The Peter Attia Drive - #120 - AMA with Dom D'Agostino, Ph.D., Part II of II： Ketosis for cancer and chronic disease, hyperbaric oxygen therapy, and the effect of ketosis on female health

00:00:00.000 Hey everyone, welcome to a sneak peek, ask me anything or AMA episode of the drive podcast.

00:00:16.500 I'm your host, Peter Atiyah. At the end of this short episode, I'll explain how you can

00:00:20.460 access the AMA episodes in full, along with a ton of other membership benefits we've created,

00:00:25.440 or you can learn more now by going to peteratiyahmd.com forward slash subscribe.

00:00:31.140 So without further delay, here's today's sneak peek of the ask me anything episode.

00:00:39.260 Hey everyone, welcome to part two in our AMA series with Dom D'Agostino. As a reminder,

00:00:45.860 you'll note that this interview had been scheduled for a very long time. And just when it was about

00:00:49.920 to happen, I had to go to Mars on a spaceship that did not contain a Zoom setup, and I was 0.84

00:00:56.480 unable to be a part of it. But both Dom and Bob Kaplan, my head of research, graciously agreed

00:01:02.980 to do it in my absence. And so you will once again be graced by the presence of Bob and Dom

00:01:08.220 speaking instead of having to listen to me. In this second episode, Bob and Dom dive deep again,

00:01:14.880 this time really focusing on the effects of ketosis on various chronic diseases. Dom's work

00:01:19.940 with hyperbaric oxygen therapy and its numerous applications, as long as the applications of

00:01:25.040 ketosis on female health and performance. This is a topic that I know very little about outside of

00:01:30.660 some reproduction. And also it's something that many of you have been asking about. And frankly,

00:01:34.580 there's just not enough information out there on such topics. Dom is an associate professor at the

00:01:39.300 University of South Florida, where he teaches at the College of Medicine and in the Department of

00:01:43.760 Molecular Pharmacology, Physiology. He focuses on neuropharmacology, medical, biochemistry,

00:01:49.740 physiology, neuroscience, and neuropharmacology. He's also a research scientist at the Institute

00:01:53.960 for Human and Machine Cognition to assist with their efforts towards optimizing the safety,

00:01:58.760 health, and resilience of warfighters and astronauts. Lastly, it's important to note that while Dom is

00:02:03.540 answering specific questions and scenarios, he is not giving medical advice. Everything in this podcast is

00:02:09.620 for general informational purposes only and does not constitute the practice of medicine,

00:02:13.320 including the giving of medical advice. So without further delay, please enjoy

00:02:18.400 part two of the AMA with Dom D'Agostino.

00:02:28.020 So we're going to switch gears to ketosis and disease. And the first up is cancer and

00:02:34.900 a lot of questions around updates on press pulse therapy. Since a couple of years ago, when you're on

00:02:40.480 the podcast, you mentioned the press pulse in the paper that you did with Tom Seyfried. Talk about

00:02:45.020 that a little bit.

00:02:46.560 I have to say I was not formally trained as a cancer biologist or cancer researcher. It just sort of

00:02:52.640 fell in my lap, so to speak, I guess around 2010. And I think maybe I went into that on the first podcast.

00:02:59.560 And I have to say I've been extremely lucky to have brilliant students come into my lab. And that has made all the

00:03:08.720 difference in the world. Because as the other PIs or professors, they just get students that and they're kind of stuck with

00:03:14.680 them for five years. But I've got the upper echelons, like the top of the top students in the program I always have. And not only are they

00:03:22.480 brilliant, they just have a genuine interest in in this topic. So they were able to basically be the engines behind a lot of the

00:03:30.480 research that we did that started laying the groundwork, I think, or the groundwork was already sort of laid because people were

00:03:37.480 already doing ketogenic diet studies like Tom Seyfried, who's been on the podcast before. But we sort of picked it up and took it in other

00:03:45.500 directions. And we kind of worked on that Press Pulse review that sort of encompasses this idea using, I guess, what you

00:03:54.800 would call ketone metabolic therapy or therapeutic ketosis, and other modalities to compromise tumor growth and

00:04:02.880 proliferation. And that weakens the tumor, if we're talking about a solid tumor, to be more amenable to other

00:04:10.780 modalities, which could be the one thing that we experimented on years ago, that one of the first

00:04:17.380 papers we put out was the ketogenic diet and hyperbaric oxygen therapy. And there are a number

00:04:23.280 of reasons why they are synergistic. So being in a state of therapeutic ketosis suppresses insulin

00:04:28.800 signaling, which drives PI3 kinase, it lowers glucose availability to the tumor, it elevates ketone

00:04:35.780 bodies, which as an alternative fuel, cannot be readily utilized by cancers, most cancers as a 0.82

00:04:42.860 source of fuel, perhaps anabolic processes, but they're not a good fuel source for cancer cells,

00:04:48.800 most cancer cells. And they also do things like they impair antioxidant pathways that the tumors use to

00:04:56.180 defend itself. And a tumor is resilient because it has upregulated endogenous antioxidant pathways

00:05:03.720 by high levels of glutathione. So the pentose phosphate pathway, for example, generates more

00:05:11.520 glutathione in cancer cells. And that is being fed by glucose. So if you reduce glucose availability,

00:05:19.080 inhibit insulin, which enhances glycolysis, so you're suppressing glycolysis, you're creating a scenario

00:05:26.140 where if you give an oxidative challenge with hyperbaric oxygen therapy, you can potentially kill

00:05:33.440 the cancer cells. So this is what I observed using a hyperbaric laser scanning confocal microscope.

00:05:40.200 So we adapted this technology for use inside a hyperbaric chamber for Department of Defense

00:05:44.880 and Office of Navy Research related projects on CNS oxygen toxicity, which manifested seizures. So we

00:05:51.520 are looking at a variety of different cell types. And one cell type curiously had a tremendous oxidative

00:05:59.140 burst. And we were measuring superoxide anion with dihydroathidium. So dihydroathidium is taken up

00:06:06.220 into the cells and then reacts with superoxide anion and forms this ethidium cation, which binds

00:06:13.560 to nucleic acids and it lights up. So the lighting up inside the cell, as the cells light up, that indicates

00:06:20.760 reactive oxygen species are being produced. And when I started looking at the first cell was U87

00:06:27.580 glioblastoma cells. And these were taken from like a 40 some odd year old glioblastoma patient. And now

00:06:34.440 it's a cell line that a lot of people use. The intensity of the cell indicative of superoxide

00:06:40.560 anion production skyrocketed above and beyond anything I'd ever seen before. And then the more

00:06:47.140 hyperbaric oxygen I gave, I saw the mitochondria starting to disappear. They lit up too, because they

00:06:52.860 have their own DNA. It was mitochondrial superoxide. I think we went on to look and explore and use

00:06:59.320 various mitochondrial specific superoxide detectors. But the cells started dying. And I didn't see that

00:07:06.040 in other cell model systems. So we figured something was going on there. And this is looking at cells. So

00:07:11.780 Dr. Angela Poff, who was one of my first PhD students, studied the ketogenic diet with hyperbaric

00:07:18.120 oxygen delivered at 2.5 atmospheres of oxygen, 60 minutes, three times a week. And that protocol

00:07:25.820 combined with a modified ketogenic diet proved to decrease tumor burden and extend lifespan in this

00:07:34.380 animal model of metastatic cancer, which is the VMM3 model that Thomas Seyfried developed.

00:07:40.420 And I think it's a remarkable model of metastatic cancer.

00:07:43.100 So now there are many different things that you can combine in press pulse therapy. So I think the

00:07:51.080 idea would be to, from a press perspective, going back to the glucose ketone index and that paper,

00:07:58.020 if you just Google glucose ketone index, and maybe I think it was in nutrition metabolism,

00:08:03.380 Tom Seyfried published this and really laid out all the science to support that a glucose ketone index,

00:08:11.380 the lower that is ideally in the one to two range below one, if possible, getting a glucose ketone

00:08:18.240 index, which is the level of glucose over the level of ketone in millimolar concentrations to one or

00:08:25.120 two, that sets the stage, slows tumor growth and proliferation, and makes the tumor more vulnerable to

00:08:33.900 what I mentioned, hyperbaric oxygen therapy, but other cancer specific metabolic drugs.

00:08:38.560 And we really want to try the PI3 kinase inhibitors that Lou Cantley is on. I just started listening to the

00:08:45.140 last podcast, fantastic podcast you guys did with him. We've been using 2-deoxyglucose, which is basically

00:08:52.880 also inhibits hexakinase and inhibits glycolysis. 3-bromopyruvate is something we want to use.

00:09:00.100 We've used DCA, metformin. We've done experiments with vitamin C, high doses of vitamin C, and that was a project of

00:09:09.960 one of my undergraduates. To publish that work, vitamin C has some interesting effects. And then there's the SGLT2

00:09:16.460 inhibitors that we're also interested in. So there's all these things out there, but we haven't really put it together

00:09:23.400 into a therapy. We're just, you need to test these things sort of in isolation and then combine certain

00:09:31.540 things together. But how they all work together, the Press Pulse review that we published was more of an

00:09:38.400 idea. And it was sort of in the preclinical stages. But there are a number of papers coming out. One just

00:09:45.980 came out this morning in science communications, looking at, it was a Walter Longo study, looking at

00:09:52.020 fasting with IV vitamin C, I believe. And it showed in KRAS, basically tumors that are aggressive and very

00:10:00.980 hard to treat that had the KRAS mutation. He had remarkable effects. It was a mouse study, I believe,

00:10:08.440 and I still, it's on my desk. I got to read it because it just came out this morning. I saw it

00:10:11.680 just showing a remarkable effect, completely non-toxic combination of fasting with vitamin C,

00:10:19.540 intravenous vitamin C. And there was also another paper that came out, just came out like a week or

00:10:24.800 two ago, metastatic thymoma. Female, she was 37 years old, I believe. Very difficult to treat cancer,

00:10:33.680 not a curable cancer at all. Pretty light, like maybe 50 or 60 kilograms, stage 4A. And she did

00:10:41.660 fasting, ketogenic diet, then fasting. I have to look at all the protocols that were used, but I

00:10:47.140 think they used prednisone too, 40 milligrams per day, which is kind of high. But come to find out

00:10:52.220 that can trigger apoptosis in cancer cells. But they had like a 90%, 96% decrease in tumor burden

00:11:00.240 with this therapy. And it was like using relatively non-toxic approach. I mean, there was some drugs

00:11:05.660 throughout some immune-based therapies, but it was basically water fasting with ketogenic diet

00:11:11.780 and then periodic water fasting with different immune-based therapies. So it's another paper on

00:11:17.700 my desk. I got to read. Tom actually emailed that paper to me. Yeah, I recently read it and

00:11:22.480 it was remarkable. And one thing that I noticed, the authors pointed it out, that the woman had,

00:11:28.600 she had a couple of episodes, correct my pronunciation, myasthenia gravis. So she had a couple of those

00:11:34.420 cases. And it looked like during those two cases that something, the remark was something about a

00:11:39.960 remarkable decrease in her intake of food or oral intake. And on the second, her second episode,

00:11:46.500 she lost about, I think it was about 15 kilograms. And like you said, she was already, let's say she 1.00

00:11:51.860 was like 110 pounds. She went down to 80 pounds. And the second, I don't know if it was the second 1.00

00:11:57.340 imaging or one of the later imaging, her tumor went from, it looked like whatever you want to call it,

00:12:02.300 the tumor burden. They were measuring it in cubic centimeters. It slowly progressed. It was pretty

00:12:07.160 stable. It looked like, and I want to say, it sounded like, and if you look at the pictures,

00:12:11.580 it looked like she had an extra lung in terms of the mass that you could see right in the sternum 1.00

00:12:15.800 in that area. So it went from something like 600 cubic centimeters to, I don't know if it was like 30.

00:12:22.540 I mean, I went on Google and tried to figure out how does that compare to like different size balls.

00:12:26.880 And it looked like it went from like a football to a golf ball or there's something to that effect

00:12:31.900 where it almost seemed like the ketogenic diet. I was wondering, it's almost like paired with this

00:12:36.880 idea of Coley's toxins, that kind of thing that she had this episode, but essentially, I don't know

00:12:41.520 how long she was fasting for, but if she lost 15 kilograms during that time, and it also looked

00:12:46.160 like her tumor just was being wiped out over that period of time. But there's a few case studies like

00:12:51.400 that too, that I know that Tom's been a coauthor on. I don't know if you mentioned it in your podcast or

00:12:55.560 his, yeah, his, like a person with triple negative breast cancer and somebody with glioblastoma.

00:13:01.120 But I wanted to come back to something too. You mentioned vitamin C, you mentioned IV vitamin C.

00:13:06.280 And I know that in the previous podcast, this was eye-opening when you talked about radiation and

00:13:10.800 perhaps up to 80% of its effects are the reactive oxygen species that something like radiation can

00:13:17.260 induce. And it sounds like hyperbaric oxygen, somewhat similar. And so then you think the tumor cell

00:13:23.100 part of the defense is the upregulation of all these antioxidants. And a lot of people will think

00:13:28.360 about vitamin C and they'll go, well, wait a minute, vitamin C is an antioxidant. I also think

00:13:32.560 is it at IV doses, it can be a pro-oxidant. Is that part of why you think it might be effective?

00:13:38.080 Yeah. I'm so into the pro-oxidant effect of vitamin C and down to the redox pathways that I don't even

00:13:44.440 think about as an antioxidant anymore. We use really high concentrations. So that's right. So hyperbaric

00:13:51.240 oxygen. So it's well known that radiation therapy kills cancer cells by 80 to 90% just through Ross

00:13:58.140 generation, maybe 10 at most 20% just by directly nicking the DNA like double strand nicks. But

00:14:05.640 you're generating reactive oxygen species and then they are toxic tumor cells. So the efficacy of

00:14:11.360 radiation therapy is proportional to the PO2 of the tumor. So if you oxygenate the tumor and then radiate it,

00:14:17.260 you're going to do a lot more damage. It's directly proportional to oxygenation.

00:14:21.940 So tumors tend to grow and outstrip their blood supply. So they're hypoxic. So when you radiate

00:14:26.880 them, they become resistant to radiation because they're hypoxic. So if you were to have hyperbaric

00:14:33.360 oxygen therapy during radiation, like a targeted radiation, we know that that would dramatically

00:14:38.580 sensitize it. Like this is well known and accepted. But what isn't really firmly established is

00:14:44.420 if you have hyperbaric oxygen therapy before or after radiation therapy, like say you have

00:14:50.780 hyperbaric oxygen and then you get out of the chamber and go have radiation, the PO of the tumor

00:14:55.980 will drop, but you'll have a residual elevation of reactive oxygen species for hours after.

00:15:02.760 So, and it'll be somewhat site-specific increase in reactive oxygen species because various mitochondrial

00:15:09.880 abnormalities, I should say, there's a debate whether the mitochondria are damaged or they are

00:15:16.140 not damaged. I'm 100% certain that the mitochondria are aberrant in a way. So they are dysregulated in a

00:15:24.560 way that they overproduce oxygen, reactive oxygen species in response to an elevation of the PO2 of the

00:15:31.120 tissue. So this is well documented. And it occurs because there's defects in the mitochondrial

00:15:37.440 electron transport chain. There's a lot of free heme available. That free iron that's available

00:15:43.940 drives the fenton reaction. So if you remember biochemistry or organic chem, so the fenton reaction

00:15:51.500 is when you have a lot of free iron, it drives the production of hydroxyl radical, which is like a super

00:15:57.400 reactive oxygen species. And that can kill cancer cells very dramatically. So the combination of hyperbaric

00:16:06.280 oxygen therapy, radiation and IV vitamin C, or if you were to take radiation out of it and just do

00:16:12.140 hyperbaric oxygen and IV vitamin C can be a potent pro-oxidant therapy. So another interesting thing

00:16:18.400 about dihydroascorbic acid is that it uses, which is the oxidized kind of form of vitamin C, is that it

00:16:27.080 uses the glucose transporter to get inside cells. So if you elevate vitamin C or ascorbic acid into

00:16:35.140 millimolar concentrations in the blood using an IV route, it functions as a glucose antagonist.

00:16:42.300 So you are not only inhibiting glucose transport, and you might actually get some hypoglycemic symptoms

00:16:47.840 out of it. So I did when I had IV vitamin C. So you are delivering a glucose antagonist that's also

00:16:55.580 dramatically increasing reactive oxygen species in cancer cells because tumors have a lot of free iron

00:17:01.860 because there's a lot of heme. Cells are necrotic. Cells are dying in tumors all the time just because

00:17:07.460 they're hypoxic, but they're proliferating. So you have dead cells and live cells. But the important

00:17:12.840 thing is that there's a lot of heme iron. They have a lot of free iron. So reactive oxygen species is

00:17:18.440 like really, really high. And vitamin C is really sort of driving that reaction in addition to the

00:17:26.020 glucose antagonist effect. So we're pretty enthusiastic about vitamin C. We've done quite

00:17:31.340 a bit of work. We need to publish more. We've published it in abstract form. I had a super

00:17:35.780 awesome undergraduate, Janine DiBlasi. She did her honors undergraduate with me, but then went to 1.00

00:17:41.420 Oxford to study cancer and radiation. And now she's at Moffitt Cancer Center under a different mentor.

00:17:47.420 But I would love to kind of reinvigorate her honors undergrad project and start doing more vitamin C 0.91

00:17:53.540 work. But yeah, that's a really important component now, we think, to press pulse concept of cancer

00:18:01.400 management. And I think this is probably part of the original press pulse, but I know that Tom's done

00:18:07.580 some work subsequent to that. I don't know if you're involved with that or you're aware of this as well,

00:18:13.160 where he talks about mitochondrial substrate level phosphorylation with glutamine. And so he thinks that

00:18:19.940 the tumor cells are, I think that that's actually, that's not controversial that you'll read papers.

00:18:24.860 If you look up PubMed and you type in glutamine addiction tumor cells, you'll see a lot of papers

00:18:30.600 come up on that and that they tumor cells quote unquote love. I don't like to use like the teleology,

00:18:36.160 but they're addicted to glutamine. I remember he did a paper recently. He has, like you said,

00:18:40.420 the VMM3 glioblastoma mice. Yeah, yeah. It's a glioblastoma that metastasizes. So it's transformed

00:18:49.740 in a way to become highly metastatic. If you eject it into the flank, then you even have brain mets,

00:18:55.640 the lung, liver. It is the most deadly animal model of cancer that I know about. And so it makes it kind

00:19:04.280 of a fantastic model system to study. So I remember Tom told me, if you can cure cancer in this model

00:19:10.480 system, then you've cured cancer. And, and we're still trying to do that because it's such an

00:19:15.020 aggressive form of cancer. And we just published a paper. First author was my graduate student. He

00:19:21.500 just graduated Andrew Kutnick and he demonstrated in that it's an amazing model to study cancer cachexia.

00:19:29.500 So not only is the VMM3 model, probably one of the best models of metastatic cancer. And we need

00:19:36.680 way more research into metastatic cancer. Studying just a consolidated tumor, whether it shrinks is not

00:19:42.180 really that informative because people really don't die of a tumor. They die of metastasis and

00:19:47.420 invasiveness of the cancer. This is a tool to do that. And so I'd encourage cancer researchers out

00:19:53.560 there to, to use this model. It's really good. And now we've demonstrated through the work of

00:19:59.220 my former grad student, now Dr. Andrew Kutnick, that it's an amazing model, the best model that

00:20:06.460 we know of, in my opinion, to study cancer cachexia, which is a really important understudied

00:20:12.820 phenomenon of cancers. It's funny. I was going to mention the same thing that what I heard,

00:20:18.240 I think this is actually an Italian, I can't remember the guy's name, an Italian researcher.

00:20:23.040 He may have told this to Gary Taubes. Gary shared this with me where he said, he was talking about the

00:20:28.280 field of cancer and mice and said, if you can't cure cancer in a mouse, you need to get out of

00:20:32.560 this field because it's so easy. And then I would think to like Tom's mice and Tom's like, I'll give

00:20:37.260 him the VMM3s. You try curing cancer in that mouse. You come back to me and you tell me how that is.

00:20:42.340 But Tom, he did a paper, it was 2019. I will be able to pull this. It was Nature Communications.

00:20:48.520 And he combined his ketogenic diet, calorie restricted ketogenic diet. And he looked at,

00:20:53.340 and he's done that study before where he looks at just the ketogenic restricted diet versus

00:20:58.280 standard diet. And then he looked at, I think, standard diet plus DON, which is a glutamine,

00:21:04.780 either the glutamine antagonist, glutamine inhibitor.

00:21:07.300 Yeah. Inhibitor, antagonist. Yep.

00:21:09.720 Six diazo5 norel leucine, something, something to that effect, right?

00:21:14.620 Yeah. And it's one of those things, if you look at a Kaplan-Meier curve, if you know how those work,

00:21:19.240 where every death of a mouse or an organism or an individual is going to tick the little plot down

00:21:24.840 towards percent survival to zero. And I looked at, it's probably the first figure in the paper,

00:21:29.760 and he has the mice that are calorie restricted ketogenic diet plus DON, and it's like this purple

00:21:35.620 line. And it starts right at the top at 100, and it just goes all the way, just a horizontal line.

00:21:41.880 None of the mice are dead. I just remember emailing him saying like, did you follow it up?

00:21:46.020 I don't know why this reminds me of Seinfeld. There's an episode of Seinfeld where

00:21:49.600 they're almost on an empty tank of gas, and they want to see how far they can take it.

00:21:53.340 Yeah.

00:21:53.840 They're test driving a car. And I just thought, tell me the end of that story. I'm not sure how

00:21:58.920 long they lasted, but his Kaplan-Meier curve went out 40 days, and there's no deaths. And if you look

00:22:03.580 at standard diet, I think this is pretty typical, that the mice, after implanted, they're between

00:22:08.440 about 15 days, all the mice are dead with a standard diet. And he's made some headway with a

00:22:13.480 ketogenic diet. And he says, it's not a cure-all. At least it's not curing cancer in these mice.

00:22:18.820 And then he added this glutamine inhibitor, which is pretty interesting. I think that would probably

00:22:24.280 be his pushback on this idea that a lot of people talk about the cancer cells having normal

00:22:29.180 mitochondria. And I think their justification is that it's consuming oxygen. And so it's that

00:22:34.520 you'll see OCR, oxygen consumption rate. But I think what Tom is arguing is that, yes,

00:22:39.400 it may be taking in oxygen, but it's not producing ATP via oxfos. It may be that the tumor is not just

00:22:46.720 getting energy from the Warburg effect or aerobic fermentation, but it also might be fermentation of

00:22:52.180 glutamine. And I remember, full disclosure, I sat in on Tom's class twice at BC. He was kind enough

00:22:57.400 to let me sit there.

00:22:58.600 That's awesome.

00:22:59.220 It was great.

00:23:00.020 I taught in that class one time. I gave a departmental lecture, sat in that class,

00:23:04.220 which was really fun. I'm a course director for a kind of a metabolism and signaling course. And

00:23:10.020 we went over Tom's papers and stuff. But the whole course was not on cancer, but it was fun. It was a

00:23:15.600 similar kind of course. They were the best kind of courses. So I'm sure it was a lot of very spirited

00:23:20.240 discussion.

00:23:21.700 Oh, absolutely. It's pretty brilliant what he does, actually. So he has his cancer as a metabolic

00:23:25.840 disease. And a big question, I think, that actually Peter gets, and I'm sure you get as well,

00:23:30.940 as with all the stuff that you have going on, you're writing grants, you're doing this, you're

00:23:34.280 doing that, you're teaching. How do you keep up with the literature? How do you stay abreast of

00:23:38.280 everything? And he essentially has every one of his students come up with a paper that tries to

00:23:44.560 essentially shoot down his hypothesis as cancer is a mitochondrial metabolic disease. And so it's

00:23:50.460 actually a brilliant way for him to keep up with the latest research and the things that, how he might

00:23:54.820 be fooling himself. It's pretty fascinating. Obviously, he's very passionate about it.

00:23:58.920 So Journal Club is a good way to do that. And there is no lack of papers out there and brilliant

00:24:06.100 scientists out there who basically are presenting work showing that cancer is perfectly normal and

00:24:12.620 the mitochondria are perfectly healthy in cancer cells. So I think there's sort of a happy medium.

00:24:18.580 We know that the mitochondria are transformed in ways to enhance biosynthetic processes. The expanding

00:24:24.720 biomass of the tumor, those needs need to be met. And the mitochondria are transformed into ways that

00:24:31.680 achieved that goal. And of course, glycolysis is elevated tremendously. And then glutamine elysis

00:24:39.340 too drives a lot of the anabolic processes and also ATP generation too, to some extent.

00:24:45.400 So targeting glutamine with Dawn is a very great strategy in theory, but Dawn is toxic.

00:24:51.380 So, I mean, it's a dose dependent thing, but we need to come up with better molecules that could

00:24:57.460 reduce glutamine levels in the blood and tissue and also just function as a glutamine antagonist.

00:25:03.380 Yeah. He mentioned, I think it's mentioned in that paper that giving Dawn on the standard diet,

00:25:09.460 at least again, we're talking about mice, it was the toxicity I think was a lot higher

00:25:13.940 than the ketogenic diet. And I'm actually, I'm thinking about if you have any thoughts on

00:25:18.860 either radiation or hyperbaric oxygen, that if you're doing either one of those interventions,

00:25:22.500 do you think that there's a benefit of being in a state of ketosis while you're actually receiving

00:25:26.520 either intervention? Yeah, absolutely.

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The Peter Attia Drive - July 20, 2020

#120 - AMA with Dom D'Agostino, Ph.D., Part II of II： Ketosis for cancer and chronic disease, hyperbaric oxygen therapy, and the effect of ketosis on female health

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