SGU Episode 942

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SGU Episode 942
July 29th 2023
"Scientists have announced the development of a room-temperature ambient-pressure superconductor."  Click for further caption "Superconductors transmit electricity without resistance and have magnetic properties that make them invaluable in technological applications. Usually they need to be cooled down to very low temperatures; superconductors capable of working outside the lab in regular conditions would be revolutionary."
SGU 941                      SGU 943
Skeptical Rogues
S: Steven Novella
B: Bob Novella
J: Jay Novella
E: Evan Bernstein
Quote of the Week
Critical thinking is an active and ongoing process. It requires that we all think like Bayesians, updating our knowledge as new information comes in.
Daniel J. Levitin, American-Canadian cognitive psychologist
Links
Download Podcast
Show Notes
Forum Discussion

Introduction, hot water...hot world

Voice-over: You're listening to the Skeptics' Guide to the Universe, your escape to reality.

S: Hello and welcome to the Skeptics' Guide to the Universe. Today is Thursday, July 27^th, 2023, and this is your host, Steven Novella. Joining me this week are Bob Novella...

B: Hey, everybody!

S: Jay Novella...

J: Hey guys.

S: ...and Evan Bernstein.

E: Happy almost birthday, Steve.

S: Yeah, two days.

E: Yeah.

B: Yeah, man.

S: My daughter's birthday is tomorrow.

E: Right, Julia.

S: Yeah, the day before I was on the calendar.

J: That's pretty cool.

E: That's very cool.

S: It was, we didn't know if she could have been born on my birthday. It was getting pretty close. Yeah, but she came out a day before. So it's good. So now we always do like the doubleheader. She always has her special day, but it is nice that, it actually is convenient to have the doubleheader birthday.

E: Definitely.

S: She's coming up this weekend. Looking forward to it. So Cara's not here.

E: Yeah, what happened?

S: There's a storm brewing. She's having some nasty weather in Florida and her power's out. And there's simply no way. She still has her phone. So she's like texting me on her phone. And I just asked, is there any possible logistical way we could still do this with the power? I think, we could talk over the phone. You could just record off on your laptop on battery power. But the microphone doesn't work without power. So she has no microphone. So we're done.

J: So did you guys hear that the ocean temperature in Florida is bathtub hot?

S: Yep. Over 100 degrees.

E: Over 100 for Fahrenheit. Crazy.

J: That's got to be uncomfortable to go into.

S: Yeah.

E: Think about what the everything that lives in that ocean. Oh my gosh.

B: Yeah. But at what depth are we talking about? I could see a five foot depth being that hot. But once you get out into the deeper water, I guess it could still be the surface.

S: Colder water is heavier than hotter water down to four degrees Celsius. So it's always going to get called colder as you get deeper. And the water at the bottom of the oceans is going to be four degrees Celsius. But yeah, so they must be talking about this water, like the surface temperature.

E: Yeah. Buoy I suppose, measures it. So that would be surface, right?

J: Cara's weather is going to be basically like torrential downforce for the next week. Jesus.

E: Oh boy.

S: She may join us later if she somehow gets her power back, but we can't count on it.

J: This is, and the thing that scares me is this is just the beginning of the global warming effect. This is it. We're not like 50 years into it. It's going to get so much worse than it is now.

S: So there was a recent study out where the scientists were basically calculating what's the probability that we would be having the heat wave that we're experiencing now? Were it not for global warming, like the increase in the average global temperatures in the last 50 years? And it basically said it wouldn't be happening. It would be "virtually impossible" without human induced climate change. So, and of course, we've read sources that are saying, it's not climate change. It's El Niňo. Well, it's both, as I think we said last week or the week before, there are two different things happening and now we're getting both the peaks overlapping. So yeah, it's warmer than average because it's El Niňo, but it wouldn't be this warm without global warming.

E: That makes all the sense in the world actually.

S: Yeah. I hate it when people do that. It's like, it's not, hey, it's B, it's everything, right? It's every factor that goes into it combined. And it makes no sense to pull out one factor as it, as the cause. I remember a funny example of that. We remember this guys. I know you remember Evan, cause you, you hated this. We were coming off from dragon con and we missed our plane. It was, it was me, Evan and Bob. I think Jay was not there for some reason.

E: And it was only for one reason, right Steve?

S: It was only for one reason. Of course there was, there was literally like about 12 different things, each of which made us a few minutes late. And it was the toll. And of course there was the argument, we're late because you had to go to the bathroom at the last minute. It's like, no, because Bob tried to get his dagger onto the plane and, no, it was because they changed the gate on us at the last minute. We had to go to a different gate.

B: It was an awesome dagger.

S: Yeah. But it was, it was obviously the combination of factors that did it. It was true that any one of them were not present, we wouldn't have missed the plane because we'd literally closed the door one minute before we got to the gate.

B: And I remember, do you remember we actually walked by our new gate and didn't know it. And then we, we got to our old gate and they said, no, you got to go to your new gate. We backtracked.

S: Comedy of errors.

E: But hey, it's good to have a scapegoat. So, yeah. Sorry, Bob.

J: Missing an airplane like that, that is an intensely stressful situation.

S: Very stressful.

E: Oh my gosh.

S: Oh, they were on standby. It was terrible. I only missed a plane one other time in my life. I was coming home from Chicago. I was by myself and I left for the airport like three hours before my flight. Coming from the airport to the hotel was like a half an hour trip, right? So I said, all right, I'm going to leave three hours before my flight time. And the, we were in traffic the whole time. I literally, it was literally a four hour trip to the airport. And you know how like you're sitting in the car and time's going by and you're like, am I going to make it? Am I going to make it? I'm not going to make it. Like it just, it's a slow creeping lateness. That's just painful. But fortunately they literally just put me on the next flight like 30 minutes later. It was, it turned out to be nothing.

B: That's the benefit of using a big airport. They got lots of flights.

Quickie Followup with Steve (5:38)

• Alzheimer’s drug donanemab helps most when taken at earliest disease stage, study finds 
   (Note: no article was given from the SGU show notes page)

S: All right. I'm going to start off with a quickie. This is just a follow up, follow up to my news item from a couple of weeks ago. Remember back two weeks ago when I was talking about can be that new monoclonal antibody Alzheimer's drug as the latest and greatest, literally a week after I spoke about that news item, yet another one got approved by the FDA. There are now three, three drugs that are disease modifying in Alzheimer's disease. I mean, they're not just symptomatic. They actually change the course of the disease. They're all monoclonal antibodies. So there's aduhelm or aducanumab, which was got the accelerated approval in 2021 still being studied. And they have, and I think another year to prove clinical efficacy and get their full approval. And then there was leqembi, which is a lecanemab. And that got full approval a couple of weeks ago based upon clinical data showing a reduction in certain clinical measures of Alzheimer's disease by 27%. And now a large clinical trial shows that a third drug, donanemab reduces Alzheimer's disease by 35%. This is interesting because these drugs are targeting amyloid, which is the protein that is abnormal in Alzheimer's, and they clump together and form the plaques. And then it's part of the progress of the disease. And we weren't really sure if they were just a marker of the disease or if it's really causing the disease. And this is the first time with these three drugs that we've closed the loop. And it's like, oh yeah, it's actually probably contributing to progression because if you treat the amyloid, if you bind to the amyloid, it actually reduces the progression of the disease. Now the leqembi binds to the amyloid precursors and the donanemab binds to the plaques themselves. They have different targets. The advantage of the donanemab, the new one, is that if you treat patients for like a year, it takes away the plaques, the existing plaques, and then there are persistent benefits even after you stop taking the medication.

B: Wow. I love when that happens.

S: But we don't know for how long. We'd have to follow up for longer. So anyway, couple of things to keep in mind. These drugs are all expensive. They all have side effects. Some of those side effects are severe, bleeding in the brain, and even death. Even there are some patients who die on the drug, more than the placebo. And the clinical benefits, I'm saying 27%, 35%, but that translates into a very modest benefit. You know what I mean? It's like, yeah, you'll maintain your function for a few more months than somebody who wasn't being treated. But just the mere fact that they do decrease clinical progression, again, I think that's a huger deal than the actual benefit that individual patients are going to get. Again, Alzheimer's is a terrible disease. Any benefit is a boon and is arguably worth it. But the benefit to just our understanding of Alzheimer's and going forward. So of course, again, the hope is that this will lead to more better things. Maybe there'll be yet a third drug, maybe targeting another protein like tau or a different type of amyloid. And maybe they need to add two or three of them together.

E: Yeah, a cocktail?

S: Get a cocktail going that starts to get to really clinically significant decreases. Hopefully they'll be able to figure out ways to reduce the side effects. Although I suspect it's kind of inherent to the mechanism of action. We're sort of binding to these proteins and targeting the immune system at them. And it's leading to inflammation. Of course it is, because we're targeting the immune system at them. And it's that inflammation which is causing swelling and predisposing to bleeding in some cases. So I don't know. It's like chemotherapy. It's like the side effects are part of the effect. You can't really get the effect without the side effects. It's kind of inherent to the mechanism of action. But it's basically a different world than it was before these three drugs came out. At least now we have this proof of concept that, okay, this does have the potential to really alter the disease. These three drugs, well, two of them have really been shown to be clinically effective. The aduhelm hasn't really shown the clinical piece yet. And I know people who were planning on going into a clinical trial, and now they're just going to get prescribed donanemab, because it's available as a prescription now.

E: But you said it's expensive. So how does that work?

S: Insurance will cover it.

E: It will.

S: The other thing is that they're really only indicated for early Alzheimer's disease. If you're altering the slope, it really only gets significant if you start really early. You need that slope to separate out from the untreated group over a long period of time for it to become significant. And that's probably why, basically for 30 years we've been trying to treat amyloid, and it hasn't worked. And the researchers that are involved with these studies are saying, well, that's probably because we didn't go early enough or big enough, right? Now that we've done it with a big enough dose and early enough in the disease, that's why we're seeing some effectiveness. So I suspect insurance companies will be paying for it, but probably only for some criteria, like with early onset by some cutoff. The other thing, and then I think as I mentioned last time, is that the other way in which we could see this leading to really significant, clinically significant, not clinically modest treatments is if we combine it with early diagnosis. Imagine being treated two years before you would have been symptomatic based on some blood tests or CSF tests. That may be the world we're heading towards. Oh, you're at high risk. You have a family history or whatever. We do a blood test. Yeah, it looks like you got the type. We're going to start this treatment before you're even symptomatic, or maybe with like really pre, what we would call minimal cognitive impairment. You're not even really demented yet, but you have just an inkling that maybe it might be happening.

E: The drug that received the FDA approval a few weeks ago, once you're on it, you take it the rest of your life.

S: Yeah.

E: So is that also true with this?

S: No, the new one, it's like you take it for a year and you're good. They're thinking that maybe you just need some tuneups. Like every year you might need a couple more rounds or something.

E: Oh my gosh, that's such a difference between needing a drug for the rest of your life and an IV, right? It's an IV.

S: It's an IV infusion. Yeah.

B: How many other monoclonal antibody treatments are in the pipeline?

S: Ton. A ton.

B: The second one, I mean, you told me about it. I was like, wait, we just talked about it on this show.

S: Do you mean for Alzheimer's or just for anything?

B: Both.

S: Yeah. So there's a lot. There's a lot in the pipeline. There's a lot already out there. I mean, there has been a monoclonal antibody revolution in the last five to 10 years. I mean, antibodies have been around since the 80s, 90s. But we just got to this threshold where the technology was just viable. It's like we got the humanized version so that they're good for large dose infusions. And we got monoclonal antibodies for everything now. A couple years ago, a whole slew of monoclonal antibodies for the prevention of migraine headaches came out. Those are the ones that I'm the most familiar with that I use because I'm a migraine specialist.

J: Do you think that this might help anxiety and depression one day?

S: I mean, I don't think if you can make a drug to bind to a receptor, you can make a monoclonal antibody to bind to a receptor. You know what I mean? It's just a different way of acting on some therapeutic target. And it's kind of a superior technology in certain ways because it's not really a chemical. So you don't really get the chemical side effects. Like you don't have to worry about liver and kidney and other kinds of side effects. It's a protein. It's literally an antibody. But that causes other side effects. I think all things considered, you can make a reasonable argument that it's a superior technology to chemical drugs, but they're expensive. They're all really expensive because they're biologics.

E: How does the price come down eventually on these?

S: I guess that the hope is that with the technology, the technology will advance to the point where it gets cheaper and cheaper to mass produce them and economy of scale. But I don't think it's going to be cheap anytime soon. But you never know. There may be the crisper of monoclonal antibodies will come out. Somebody figures out, oh God, we could make these orders of magnitude cheaper. That could happen. For now, it's just like, okay, we have these really expensive, really awesome drugs and we just have to use them wisely, use them judiciously for people who really need them.

:E My gosh, there are going to be people who will want to take it sort of as a preemptive strike against even if they're not otherwise a candidate to take these things, they're going to want it.

S: You won't get them unless you meet some criteria. For the Alzheimer's drugs, you need to have the positive blood tests. You need to make sure you have the target. You have the plaque or the abnormal amyloid or whatever. But now, more than anything, and one of the ways that the practice of medicine has evolved over my career is that cost effectiveness is becoming more and more important. It was always important, but now it's like really the order in which we go through drugs is cheapest to most expensive. If you have a bunch of clinically basically equivalent drugs in terms of the probability that they may work for a patient, we start with the cheapest ones and then go from there. That's the predominant feature now in many contexts that guides our decision making. For those people who don't like that, I also see the other thing. I've seen, like for getting back to migraines, that's what I have the most experience. I get referred patients who get started on these newer, more expensive drugs prematurely. It's like, really? He went right to the $7,000 a year drug and you didn't even try any of these other ones? But they're by non-experts and that's why they're getting referred to me. But that's one of the mistakes that they make. They just go right to the new shiny, really expensive drug. It's like, you should not do that. You're ruining it for the rest of us. Because when they do that, then insurance companies clamp down. Then they make it harder for the patients who really needed to get the expensive drugs because then they throw up all these barriers to prescribing them because they're being overprescribed as first and second line drugs when they really need to be third and fourth line drugs. So it's added a layer of complexity to the whole decision-making process. Because if we don't make, as practitioners, if we don't prescribe in an economically responsible way, especially with now access to so many really expensive options, the bean counters are going to take it out of our hands, which they're already doing, but they'll make that worse. If you practice in a country with single payer, it'll be the government. If you practice in the United States, it'll be the insurance company. It'll be somebody, but it'll be somebody other than the practitioner basically making that decision based upon economics, not on clinical concerns. You know what I mean?

B: Steve, go ahead 50 or 100 years. Where do you see monoclonal antibodies at the peak?

E: Over the counter.

B: Besides the obvious like, oh, there'll be fewer side effects and it'll be cheap. Is there anywhere else you can go to improve with better tech, like sci-fi tech? What could we potentially see, you think?

S: Well, if we want to go to sci-fi tech, I think the progression will be we're going to get more and more applications. The technology is going to incrementally improve. The prices will come down somewhat. We went over lots of technologies that could transform this. Imagine if you're essentially like 3D printing these things or whatever. You have some kind of a machine where it's like, okay, here's a drop of my blood. It not only makes your diagnosis, it personally crafts a monoclonal antibody for you and gives it to you. You know what I mean? Just essentially like the equivalent. It wouldn't be like really a 3D printer, but I'm just saying like the equivalent of that where you're just-

B: Bioprinting.

S: Bioprinting personalized drugs based upon your genetics, your disease, your protein, whatever it is, not just based upon the study of other people. And that could be on demand. On demand, personalized pharmacotherapy with monoclonal antibodies. That's totally plausible. All right. Let's move on to some news lines. That wasn't really much of a quickie, but-

E: It's a not so quickie.

News Items

S:

B:

C:

J:

E:

(laughs) (laughter) (applause) [inaudible]

Can AI Learn Like Humans? (19:06)

• Future AI algorithms have potential to learn like humans 

(Transcriptionist's note: Another AI news item, "AI and Politics" is noted on the shownotes page, likely the news item Cara would have covered if she had regained power.
The associated article: The Conversation: 6 ways AI can make political campaigns more deceptive than ever)

Room Temperature Superconductor (30:49)

• First Room-Temperature Ambient-Pressure Superconductor Achieved, Claim Scientists  

A Galaxy Without Dark Matter (45:48)

• A Galaxy Without Dark Matter 

Men Convicted For Mineral Solution (59:19)

• Federal jury convicts 4 Florida men for selling bleach solution as ‘miracle’ cure for diseases 

Who's That Noisy? (1:08:45)

Answer to previous Noisy:

Sound of water freezing and crystallizing

New Noisy (1:11:58)

[squeaking, as of birds or wheels]

J: ... what this week's noisy is

Questions/Emails/Corrections/Follow-ups

Question #1: Talent vs Skill (1:16:58)

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Science or Fiction (1:28:08)

Item #1: Scientists have been able to reanimate nematodes taken from Siberian permafrost that were frozen for 46 thousand years. Item #2: New research finds that, despite diverging evolutionarily 179 million years ago, the honeycomb design of honey bee and paper wasp nests derives from a common ancestor. Item #3: Researchers were able to transplant mitochrondria into damaged kidney cells improving energy production and reducing toxicity and physiological stress.

Answer	Item
Fiction	Honeycomb: common ancestor
Science	Reanimated nematodes
Science	Mitochondria transplantation

Host	Result
Steve	clever

Rogue	Guess
Evan	Mitochondria transplantation
Bob	Reanimated nematodes
Jay	Honeycomb: common ancestor

Voice-over: It's time for Science or Fiction.

Skeptical Quote of the Week (1:45:36)

Critical thinking is an active and ongoing process. It requires that we all think like Bayesians, updating our knowledge as new information comes in.  – Daniel J. Levitin (1957-present), American-Canadian cognitive psychologist, from A Field Guide to Lies: Critical Thinking in the Information Age

Signoff (1:48:07)

S: —and until next week, this is your Skeptics' Guide to the Universe.

S: Skeptics' Guide to the Universe is produced by SGU Productions, dedicated to promoting science and critical thinking. For more information, visit us at theskepticsguide.org. Send your questions to info@theskepticsguide.org. And, if you would like to support the show and all the work that we do, go to patreon.com/SkepticsGuide and consider becoming a patron and becoming part of the SGU community. Our listeners and supporters are what make SGU possible.

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Today I Learned

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