some the "father of American anthropology," and really sets a precedent for a lot of
this collecting in his book, Crania Americana, that really encourages people, especially around the
era of the Civil War, to view race a particular way and also get in on the act of collecting.

0:36:57.7 SR: As I went through these museum records, one thing that really stood out to me as
surprising is that it wasn't just these major big name scientists, it was farmers, and missionaries, and
amateurs, and military officers, and medical officers, and many, many, many other people who
somehow caught wind of this, somehow knew that there was a project to collect human remains at
the Smithsonian Institution, and were glad to box these up and send them. Sometimes at their own
expense. To the Smithsonian. So that's what I became really interested in. Where does this
intellectual history that we often think we know in relation to Samuel George Morton and figures
like Aleš Hrdlička, who I should say, becomes the first head of the Smithsonian's Physical
Anthropology program, and takes it from a collection of about 4,000 sets of human remains and
builds it, maybe doubles, triples the size of the collection.

0:37:53.0 SR: And he does it not just collecting on his own, which he does, he goes down to places
like Peru, he goes to Alaska, but he's also collecting remains through these almost like whisper
networks, that we haven't really unpacked and talked about how they play a role in this. Because it's
interesting to me that Morton collects a couple hundred skulls, but how do you get 30,000 skulls at
the Smithsonian, or 30,000 sets of human remains, I should say. It seems like there's a little bit of a
gap there that I wanted to try to fill in with the book Bone Rooms.

0:38:23.1 AS: And that's one of the fascinating things about your book is that it's almost this huge
national project, or international project, of citizen science or citizen race science, even, that
everybody is getting in on it. And it was very opportunistic, the way that you describe how
particularly the remains of indigenous peoples were collected with very little care about how
communities might feel about this, and obviously in almost all these cases, they would have been
shocked at this kind of collection, and yet people didn't seem to mind. They did it anyway. Why on
earth was that seen as acceptable to just grave rob in that way?

0:39:02.8 SR: Great question. Of course, like we've been talking about, the context is really
important. And one of the things that I think when we think about this story, sometimes we are so
connected or so thinking about the intellectual history of how these people are debating these
phenomenon in Europe and in the United States, that sometimes we lose sight of what I might call
the cultural history or the social history. Involved in that, of course, is as this is emerging are
phenomenon like we've touched on already like the Civil War and debates about the place of
African-Americans and these freedmen after the war. Should they be citizens? How should they sit
within the national fabric?

0:39:41.7 SR: Well, of course, Native Americans at this time are still not considered citizens, they
wouldn't be until the 1920s. They have this unique tense relationship in many respects with people
in the United States. There's this idea, this sort of contradictory idea that people want to wedge out

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American Indians and push them to the side. And yet, they're also... Their "antiquities" as far as
material remains are somehow considered part of the national heritage in the United States, and they
make us different than the colonial powers in Europe. This is seen in some ways as an asset.
Especially, there's a major turning point with the 1906 American Antiquities Act, where people start
viewing this as more of an asset. And burials and remains, as I show in Bone Rooms, figure in
prominently to the conversation around that Act.

0:40:31.0 SR: I think, yes, we need to think more about this national story where Native Americans
fit in, and they've always fit in sort of uncomfortably, but they're exploited to this extreme degree.
This represents this fundamental problem or tension between this emergent science with this very
thin line, you're right, between the evolution of archaeology and outright grave-robbing, where
there were letters that I found in the archive that I describe that ultimately ends up in the
Smithsonian collection, where Army medical officers or Army officers say, "I stole this off of a
funeral pyre. Native Americans were shooting arrows at me as I was doing this act of theft, but the
teeth on this individual were so beautiful that I kept it on my mantle for 20 years before sending it
to you, the Smithsonian Institution."

0:41:27.0 AS: It becomes almost like a trophy in that sense.

0:41:28.6 SR: 100%. Sometimes when we're rendering this from reverse, we see this in an
anthropology collection or an archaeology collection, and we think of it as co-joined with the
history of those sciences, which indeed they are in some ways. But it's this big complicated
collection where there are indeed examples of outright theft and grave-robbing. There are many,
many more mysterious examples where things just showed up into the collection with very limited
information. A part of me, without a doubt, says all of these remains should go home, as I encounter
these really gut-wrenching stories that from my view suggest very little attunement to the wishes of
the deceased or their ancestors or anything remotely resembling that.

0:42:16.4 AS: And it is something that museums and scientific institutions are having to confront
now. There's this very big reckoning happening within the sciences when it comes to race and
particularly human remains. There have been attempts at repatriation and dignified burial. What are
your thoughts on what's happening right now? How are scientists behaving in this moment?

0:42:37.9 SR: In 1990, a law was passed in the United States called NAGPRA, for short. Or, the
Native American Graves Protection and Repatriation Act. And that law without a doubt, even if we
look at it now as incomplete or with some degree of right-minded cynicism, it's a major turning
point in thinking about this whole story in the United States, in that recognized tribes, federally
recognized tribes, were able to legally demand the return of burial goods, objects of cultural
patrimony, so significant across the whole tribe or human remains. And that was a major step, but
there were barriers thrown up, people were very often abiding by the letter of the law and not the
spirit of the law, and it was very specifically written that it was an Act about grave sites. It's
intended to address this problem of looting. There are very real problems that this connects to, but it
also misses a whole bunch of things.

0:43:40.4 SR: For example, a question that I think has come up in 2021 and 2020, why is it that this
law should govern the collection of Native American remains when many African-American

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remains were collected under similar ethical guises with problems associated with that, but they
don't have that same legal recourse. The remains that really were probably most hotly contested this
year in the United States involved, here we are in the pandemic, we're doing a lot of things, remote
learning and via the internet, and a professor at the University of Pennsylvania utilized in her
teaching or used some remains of a bombing victim from 1985 who died in a police action, what's
called the MOVE bombing in Philadelphia.

0:44:26.8 SR: That hit people, from my view, in a really visceral way, to know that there were
people's living ancestors who were there and that didn't know what had happened to these remains.
It struck people as intensely problematic and a breach in ethical norms and behaviors, even if the
science maybe hadn't caught up with that yet. And I think that's an important point, that the
scientific best practices or ethics may have allowed for this, but in the court of public opinion, it
was an egregious violation of ethical norms.

0:45:03.2 AS: Thank you, Samuel Redman, it's been a pleasure. And thank you at home for
listening. I'm Angela Saini, and I hope you'll tune in for our next episode, one month from now,
with Professor of Medical Science, Lundy Braun, discussing her book, Breathing Race into the
Machine.

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0:45:19.7 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 this 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. You can subscribe there or anywhere you get your podcasts.

0:45:40.7 SC: This show was edited and produced by Sarah Crespi, with production help from
Podigy, Megan Cantwell and Joel Goldberg. Special thanks to intern Claire Hogan. 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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