Speaker 1: Pushkin from Pushkin Industries. This is Deep Background, the show
Speaker 1: where we explore the stories behind the stories in the news.
Speaker 1: I'm Noah Feldman. Research into the novel Coronavirus is happening
Speaker 1: and being published or sometimes just press released at breakneck speed.
Speaker 1: Every few weeks, we hear about a possible new breakthrough
Speaker 1: or a potentially interesting avenue of research. But often that
Speaker 1: breakthrough it turns out to be too good to be true,
Speaker 1: or to have less effect than we might have imagined.
Speaker 1: To help us make sense of the latest about the
Speaker 1: novel coronavirus, which studies to watch, which studies are too
Speaker 1: soon to interpret, and where we are in the progress
Speaker 1: towards a vaccine, We're joined by doctor Sad Omer. Doctor
Speaker 1: Omer is a professor of infectious disease and epidemiology at
Speaker 1: the Yale School of Medicine and at the Yale School
Speaker 1: of Public Health. He's also director of the Yale Institute
Speaker 1: for Global Health. In short, he's perfectly qualified to talk
Speaker 1: about these questions. So thank you so much for joining me.
Speaker 1: I'm very grateful. I wonder if we could begin with
Speaker 1: some of the latest publicized developments in therapy. There's a
Speaker 1: large randomized study out of the UK, which we only
Speaker 1: see in so far in press release form, although we're
Speaker 1: getting used to that, involving the use of the steroid dexamethasone.
Speaker 1: What is your takeaway from that study. It's a very
Speaker 1: encouraging study for several reasons. First of all, from the protocol,
Speaker 1: it seems that it was a well conducted study. They
Speaker 1: showed an impact on mortality, not on everyone, but those
Speaker 1: who were on vents. The third thing is that it's
Speaker 1: a widely available drug. So whenever you are dealing with
Speaker 1: these public health emergencies, one concern, one major n is equity.
Speaker 1: At least in the initial few months after a drug
Speaker 1: is evaluated successfully or it comes out, etc. You're really
Speaker 1: concerned about getting that to the most vulnerable. Since this
Speaker 1: is a widely used drug already, we have broader availability.
Speaker 1: So that's the good news. The caveat, as you pointed out,
Speaker 1: is that all we know at this point is a
Speaker 1: press release, a press release from a credible group. But look,
Speaker 1: I would like to see at least data, maybe not
Speaker 1: a full flash paper, but they worst probably somewhere some
Speaker 1: discussion at their data Safety Monitoring board or somewhere where
Speaker 1: they presented those slides. At least share those slides. Now.
Speaker 1: I understand that there's a lot of time pressure on investigators,
Speaker 1: but if the data are good enough to be shared
Speaker 1: publicly in a press release, they should be good enough
Speaker 1: to be shared more broadly. The effect on mortality on
Speaker 1: deaths reported in a press lease was a one third
Speaker 1: reduction for those people who were so sick that they
Speaker 1: were on ventilators, and I believe a one in five
Speaker 1: reduction in deaths for those who were sick enough to
Speaker 1: be on oxygen but not oxygen delivered via a ventilator.
Speaker 1: And then for those who were very sick and in
Speaker 1: the hospital but we're not on oxygen, they reported no effect. Obviously,
Speaker 1: I'm asking you to reconstruct something that's not so simple
Speaker 1: to reconstruct. But why would one have expected those sorts
Speaker 1: of results specifically from this treatment. Yeah. So, look, we
Speaker 1: are learning about the disease as we go along, and
Speaker 1: sometimes what works in terms of treatment tells you as
Speaker 1: much about the disease as it tells you about the
Speaker 1: intervention itself. But in this case, and you know, these
Speaker 1: results combined with our previous current understanding of what's happening
Speaker 1: with the patient with the individual after you get the disease,
Speaker 1: is that there is this maladaptation and then this exaggerated
Speaker 1: response of the immune system. And so the contrast is
Speaker 1: higher when you have an intervention that is attacking the
Speaker 1: condition by dampening broadly the immune response at a stage
Speaker 1: when it's exaggerated. So that contrast would be highlighted in
Speaker 1: more severe patients because, for example, the cytokine storm is
Speaker 1: happening in more severe patients, So if you're attacking that,
Speaker 1: that's where the contrast is. So that would be in
Speaker 1: line with these results, and that's because steroids are broadly
Speaker 1: speaking anti inflammatory, but maybe going on in these most
Speaker 1: sick patients is some kind of the cytokinde storm, which
Speaker 1: is a kind of exaggerated immune reaction, exaggerated maladaptive. So
Speaker 1: it's not just the quantity of the immune response, but
Speaker 1: the type of immune response. But but essentially focusing on
Speaker 1: the type of response and the quantity of response and
Speaker 1: sometimes dampening it broadly speaking can have these benefits. So
Speaker 1: that would explain it. So if I just to make
Speaker 1: sure I'm understanding you correctly, because the sicker patients actually
Speaker 1: benefited proportionally more from the steroidal intervention that provides some
Speaker 1: indication that at least in those very very sick patients,
Speaker 1: what's going on is the kind of thing that might
Speaker 1: be responsive to steroids and therefore fits the theory argued
Speaker 1: for by some of your colleagues at Yale and others
Speaker 1: of the cytokind storm. Yeah, exactly. Let me ask you
Speaker 1: about this large genome wide association study that's being reported
Speaker 1: on in Europe. Again, I think we don't have the
Speaker 1: full final paper yet in which an argument is being
Speaker 1: made for an association of blood type, surprisingly enough with
Speaker 1: probability of suffering from COVID, not exposure to the virus,
Speaker 1: but suffering from the disease if you are exposed to
Speaker 1: the virus. And then there's it's not the blood type itself,
Speaker 1: according to the theory, at least, it's a some set
Speaker 1: of genes that are associated with the same gene area
Speaker 1: as the blood type. If I'm getting it right, say
Speaker 1: a word about that place. From my perspective, it's too
Speaker 1: early to say anything definitive about this. It's a signal generation.
Speaker 1: I think there needs to be a lot more work
Speaker 1: to look at. First of all, if the signal is
Speaker 1: credible because a lot of times when you do these
Speaker 1: observational studies in sick patients, you're not able to match
Speaker 1: appropriately you control for underlying confounding and so therefore that's
Speaker 1: one of the reasons we would like to see more
Speaker 1: detailed data, etc. To figure that out. I think this
Speaker 1: one is too early to say anything definitively. I think
Speaker 1: it's certainly something that needs to be followed up that
Speaker 1: could have further implications. So I would put it in
Speaker 1: the bucket of signal generation more than or hypothesis generation
Speaker 1: more than anything beyond that. It was fascinating to me
Speaker 1: because it reminded me of some of the other high
Speaker 1: profile GA genome white association studies, where you know, the
Speaker 1: researchers look potentially at hundreds of thousands in some cases
Speaker 1: of people with some condition and then they just literally
Speaker 1: mind the data, which is what scientists we're supposed to
Speaker 1: not do in the bad old days or maybe the
Speaker 1: good old days, and they say, well, we're minding the data,
Speaker 1: and here's what we see. You know, these are these
Speaker 1: associations that we find in the data, and therefore they
Speaker 1: must have some effect, and now let's try to figure
Speaker 1: out what that effect is it's sort of the opposite
Speaker 1: of what we were all taught. The scientific method is
Speaker 1: supposed to be, and yet it has caught on as
Speaker 1: a real methodology, and it often yields fascinating things. But
Speaker 1: of course there's some statistical reason to think that some
Speaker 1: things should be yielded anyway. Yeah. No, So here's the
Speaker 1: interesting thing DWAs. And big data techniques, whether applied directly
Speaker 1: to biology, to or to other sources of data, give
Speaker 1: you great power and for a lack of bettle example,
Speaker 1: you know, i'd quote spider Man, power comes great responsibility.
Speaker 1: Actually Voltaire said it before, but you know, you know
Speaker 1: spider Man, or actually his uncle Ben said it with
Speaker 1: more flair. So with this kind of these kinds of tools,
Speaker 1: it's okay, it's reasonable to apply these tools, but a
Speaker 1: lot of it is in what you do when you
Speaker 1: find something. So if it's taken as a signal hypothesis
Speaker 1: generation exercise to then do a sort of a hypothesis
Speaker 1: testing set of studies, this kind of an approach can
Speaker 1: add value. But if it is taken as hypothesis testing exercise,
Speaker 1: then you get into some of those other issues that
Speaker 1: you mentioned a little bit earlier. Two vaccines are getting
Speaker 1: very close to trials that are going to tell us
Speaker 1: probably whether they work or not. The Maderna vaccine RNA
Speaker 1: based vaccine, and then the Oxford vaccine, which is a
Speaker 1: trojan horse vaccine. These are both brand new techniques, neither
Speaker 1: of which, according to guests I've had here before, has
Speaker 1: ever generated a successful vaccine that went to market. Yet nevertheless,
Speaker 1: we're all extremely excited and eagerly anticipating the results. Everyone
Speaker 1: has some instinct about this. You're in a position to
Speaker 1: actually have an intelligent instinct. What is your instinct about
Speaker 1: these possible vaccines? So first of all, I add in
Speaker 1: a little bit of nuance to these are two Western
Speaker 1: vaccines that are two of the more prominent ones. There
Speaker 1: are a couple of Chinese vaccines that we should keep
Speaker 1: an eye out for and we should track. So one
Speaker 1: is produced by the company's Signo vac and then the
Speaker 1: other one is can sign on. But coming to these vaccines,
Speaker 1: the Modern vaccine and the Oxford vaccine are some of
Speaker 1: the earliest vaccines that are being evaluated or likely to
Speaker 1: be evaluated in large trials. The Oxford vaccine has an
Speaker 1: innovative trial design where they had a rolling Phase two
Speaker 1: three trial where they have already enrolled a bunch of people,
Speaker 1: not they're not close to their final sample size. And
Speaker 1: one of the complications, one of the nuance that has
Speaker 1: been added is that some of the earlier projections of
Speaker 1: their timeline, as I understand, was based on the incidence
Speaker 1: in the UK because that's where the main core of
Speaker 1: the investigators is located. So that the disease incidence going
Speaker 1: down seems to have complicated things a little bit. And
Speaker 1: they are going to Brazil now to recruit, which is
Speaker 1: very reasonable and this is how it should be done
Speaker 1: in a pandemic. But the reason I'm highlighting this is, look,
Speaker 1: this is one of the reasons why we should stay
Speaker 1: away from predicting that the vaccine will be available in
Speaker 1: three months. You can say that it will be available
Speaker 1: in the near future or the prospects look good, because
Speaker 1: there are a lot of things that can slow down
Speaker 1: your development process. But coming back to your original questions,
Speaker 1: so the main question that these are a new approaches,
Speaker 1: I think they're based on pretty sound biology. Then there
Speaker 1: should be in the front line of things where the
Speaker 1: global community and national programs invest Having said that things
Speaker 1: can go sideways you can have unexpected things. So what
Speaker 1: do we do about that? A First of all, have
Speaker 1: realistic expectations about the timelines. If they go early, that's great,
Speaker 1: but we should all have a little bit of humility
Speaker 1: about our projections, especially for new products. The other thing
Speaker 1: is we should all hedge our bets. So it's a
Speaker 1: good approach to have a diversity of technologies, some new,
Speaker 1: some old. So having a couple of live attenuated products
Speaker 1: in the mix, having a couple of recombinant vaccines in
Speaker 1: the mix helps us even out that risk. And so
Speaker 1: these are the few implications of having a vaccine program
Speaker 1: or a vaccine development program that has a few new, novel,
Speaker 1: innovative products. Can you say something about the two Chinese
Speaker 1: vaccines that you mentioned, because those have not gotten the
Speaker 1: same amount of coverage in the US media. But my
Speaker 1: understanding is one of them is a live attenuated vaccine,
Speaker 1: good old fashioned vaccine. Yeah, exactly. You take the virus
Speaker 1: and you primarily through serial passage through culture, take away
Speaker 1: the disease potential, but ideally maintain the replication potentials. So
Speaker 1: that's the live attenuated vaccine. There's another vector vaccine that
Speaker 1: is also in more advanced stages. So these are the
Speaker 1: two vaccines that are ahead of the pack in China.
Speaker 1: They also seem to have issues in terms of Phase
Speaker 1: three trials because of the successful control they have achieved
Speaker 1: in reducing the incidence of the virus in their own population.
Speaker 1: One of the most important things I think that you
Speaker 1: just said is that we need to realize that even
Speaker 1: just running the trials can take longer than one expects.
Speaker 1: Even if these are great, the durational issue isn't easily
Speaker 1: manageable because these aren't challenge trials. No one is being
Speaker 1: at this point intentionally exposed to stars Covy two virus.
Speaker 1: There have been people who've talked about the value of
Speaker 1: doing that. Under the circumstances, I have actually been opened.
Speaker 1: I understand ethical challenges. I've been sort of opened to
Speaker 1: the ethical argument that when many people are dying and
Speaker 1: the economic effects are as great as they are, if
Speaker 1: there's ever a time for challenge trials where people are
Speaker 1: intentionally exposed, this is it. It sounds as though you're
Speaker 1: not convinced, well, I'm actually I haven't made up my
Speaker 1: mind in terms of specific challenge trials, And here's the
Speaker 1: reason why I think they're a legitimate policy option that
Speaker 1: should be explored. But in order to going forward with
Speaker 1: an actual challenge trial, I think we need a few
Speaker 1: more things, and I like the WHO approach, so they
Speaker 1: issued ethical guidance about if to do it, this is
Speaker 1: how you do it. It's not straightforward to do a
Speaker 1: challenge studies because you have to have a standardized challenge
Speaker 1: doors for humans, you have to have a more rigorous
Speaker 1: set of protocols facilities. The ability to do that and
Speaker 1: the ability to conduct challenge trials is actually way more
Speaker 1: limited than to do efficacy trials throughout the world. So
Speaker 1: there are fewer centers in the world that have done
Speaker 1: human challenge studies. So obviously animal challenge studies are different.
Speaker 1: And so one of the thinking that that is there,
Speaker 1: which is not discussed too much in the public discourse
Speaker 1: or discussion, is what is the added time gain if
Speaker 1: you have to take these several steps that require you know,
Speaker 1: some time to iron out. Having said that, you know,
Speaker 1: developing it as a parallel policy option is very reasonable,
Speaker 1: but it should be done with not just policy discussion,
Speaker 1: but detailed call discussion. I want to ask you about
Speaker 1: asymptomatic transmission as sort of our last topic of conversation.
Speaker 1: I guess the question that I'm really interested in is
Speaker 1: we all understand that there's droplet transmission from coughing sneezing.
Speaker 1: We also understand that there is presumably some sort of
Speaker 1: aerosolization transmission where the droplets are much much, much much tinier.
Speaker 1: I think a lot of people are trying to figure
Speaker 1: out how they should think about those two aspects of
Speaker 1: transmission and what it means for masks. So within the
Speaker 1: symptomatic they can be sort of different modes of transmission.
Speaker 1: It could be from surfaces or full mites, mediums, large
Speaker 1: sized droplets as well as small sort of aerosols. Although
Speaker 1: that the data are being generated, there's a few things
Speaker 1: to keep in mind. First of all, the classifying the
Speaker 1: type of the size of droplet and the probability of
Speaker 1: something being aerosolized versus not so. Hanging out in the
Speaker 1: air for some periods and sort of transmitting through air
Speaker 1: is different from aerosualization, which stays much longer in the air.
Speaker 1: We do know that the risk of aerosolization is way
Speaker 1: higher in some higher risk procedures such as intubation, enduring
Speaker 1: medical procedures, and even you know specimen taking is likely
Speaker 1: to be especially in Nize with angel swabs, etc. So
Speaker 1: therefore healthcare workers need to have PPE for some of
Speaker 1: that stuff. The good news is if you have good
Speaker 1: personal protective equipment in healthcare settings, even with aerosolization, we
Speaker 1: seem to have fairly low transmission wherever PPE was available,
Speaker 1: So that's setting that aside. So now for mass transmission,
Speaker 1: what you're dealing with is a surface paced versus you know,
Speaker 1: these droplet transmission, which is not quite a rasalized but
Speaker 1: these droplets can travel, you know, reasonably far beyond six
Speaker 1: feet sometimes, and those droplets there is evidence, or again
Speaker 1: it's not definitive evidence, that you decrease the probability of
Speaker 1: that spread if you are wearing masks, but the effect
Speaker 1: size on an individual level is relatively modest. So the
Speaker 1: thinking is because it's not a very intrusive intervention, if
Speaker 1: you have masks compliance with mask wearing, you decrease the
Speaker 1: probability to an extent that you can see a substantial
Speaker 1: population impact. That last point is fascinating and one that
Speaker 1: has not I think been fully stated, partly maybe because
Speaker 1: people in the public health space don't want to state
Speaker 1: it as explicitly as you just did. So let's just
Speaker 1: go over it for clarity. What I hear you to
Speaker 1: be saying is that although the data on masks, not
Speaker 1: in the hospital context but in the public context, are
Speaker 1: not necessarily that definitive, and although the effects actually might
Speaker 1: be relatively small, there's a kind of public health judgment
Speaker 1: that says, well, it's very low cost for everybody to
Speaker 1: wear masks, and let's insist that people wear them, in fact,
Speaker 1: regulated by law in many places, including where I live
Speaker 1: in Massachusetts. And then we think that cumulatively, that is
Speaker 1: likely to have a harm reducing effect, and the theory
Speaker 1: is sort of that there's not that much downside. If
Speaker 1: that's the case. I do think there's a little bit
Speaker 1: of subtlety there, because it involves a value judgment about
Speaker 1: how low cost it is to wear a mask, and
Speaker 1: I think that may vary from person to person, and
Speaker 1: there are regional variations and how people feel about it,
Speaker 1: There are cultural differences in different places. So I'm wondering
Speaker 1: if you could just say a little bit more on that. Yeah, no,
Speaker 1: I agree, And so that's one of the reasons why
Speaker 1: public health agencies have gone back and forth on this issue.
Speaker 1: It's not a clear good issue. So there's a nice
Speaker 1: review by Oxford that try to incorporate all of these things,
Speaker 1: and they did show that at really high compliance numbers
Speaker 1: you can have a pretty substantial population level impact. What
Speaker 1: level of impact is there? So, based on the fact
Speaker 1: that a lot of these are assessments from studies that
Speaker 1: are sort of still evolving in terms of the evidence
Speaker 1: is still evolving. Because of that, I don't think we
Speaker 1: can say what is the amount of impact, but there's
Speaker 1: likely to be some population level impact. But I think
Speaker 1: you're right, we need to have some nuance in the messaging.
Speaker 1: Thank you very much. I really appreciate your time, my pleasure,
Speaker 1: and these were great questions. Sud's analysis is crisp, clear
Speaker 1: and helpful. First, and most importantly, we should not assume
Speaker 1: any specific time when we will know if the existing
Speaker 1: vaccines that are being tested work. Challenges to the testing
Speaker 1: process are endemic at a time when the virus is
Speaker 1: itself being controlled in many places in the world, and
Speaker 1: resetting up a protocol in a place where the disease
Speaker 1: is spreading faster is actually time consuming in its own right.
Speaker 1: So the fact that it is possible to get trial
Speaker 1: results sometime in twenty twenty does not at all mean
Speaker 1: that we will get those results in twenty twenty. Next,
Speaker 1: when it comes to new therapies, we need to see
Speaker 1: more data. It's very promising that the steroidal treatment of
Speaker 1: dexamethasone is helping to reduce deaths. This is the first
Speaker 1: therapy we've seen that actually specifically does reduce deaths, because
Speaker 1: the rim desvere therapy reduced time in the hospital but
Speaker 1: was not shown statistically to reduce deaths. So that's promising.
Speaker 1: But we still do not have publicly released data. What
Speaker 1: we have rather is a press release from a reputable group,
Speaker 1: Sad says. Sad also reminds us to keep an eye
Speaker 1: on the vaccines that are coming out of China, including
Speaker 1: a traditional style vaccine with an attenuated form of the virus,
Speaker 1: a topic to which we may return in a future episode. Last,
Speaker 1: but not least, when it comes to masks again, Soad
Speaker 1: calls for nuance. He points out that some studies suggest
Speaker 1: mild benefits of mask wearing, which can be magnified through
Speaker 1: the population if there's very very broad compliance, and that
Speaker 1: public health officials think that is worth doing, in part
Speaker 1: because they judge that the wearing of masks is not,
Speaker 1: in fact a high cost public intervention that raises fascinating
Speaker 1: issues about the costs versus the benefits of mask wearing.
Speaker 1: I guarantee you we will return to that issue in
Speaker 1: the near future as well. We'll be back in a moment.
Speaker 1: During the intense last couple of months, we've been so
Speaker 1: focused on getting you COVID stories that we temporarily paused
Speaker 1: a segment that we used to have on the show
Speaker 1: called Playback, where I choose a moment in the news
Speaker 1: and play it back to you for further discussion. This week,
Speaker 1: we're bringing playback back, and in particular, we're going to
Speaker 1: turn our attention where it always goes at the end
Speaker 1: of June, to the Supreme Court of the United States.
Speaker 1: That's the sound of people celebrating in front of the
Speaker 1: Supreme Court last Thursday, after the Supreme Court ruled that
Speaker 1: the Trump administration had acted unlawfully when it tried to
Speaker 1: rescind DHAKA, the Deferred Action for Childhood Arrival's program designed
Speaker 1: to protect people known as dreamers. From a moral standpoint,
Speaker 1: this is a tremendously gratifying decision. Dreamers are about the
Speaker 1: most sympathetic people you could imagine, And the fact that
Speaker 1: the Trump administration sought their deportation was again, from a
Speaker 1: moral standpoint, horrendous. That said, the Supreme Court's decision was
Speaker 1: itself surprising on the law. The decision was written by
Speaker 1: Chief Justice John Roberts, who is ordinarily a staunch conservative,
Speaker 1: and as the fact that it was a five to
Speaker 1: four decision shows, there were grounds that a conservative justice
Speaker 1: like Roberts could have used had he wanted to decide
Speaker 1: that what Barack Obama put in place, namely the DOCCA program,
Speaker 1: Donald Trump could remove. Indeed, Roberts typically has a rather
Speaker 1: expansive conception of executive power. And although we can know
Speaker 1: with one hundred percent certainty, I would say there's ninety
Speaker 1: nine percent probability that several years ago Roberts was one
Speaker 1: of the justices who voted to strike down an Obama
Speaker 1: program that was similar to DOCA but aimed at parents.
Speaker 1: So what was going on here? Why did Chief Justice
Speaker 1: John Roberts choose to leave his conservative allies and join
Speaker 1: the liberals to keep DOCCA in place. Sometimes when Roberts
Speaker 1: issues an apparently liberal decision, it's clear that what he's
Speaker 1: doing is trying to preserve the appearance of legitimacy of
Speaker 1: the Supreme Court by avoiding a scenario where the public
Speaker 1: would think of the justices as basically partisan. Roberts understands
Speaker 1: that the public knows that the Supreme Court justices have
Speaker 1: different ideologies. What he doesn't want is for the public
Speaker 1: to think that the justices vote based on the party
Speaker 1: of the person who appointed them. That may explain Roberts's
Speaker 1: vote not to entirely strike down Obamacare, the Affordable Care
Speaker 1: Act some years ago. In the DACA case, however, Roberts's
Speaker 1: motivation seems to have been somewhat different. What seems to
Speaker 1: be motivating Roberts is a kind of disrespect for the
Speaker 1: Donald Trump administration's unwillingness to cross its tees, dot its eyes,
Speaker 1: and follow the rule of law when it comes to
Speaker 1: issuing important governmental decisions. We saw this a year ago
Speaker 1: when Roberts also provided the decisive fifth vote to reverse
Speaker 1: the Trump administration's plan to put a citizenship question on
Speaker 1: the twenty twenty census. In that case, as in the
Speaker 1: DACA case, Roberts relied on a law called the Administrative
Speaker 1: Procedure Act, which is the law that gives the federal
Speaker 1: courts the authority to oversee and review decisions of administrative
Speaker 1: bodies in order to determine whether they complied with the
Speaker 1: pre jurors that the law demands. In particular, the Administrative
Speaker 1: Procedure Act requires that the government give clear, honest, and
Speaker 1: accurate justifications and reasons for why it's doing what it's doing,
Speaker 1: and both the Census case and the DACA case, Roberts
Speaker 1: ruled that the government had failed to provide those justifications.
Speaker 1: In essence, Roberts was saying, taking the action in question
Speaker 1: was within the general authority of the executive branch, but
Speaker 1: the executive branch didn't do a good enough job of
Speaker 1: explaining why it did what it did. This kind of
Speaker 1: judicial supervision of governmental action is crucial to preserving the
Speaker 1: rule of law, and it's pretty clear that John Roberts
Speaker 1: no longer trusts the Trump administration to do that. To
Speaker 1: be sure, at the beginning of the Trump administration, Roberts
Speaker 1: was willing to give Trump the benefit of the doubt.
Speaker 1: He after all, wrote the opinion in the Trump against
Speaker 1: Hawaii case, the one involving the Muslim travel ban, in
Speaker 1: which he upheld the president's authority to issue the version
Speaker 1: of the travel band that was in play at the time.
Speaker 1: What seems to have happened subsequently is that as Roberts
Speaker 1: has gotten a closer and closer look at Trump's disrespect
Speaker 1: for the courts and his disrespect for the rule of law,
Speaker 1: He's decided to take on the role of defending the judiciary,
Speaker 1: defending the rule of law, and of him making Trump comply.
Speaker 1: And it may not be irrelevant that Roberts also had
Speaker 1: to spend a good chunk of his January sitting in
Speaker 1: the Senate listening to the Impeachment Manager's condemnation of Donald Trump,
Speaker 1: precisely for his disrespect for the rule of law. So
Speaker 1: if you're wondering whether John Roberts has suddenly become a liberal,
Speaker 1: take it from me. He has not. I expect more
Speaker 1: conservative decisions from him, possibly even this week or next.
Speaker 1: But John Roberts has taken up the responsibility of the
Speaker 1: judiciary to keep an eye on this president, and for
Speaker 1: that I think everybody liberal or conservative should be profoundly grateful.
Speaker 1: Next week, we'll be taking a break for July fourth,
Speaker 1: but we will see you the week after, and until then,
Speaker 1: be careful, be safe, and be well. Deep Background is
Speaker 1: brought to you by Pushkin Industries. Our producer is Lydia
Speaker 1: Jane Cott, with mastering by Jason Gambrell and Martin Gonzalez.
Speaker 1: Our showrunner is Sophia mckibbon. Our theme music is composed
Speaker 1: by Luis GERA special thanks to the Pushkin Brass, Malcolm Gladwell,
Speaker 1: Jacob Weissberg, and Mia Lovell. I'm Noah Feldman. I also
Speaker 1: write a regular column for Bloomberg Opinion, which you can
Speaker 1: find at Bloomberg dot com slash Feldman. To discover Bloomberg's
Speaker 1: original slate of podcasts, go to Bloomberg dot com slash Podcasts.
Speaker 1: And one last thing. I just wrote a book called
Speaker 1: The Arab Winter, a Tragedy. I would be delighted if
Speaker 1: you checked it out. If you liked what you heard today,
Speaker 1: please write a review or tell a friend. You can
Speaker 1: always let me know what you think on Twitter. My
Speaker 1: handle is Noah R. Feldman. This is Deep Background.