19 Burst results for "Barzilai"

"barzilai" Discussed on The Kevin and Ryan Show

The Kevin and Ryan Show

03:41 min | 3 years ago

"barzilai" Discussed on The Kevin and Ryan Show

"So instead what restored by doing is focusing on things. Pneumonia in an ideal world, if the ever Linus study from Novartis could be reproduced you should be able to reduce the rates of pneumonia in elderly people due to the boost in immune function. Correct. And so it would almost be like met form in that way. Then it would have a primary prescription for one particular thing and actually have the outcome belong Javadi. Well, yes. Although in both both metformin rapamycin are currently available by prescription. So you glad you could technically use either these off label. What are the same metformin was not approved for longevity? If it didn't clear it for Abadi. Right. Yeah. So tame, which is that study that's hopefully going to be funded very soon led by near Barzilai, and his colleagues is also going to look at some of these other more longevity based metrics, and I believe again, I someone will can look this up and get much more accurate data. But I think restore bio has come up with a number of indications. They're looking at that are much shorter and easier to measure in clinical trials than. Obviously long jetty is the ultimate goal to produce a version of this that you know, will be sought out in mass markets on label for that purpose. You know, perhaps. Yeah. But now to your question. So what is what is rapamycin do? So when you turned down M tour, what are you doing? It seems that you are mimicking what happens to a body when it is a nutrient sparse environment. So when nutrients are well and still it more complicated. 'cause which nutrients so I would say the simplest way to explain it is m tour is probably the best thing we have at sensing amino acids amino acids, are the building blocks of proteins now, there are two amino acids in particular that are really important when it comes to nutrient levels, the first is the amino acid that seems to be most sensitive to activating 'em tour, and that's an amino acid Cobb loosing, which is one of the branched chain amino acids. And most people who listen to this who have you know, who are in defeat nece probably know that you can buy branch chain amino acids at a health food store, whatever there are three of them losing isolated valley and as their name suggests their branched chain. So they have actually have a side chain that's branched on them. And that's why they have that name. And so I think the fitness or bodybuilding community was wise to sort of realize there was something about branch chain amino acids that were really valuable, and if you wanted to grow your muscles, you had to have a lot of these things in you, and unfortunately, the industry's mostly sham. So most Brad sham. You know? Acids. Are are actually literally crushed bird feathers. Really? Yeah. As a very low concentration of these things. So there's only a handful of companies. In fact, there's only two companies I'm aware of that make a legitimate branch chain amino is everyone's gonna be asking me this now where do come and to be clear, I'm not saying that these are the only two, but these the only two that I can vouch for so one is a company in Japan called agenda motto. And they they really are the original company that they created a true. You know, pharma grade branch chain amino acid, and the other is a company in Canada called biosteel now other companies, so if someone's listening to this and saying, well, you know, how do I buy the stuff lots of companies, I believe are also now selling branch chain amino acids that contain I mean acids provided by Inomoto. But basically if a patient comes to me and says, hey, I want to be on branching amino acids. I'm putting them on biosteel because I think it's the best product out there than if they for some reason can't stand the taste because truthfully I don't like the taste that much myself. I little too sweet I say, well, let's just look for something else that at least has an Moto stamp on it. So that we know it's coming in with the right stuff side question on that though..

metformin Pneumonia Novartis Brad sham Barzilai Abadi Canada Japan Cobb
"barzilai" Discussed on The Kevin Rose Show

The Kevin Rose Show

03:30 min | 3 years ago

"barzilai" Discussed on The Kevin Rose Show

"So instead what restored by doing is focusing on things. Pneumonia in an ideal world, if the ever Linus study from Novartis could be reproduced you should be able to reduce the rates of pneumonia in elderly people due to the boost in immune function. Correct. And so it would almost be like metformin in that way. Then it would have a primary prescription for one particular thing and actually have the outcome belong Javadi. Well, yes, although in both both metformin rapamycin or currently available by prescription. So you glad you could technically use either these off label what same met form was not approved for longevity. If it didn't clear it for seventy right? Yeah. So tame, which is that study, that's hopefully gonna be funded very soon led by near Barzilai, and his colleagues is also going to look at some of these other more longevity based metrics, and I believe again, I someone will can look this up and get much more accurate data. But I think restore bio has come up with a number of indications. They're looking at that are much shorter and easier to measure in clinical trials than. Longevity is the ultimate goal to produce a version of this that you know, will be sought out in mass markets on label for that purpose. You know, perhaps. Yeah. But now to your question. So what is what is rapamycin do? So when you turned down M tour, what are you doing? It seems that you are mimicking what happens to a body when it is a nutrient sparse environment. So when nutrients are well and still it more complicated because which nutrients, so I would say the simplest way to explain it is m tour is probably the best thing we have at sensing amino acids. I mean, oh acids are the building blocks of proteins now, there are two amino acids in particular that are really important when it comes to nutrient levels, the first is the amino acid that seems to be most sensitive to activating 'em tour, and that's send amino acid Cobb loosing, which is one of the branch chain amino acids. And most people who listen to this who have you know, who were indefinite probably know that you can buy branch chain amino acids at a health food store, whatever there are three of them losing isolating valley and as their name suggests their branched chain. So they have actually have a side chain that's branched on them. And that's why they have that name. And so I think the fitness or bodybuilding community was wise to sort of realize there was something about branch chain amino acids that were really valuable, and if you wanted to grow your muscles. You had to have a lot of these things in you, and unfortunately, the industry's mostly a sham so most branch amino acids are are actually literally crushed bird feathers. Really? Yeah. As a very low concentration of these things, there's only a handful of companies. In fact, there's only two companies I'm aware of that make a legitimate branch chain amino is everyone's gonna be asking me this now where to come and to be clear, I'm not saying that these are the only two, but these that I can vouch for so one is a company in Japan called agenda motto. And they really are the original company that they created a true. You know, pharma grade branch chain amino acid and the other is a company in Canada called biosteel now other companies, so if someone's listening to this and saying, well, you know, how do I buy the stuff lots of companies, I believe are also now selling branch chain amino acids that contain I mean oh acids provided by edging Amato. But basically if a patient comes to me and says, hey, I wanna be on branching amino acids. I'm putting them on biosteel because I think it's the best product out there than if they for some reason can't stand.

metformin Pneumonia Novartis Barzilai Japan Canada Amato Cobb
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

05:31 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"And we went to this data set that Skuld clean VAR clean VAR, then head the fifteen thousand but to genyk mutation that most probably will cause a disease. Okay. Now, they have about thirty thousand. And our policies that are Cincinnati's. Don't have any of those okay. Will support the perfect. Forty four centenarians head more than two hundred thirty mutations between them another five to six mutations. The shoot have caused them diseases, and none of them had this disease in hundred years of life, and some of those mutation I'll give you the best example for Parkinson and conser and everything but Upul e four what's the in? We have to up four hundred years old people that the textbook would say they're demented at seventy dead at eighty and they're not demented. The no dead at hunter. You think this at all explains the LPGA uptick, we see because, you know, one of my favorite topics lipid, Allah g and of course, L P little a is a very variant Leiper protein, and yet centenarian seemed to have more of it than the general population act. So we actually we actually showed in a in a paper because we. The we we found a way. So basically. A week, obviously, we can have mutations that are protected because they have slow aging or longevity genes. Protect right. So how do you prove it? So we noticed that when you look cross-sectional. I hope I can make it very simply when when we put any genotype cross-section Louis. In other words, we have all ages from fifty two hundred twelve is our oldest. We see patterns if we see pattern that the general type is declining with age. We know it's killing people. Okay. If we see that it's kind of monotone eclipse increase with age like with concentrating with yet. Then means the people are surviving are surviving with this mutation. That's why we have Maureen on rid like the example of Roman receptor going for three to twelve. In Montana Kway. So we looked at L P lay. Exactly. And this is the most confusing of them all because I don't see any compelling evidence. That LP little a is anything other than Athar genyk. And so it begs the question, why would it concentrate in centenarians as opposed to just rise commensurate with the population? Exactly. So this is the Unser. Okay. I the all we shall cross-sectional that LP drops until the age of eighty by half. In other words, highly like crazy until it's not right? And then and then you look at it, and you kind of try to send just a minute. Now. This thing that killed now. All of a sudden centenarians have even more it should stay flat after these right? It should be fled wise, it increasing. Will because it's a protected aging, gene. In other words, it was obviously during evolutionary times, are you saying that the the thing that LP lay did for us five hundred thousand years ago that is no longer beneficial in his lousy environment. The centenarians have managed to tap into its properties of. No, no. So what we did what we did in. It's all published in computerization biology journals, we took everyone of longevity, gene that we have. And we did gene to gene interaction. In other words, we try to see if there's interaction between the bed genotype and the good genita- good longevity genotype, and we didn't to variety of those U-shaped, right? I'm I'm telling you, there's a U shape. Don't always goes down with aging. And then it's good incentive. And we really found statistically significant that L pill is protected by people are homeless ideas to a CT mutation that these on Jebediah mutation that we we found that's the av mutation v mutation in other words, most of the people with the L P lay that are centenarians were also CTP CTP Buteau. Can we tell people what that phenotype is? So I've talked on his podcast a lot about see tap and its role in reverse cholesterol, transport cetera. Talked me about what what does the lipid panel like for someone who is v plus or minus LP little so those would C P V they have higher HDL levels. They have larger life approaching particle size, and they have lower CTP levels. That's their fennel type. In this city has is being protective against several age related disease. The most dramatic is cognitive decline. And by the way, the two upper four are also CPV carriers..

Skuld LPGA Cincinnati Parkinson Montana Kway Maureen five hundred thousand years four hundred years hundred years
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:07 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"Decreases, some other singling fuck signaling and some other stuff dramatically. So there's a micro Aurigny targeting of the growth hormone idea for sceptre in about thirty percent of our centenarians, then twenty two percent of our centenarians mutation in folks three that Sukumar new tation in centenarians. So you start to percent and twelve present tell people at FOX three does folks folks are three A is another holiday say just house. How stays? Yeah. Housekeeper that lets in good stuff in change things in things in stop. It's too complicated to go more. But it is part of the Terim insulin actor at at regulating Hamis, sailor harmonizes, and that's not a great explanation. But yeah. It isn't FOX the most prevalent genetic difference between if you were to just isolate them by by Gina type, if you look at C Tappin C three and FOX, oh and g h and I Jeff I mean, if my recollection is that FOX might be the single most prevalent of folk so a mature through with FOX's three A is common in all centenarians population around the world. Not every population has the same you Teychenne's. In fact, what we're doing? Now, when we have the XM sequencing of all are subject, you know, almost three thousand XM sequencing, the important thing to do is to assign them to pathways because you know, we're doing something really silly with genetics. When when we had these Jesus, we we said we have meaning snips around the genome, we'll find diseases every disease in the world. And one of the stupidest thing we did we took one sleep at the time. Okay. Let's see this nip is significant, but we're not build of Swansea of time and certain population. There is down that down despotic there'll be another sneak that will change the function. So you need unique to our analyses now is totally different than how we started. But this, you know, I agree with you completely. But I don't think most of the world is listening near. I mean, if I had a dollar for every time one of my patients. Came with their, you know, complete sequence. And you know, they want me to interpret them. I have the same discussion so many times. Okay. You have twenty thousand genes to my last counting may be seventy eight of them have deterministic relationship with disease. You have none of them. And we know you have none of them because if you had any of them, we would know by now, there's no chance you got here with the Huntington's disease, and we sort of missed it. Or there's no chance you have some inborn error of metabolism that somehow got missed and then we get into this whole g waas morass. And you know, it's hard to explain to people. How multifactorial these issues are. And I find myself, maybe you do as well somewhat frustrated by these discussions and the over emphasis on this genetic, you know, it's a little bit of the drunken the streetlight problem. Right. When the guy standing with other street, light, and you. Say what are you doing here? And he says I'm looking for my keys, and you say did you drop them here? And he says, no. But this is where the light is. So let me not increase the complexity but give you another munition. Okay. So we did, you know now several years ago because of funding we did our forty four best, you know, first centenary ans their whole genome sequencing so think about it. We have a study without control richest have forty four centenarians, and we do the whole genome sequencing and our question was do cinemanow have this perfect genome. I mean, maybe one out of ten thousand they just don't have all these crap from the genus those snips for hearten out severance of they're just great..

FOX inborn error of metabolism Sukumar growth hormone Hamis Teychenne Swansea Gina type Jeff twenty two percent thirty percent
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

05:20 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"I'm saying common because it's like three four percent in the population where they have a completely tion of XM three in the growth hormone receptor. Okay. So one of the Exxon's the, you know, one of the things that are important for the integrity of this hormone right is the league. And of course, you would think that that means that the growth hormone is less effective and Gillet Smail was fellow with me brought me this data to suggest that while it's three four percent in our control population. It's twelve percent in our centenarians. So I asked so what's the idea one level, and he showed it slower. And I said what's the height of the people? He said, well, that's the problem. They're much taller. So I said, I cannot do anything with this study just makes no sense. I don't know how to write to them people with lower idea. But the mutation was in the Exxon of the girls from on receptor, so they had lower Jeff five, oh this function of the receptor theory. So less idea, and we know that it was fully penetrated all their life. In other words, we there's no chance that it didn't start showing up until they were in adult WALE. Will come back to that. But the mutation didn't change and by the way, just give me some numbers here. How lower the ri-. Jeff's. I don't wreck Tionling. We're talking about like less than a hundred or less than two hundred. Okay. Yeah. Hundred is about the median level of GIF for somebody over sixty five. Yeah. I think in the studies that I told you the everage or the Nino whatever was ninety four something like that. I don't remember to answer about those people. Okay now. Okay. So he said what to do? I said well, first of all what you do genetics. Do replicated study. You know, you go to other populations. And you see what's going on there and second you do a functional study. Let's see if it's really a functional mutation so it took almost ten years. Right. And in ten years, we replicate the data in three other population in Amish French centenarians in the. The siege s here in the United States. And in all studies that people leave the longest head much more of those. Komo's I go cities in the growth hormone receptor. So that was a great validation second, the functional so hussy coin might might partnering UC we send him the lymph oblast of our patients affected, the not defect it than he is a growth hormone idea expert. So he incubated them Serem free. So without stimulation and with growth hormone and looked boated activation and proliferation by growth hormone so in Serra free without stimulation. They had less active, Asian and less proliferation. Huff of normal suggesting. Yeah, that's the mutation. That's the function when he incubated them with gross Ramon. It totally switched. I'm sorry. Going back. You talked about. Proliferation. But was there a functional difference in the lymphocyte in addition to its increase number? There's yet the the I was activated by in some of the okay some of the nonspecific activation. No, no specific to what growth Ramona's doing. But it really ration-. It's you know, that's an easy one. Yeah. When he incubated with gross money. It was the opposite. Rather than the slow proliferation. Low activation was high active Asian high proliferation. So what's going on with what's going on? When do we have high growth, months Repubic? So with high gross Ramon something has changed in declaration from log division jump to high evasion for reason with the Malacca the real mechanism. We don't know really. But that's what happened when you have high growth hormone. So they all were Toler, and then when growth hormone go down for the rest of their life. They shut off. Okay. So so, okay. So this is twelve percent of our people then Yutian sued who's a geneticist that's working on this. She was interesting micro Rene. That's another EPA genetic thing. That's comes we we haven't been thinking about. But those are our that comes from certain region of the gene and they bummed bind specifically to active region of the, gene. And they multi late will thirty percent of our sentiments have clusters of micro Rene that are over expressed by lot by forty times. You know, just immensely activated. One of them, for example, Micron ary Micronesia one forty two that's increased by thirty five fold when you incubated with with sales. It prevents the facilitation of the idea receptor..

growth hormone Gillet Smail Exxon Ramon Jeff ri Rene United States EPA Yutian Komo Huff Ramona Toler Malacca three four percent twelve percent ten years thirty percent
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:04 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"Let's let's keep going down that rabbit hole. So I was saying that one of the worries about low growth hormone idea is affect on the muscle because people think that growth hormone effects muscle function muscle size. And we found that in females and males. The one level is not associated with better worse. Lots of muscle function, including grief and getting out of Charon, you know, other things. So maybe the -ffective Loide Jeff an aging are just as good as having higher fictive idea on muscle just ways it self out. Okay. But then our studies genetics. Okay. That's what we tried to do. And. Several years ago, almost I guess a decade ago, we found clusters of mutations in the. Jeff receptor those were new mutations that haven't been found before. But we found him in nine of our Cincinnati, which was two percent of our centenarians. And that was kind of a proof of concept for us. That that clusters of mutations that are functional is what we really need to look for rather than like, everybody's doing doing Jewess and find, you know, something introducing somewhere, and this was also the first proof of concept, the growth hormone, I could be relevant to Uman human aging people that those two percent of our those nine people head higher one level because they were resistant, right? It's Jeff receptors. They're resistant to I Jeff so their level was a little bit tire. But they were significantly shorter than others. Which is a great explanation of how that FINA type would play out. You would say, well, how can they be short-statured with? Hi, Jeff, and the answer is if the isn't as affected at the receptor, right? But remember that most of our people with low idea for doing better, by the way, we take the people with. Is right men men also or just women to manning those nine people, and by the way, then they're dwarfs human dwarf that called Laurent dwarfs the evening in Ecuador and hussy coin in Volta Longo in some of the people in Ecuador were looking basically, we're trying to find if they leave longer too few of them to really know, but they have less concert unless they BT's, you know, significantly less. So there's other evidence from humans came after hours that that there is a least less age related diseases. Those people certainly didn't live better life in any way that we could assess corroborate. I mean, we we always joke that. They they weren't happy with the -ffected. They're short. So they drank a lot and that's out collegium. And then when they cross the road, nobody so them, so they're died more trauma. The, but I think it's really not true. So I met some of them we were in the conference. Everybody has to to bring his Beijing Longo brought somebody from Ecuador in. I brought a centenarian from Rome. And and the guy the T bro told the different story wasn't unhappy. It was also heavily married with a big woman and had children and with the so I I don't is the defect in them at the growth hormone receptor in the liver in the league. So they make normal amount of growth hormone their liver. Doesn't acknowledge I amount of growth hormone jackals. Yeah. Yes, they have lots of growth hormone. But it's not being expressed through the liver into I. And so they have no idea. A so. We published last year paper that took us ten years to write basically, we were looking at a relatively common mutation..

growth hormone Jeff Ecuador FINA Beijing Longo Uman Volta Longo Rome Cincinnati Laurent BT two percent ten years
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

05:08 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"Right. Look, it's it's really difficult. I afford, for example, lots of the known AMP kind activties are on much higher doses of mid for me. Well, that's my point is can you clinically match them. And no because you you really don't know at the end how much mid forming easing the sill what we're doing. Now, we're doing isolated sales. In other words, we treated animals with forming, and we're taking is elated sales to just see the ability of of with formula individuals sales in amongst homogeneous tissues. Yeah. Like, we'll take pot sides sites and look at the very expression. Yeah. Right. So it's all kind of important question. But but the story still I'll tell you the story because at the end I'm going to answer you what he's doing for aging. Okay. And I don't want to rush this story because this is a great story you take your sweet time. So think about it in a scheme. You have the mid forming in the middle getting through the plasma membrane getting to the mitral congre. And on the left side. Let's say there's the Ampy kindness. Okay. Now in the right side of sorry. Just for the listener explain what AMP kind as does the high level. It's it's a hormone of what it's a hormone of nutrient deprivation, and therefore it tells the body to do what like when you don't eat for a day AM PK goes up. Why will? But it's also an exercise me medic pathway. Yes. That's what happens with exercise. Really? That's was the the hope of what the aim behind these doing. But it's. A nutrient sensing that these impart upstream of 'em Tor. Okay. But the other side of mid forming is what happens to the might to country of because in a way. And I hope I won't regret saying it here, but mitt formulas the weakside night. Okay. Look what cyanide acted at complex four. Right. But now, you just mean more broadly speaking heading the right eighteen Heeb it, so yeah, there's less arrests production, okay in then, there's less inflammation. And there's other things that's going just because it might country are his list of see the Tiv pathway going down. So this is a great example of why binary thinking doesn't very doesn't do very well in biology, right? It can't be all or none will. So now, I can go on and on and connect, although sweet due to eventually. A pillar of a, gene. But I wanna insert another thing because other things are happening, for example, insulin levels goes down. Right. Why is it just due to the reduction of paddock Lukasz output? I'll tell you why I think and then also inflammatory factors are going down. And there's a whole NF Cup be action of mid forming that might be part of the hour s and part could be independent even without my congre. Okay. It's confusing. But this is the point I wanna make I don't know which one of those is important for aging, but parts of what you're measuring is the following yueh-fei the aging on a cellular level. Okay. So the younger that the sales are younger a lot of things are correcting themselves. So I think at the end the lower insulin levels low inflammatory are not necessarily direct effect. And that's why we're we're fighting all the time a buck multiform these doing because you can measure lots of things, but the things you're measuring because aging was fixed and once agents fixed, then there's whole Hemel dynamic readjusted, or whatever you wanna call eat. And then you're measuring that everything, and this is not only typical mid form this with rapamycin with veritable. You also can see that. There's a lot of things that are improving themselves. And I think we have to get used to the FEC that when you have a drug that we argue what it's doing because everybody's measuring something some of it is true. But it's like secondary. It's you fixed it richer, and unrelated, and it's funny. You mention those three which again, I think speaks to an advantage you have with tame. So when you look at rapamycin, reservoir, trawl and metformin the big advantage of metformin. Is you already know the dose and the frequency with rapamycin over dinner tonight. I'm gonna give you my philosophy on the dose and the frequency than we can discuss it. But I can't demonstrate it to you with anywhere near the validity that you could do the same with metformin at wonderful discussion with David Sinclair and bioavailability came up on resveratrol. Right..

metformin David Sinclair FEC Heeb Hemel
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:37 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"From prescription to usage to mortality exactly, and they're probably they don't need to d- to be the identify after mortality when you're dead. You're not prime. Any more K? So they did this study. So what they've done their four arms to the study. They came and took patients who are on Sufen Lereah twelve thousand patients. Okay. And they matched them to twelve thousand people without the Beatty's. Okay. Same pharmacies same doctors controlling for some other things. And of course, the people in sulfonate Maria had higher mortality than their control. You know? Right. Doubles. Of course, they had to be taking this oftener diabetes. So that's okay. Then they took seventy eight thousand people on myth for me and seventy eight thousand people who were non diabetic again matching them and the seventy eight thousand on metformin was met form in mono therapy monotherapy first line, right? And they watch their mortality so just to. Underline again, the people on metformin had diabetes control didn't have there are more bee's than the control. They also have more diseases than the control, but they had significant less mortality seventeen percent less mortality. In the mid forming group, and you know, the sulphonate Maria group was okay. So if you get less mortality with metformin when the setup is diabetes that really shows that mitt forming has a very important affect in Newman's as far as aging. What was the median dose of metformin in those populations? They were over thousand milligrams. That's it just a thousand milligrams. They intended more, but the average was about fifty meter about you know, I don't just fifteen hundred. Yeah. No thousand Manhattan story. They. This is a discussion there. I don't think they really could volley date the dose because an elegant thing to do if you have seventy eight thousand in your database is now stratified does. Absolutely. They taking five hundred thousand fifteen hundred two thousand they couldn't do that. And I really cannot answer you if you can get back to the data or not, I really don't know. The does the does which came from other studies. But you know, that's not the only thing we know about mid form that what was the what was the time course of that. By the way, do you know how years five years more tougher five years exposure to metformin or five years of prospective mortality following? No. It's will it's all it was all prospective study. Okay. It was all perspective study when they started. Okay. They went back. They looked at everybody on it for me. I'm asking is do we know how long the needed to be on metformin to achieve the Begnaud? We don't know. Okay. So we followed them for five years of mortality in a prospective cohort. But they could have been on metformin for five years or twenty five years. We don't know. No. It's newly it's newly prescribed for me. They were not more though. So we have normalized by duration. Lutely, absolutely, no. They haven't been on. It's forming before those are newly diagnosed type two diabetes so to near that's a pretty to be blunt goddamn staggering result. So my metformin moment nowhere near as dramatic as yours. Be basically came out of a research project. I did with two analysts in two thousand thirteen and I don't even remember what prompted the question. But there is a question we had internally about what was the benefit of metformin. Oh, now, I remember the quest. The question was was the relationship between hyperinsulinemia and breast cancer. This was the question we wanted to ask and as we dug and Doug, and Doug, and Doug and Doug something kept hitting us over the head over and over and over and over again, which was with or without diabetes with or without obesity with or without hyperinsulinemia any way you slice and dice the data of.

metformin diabetes Beatty Sufen Lereah Doug sulfonate Maria sulphonate Maria group hyperinsulinemia Manhattan mitt breast cancer Lutely Newman five years seventeen percent twenty five years fifty meter
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

02:16 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"See if it really how much of it is regularly. Mediated verses not or. Yeah. Or more nerve on the you know, the nerves because we do it's not only got to me we do a little bit a generic too. But it's through this the nerves and not through a chemical reaction on the liver. You see this is the problem with metabolism near the more. I go into it the less. I know it drives me nuts. My absolute knowledge increases incrementally. My relative knowledge falls precipitously. I think I realized that you know, what to ask. So you're undermining your own abilities. But it's really it's really the integrity of metabolisms really very confusing to explain so we will define insulin resistance at the muscle. Whether it be from an aged phenotype or a diabetic phenotype as a scenario under which a fixed amount of insulin hitting the insulin. Receptor produces fewer glued for transporters. Is that a fair definition? The definition of insulin resistance is really different in very simple. It's all about the glucose uptake in the muscle rates all about that -bility of in. Insulin to clear glucose. Okay. That's the only way we define clinically insulin resistance. Although that totally misses the point because those insulin levels have different affects on different issue. But for us, the insulin sensitivity is totally related to the glucose optic. So let me give you an example. So when I use an oral glucose tolerance test with my patients, I'm a bit of stickler. So if they take their seventy five grams of glucose, LA I measure their glucose and insulin at baseline administer the glue cola, thirty minutes later, sixty minutes later, ninety minutes later, and if I'm feeling aggressive one hundred twenty minutes later, we re measure the glucose, the insulin and the FA, then maybe even the peptide, but for simplifying it just the glucose and insulin. So let's assume you have to patients who start out with a fasting glucose of ninety milligrams per deciliter and six insulin of use of six..

one hundred twenty minutes seventy five grams ninety minutes thirty minutes sixty minutes
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:54 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"So we are walking around if I bowl issue with glucose right now and your blood glucose rises from wherever it is right now ninety two two hundred let's give you an enormous bowl of glucose. I double it. So you're up to one hundred eighty milligrams per deciliter this very high screaming high level, which by the way, only amounts to an extra few grams of glucose, but nevertheless, what is the chain of events that leads to insulin being secreted and the muscle. Ultimately disposing of that glucose both actively or passively will there be obviously secretion to insulin. That's relative to your Lucas level. And so that the beta Sal is the sensor right an outcomes insulin. And now what is insulin doing to the muscle and insulin through the insulin? Receptor will. Get translocation of the glut for those of the glucose transporters that are the major glucose transporters muscle. It will go from an intracellular pool into the plasma membrane integrated in starts getting locals like crazy into the and that happens quite passively. Meaning once the glut four transporter is translocated across the cell, membrane glucose can passively rush. Incorrect, it doesn't require ATP to bring it in a great way of any sort. Correct. An infected has its own intrinsic activity. That's not the energy dependent. So he can go faster or slower by by different ways. Now is there another method by which without insulin? We can get glucose into a cell that somehow relies on AMP China's not named Py kind. But there's none insulin. Mediated glucose optic. In other words, there's a way for Lucas to get up without the incident, and we know that from hyperglycemia clamp and from. Other things that when we can move into their or keep insulin level at basil. And still there's a substantial Luca's optic. That's happening. So yeah, we know what's the mechanism of I'm I'm not sure I know it also seems to be enhanced by exercise. That's true. That's true. This ninja is the non intimidated glucose update something that is exercise dependent to mellow. That's what now industry your questions. AMP kind is just part of the net. And I I don't know that I only have one patient in my practice who has type one diabetes, but he is such an interesting patient because of his incredibly strict dietary control and his unbelievable appetite for exercise. And he I've never seen a higher level of adiponectin in a human of never seen a higher level of sex hormone, binding globulin in a human way. Which are basically, and we know how much insulin. He has because he injects it, and he injects so little insulin to himself, and yet can to you know, he has a hemoglobin A one see below six using six to eight units of insulin a day. And so what got me. That's what got me very interested in this. Non insulin dependent glucose uptake. Yeah. I'm not doing this research anymore. I used to in front of that I- glucose itself can modulate local China's activity in the lever. There's a lot of things that happening. And of course, there's coordination between the fat, and and the liver, and then I started being interested because we can do things to the hypothalamus and take over these insulin and muscle in fat and liver. We can do it all from the brain. Isn't that amazing? Well, just because I'm so fascinated by this. And I think it will help the listener to understand the complexity of what you just said if I took an animal and put a. Elision into the ventral part of the hypothalamus a normal animal. What could that do what would that change about its metabolism will that would increase basically, food intake and change a lot of the peripheral physiology? But we do basically the opposite. We give insulin to Potala mousse or glucose or or lifting. Okay. And then we see what happens to the brutal birthday, those hormone levels are not increasing adult and not only that the liver is a good target to follow because what you can do with the liver. You can do selective of gotta me and everything that you did through the brain doesn't work anymore because it needs the nerves writes all explained to the listener what that means. So the Vegas nerve connects the body through this para sympathetic system. And of course, if patient has a liver transplant or if you do an operation where you sever the Vegas nerve. You sever that connection between the central nervous system and the periphery correct? And so we can do it's experimentally an end it will help us..

Vegas AMP China diabetes Lucas ATP hyperglycemia China Luca Py I
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

02:01 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"In the end has to be the liver because it had leased has the capacity to turn excess glucose into fat, whereas all of the other organs are going to be saturated. That's true. And that's part of I think where the glucose is knowing. Okay, too fat into liver. Okay. So what am I telling you? I'm saying that insulin resistance is a protective mechanism. It's a modulator. It's a stress response something. So now, I understand why a stress response mechanism in one animal caused them to leave longer and in another animal, it's a pain in the butt. So I went and I wrote this review with with Luigi Ferruccio. I wrote this review where we took all the animals that had problems with their insulin sensitivity the animals that are insulin resistance and leave longer and the animals with insulin sensitivity that leaves shorter. And there's a huge list of it rep Amai. In is an example, right rep amazing causes insulin resistant the animals the best intervention in in rodents. There's the PT one transgenic animals, it's very insulin sensitivity, and he's has huffed the lifespan the lifespan of a wide when you say insulin resistance, insulin sensitive. Are you always referring to muscle? Are you referring to liver? How are you defining them will in this sense? It was everything it was I arrest, for example, iris one IRS to know cout, some of them owning the brain. So it was really insulin resistance everywhere is IRS one found in the muscle and not deliver. No IRS one in Irish to are everywhere, but IRAs stew is more in liver. Like, the the sort of have selective express. Right. Yeah. So just translate IRS one insulin receptor substrate substrate. So let's talk about exactly how the muscle takes glucose..

IRS Luigi Ferruccio
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:03 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"Can you just for the listener define? What is the analog of daft to Daf sixteen and us Duff to ease the insulin receptor and doffs sixteen is the fuck. So the folks oh transcription factor. But the point is at this time that you took a worm that normally lives two weeks, and you turned down its insulin receptor slightly not off correct. Right. But you made insulin resistant, and it was accumulating fat. And what was? Cy bringing into the field. I was saying the major reason for aging is this insulin resistance syndrome, and the main part of the insulin resistant is accumulation of visceral fit. And so the premise was good digs Empel was disaster. To me, I had the JC I taper adept timing press really showing with MRI pictures, how caloric restriction decreases, the visceral fed I was talking about the biology of those fed and stuff, and it was a major power Dokes for us in the field. And how we continue if we're saying insulin resistant is good for longevity and everybody diabetes news. This is a disaster. Why am I telling you that because I learned later I was thinking later on experiments that I've done out. So first of all experiment that I've done that was very conclusive was I took. Bunch of Ritz hundred fifty actually and all of them underwent surgery after puberty in some of them, I removed their visceral fat depots by surgery and in the other. It was a sham procedure just moved but didn't remove and we had three groups in the experiment. One was Ed Lee, boom, feeding the second was caloric restriction. This is the control they would leave forty percent better. And the third group was Ed Leedom feeding of the Retz that their visceral fat was removed. And I said, you know, without the visceral fat even with nutrients, they leave longer and they actually leave significantly longer than the Leedom by twenty percent. But not as much as the caloric restriction. Just make sure understand you had a two one ratio of your animals because you had no I had three groups three groups, but one of all ad lib feeding of the visceral. Fat removed that was right. And then of the ones that had sham surgery. They were randomized to ad-lib versus CR, correct? It's really showed that visceral fat, the removal of visceral fat had major effect. And when the animals who had the visceral fat removed were autopsied or whatever the word is for rat. Autopsies had they re figured out a way to reaccumulation visceral fat or where they accumulated now. In fact, when you do this procedure after puberty if you do it before puberty, they accumulate visceral fit, otherwise don't accumulate much visceral set did they have changes in subcutaneous fat. That's a good question mice heavy when you do it and Retz do not what do they ultimately succumb to? They all die from the same thing only different times. Which is what cancer? Yeah. It was Sprague doling so kidney disease cancers were the leading causing debts. So you basically got half the benefit of CR by doing this. But. Doom but without visceral fat. So you understand it's very sorry. One other question near was there any change in their health span or their spry nece? Yes. There was a helsmman. In fact, what happened to the Libby doom that lead doom starts losing weight at the end of their life and the ad lib doom with visceral fat have still gained weight after the others. You know, it was a significant change in weight. And then there's a whole hell spend their insulin levels and other things that we've been we've down in parliament..

CR Retz Empel Ed Leedom Duff diabetes Ed Lee Libby Sprague twenty percent forty percent two weeks
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:28 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"And you know, we know now that it's total collaboration. Yeah. You increase insulin resistance and the punk ass have to secrete more insulin, and we Uman's at least in the condition of our environment of BCC everything. Many of us. I would say forty percent cannot deal with it. And we become diabetic. There's the Starling curve of the punk-rock. You know, like like for the heart that increasing soon secretion at some point you cannot increase insulin. Secretion you become the basic and then insulin secretion decree decrease and so- insulin resistance was a major way. And that's why mitt forming was a good place to come with. You know, at least it it affects mainly the potty glucose production. Rather than the muscle though. I have to tell you in vitro on muscle specimen. It's an insulin. Sensitizing the muscle to. Let's talk about this idea of. Insulin resistance. I think there are a few terms that leave me scratching my head more than that one. So this is an example of something where maybe five years ago, I thought I really knew what insulin resistance was. And I think today, I'm pretty sure I don't know what it is in the sense that when you take the typical FINA type of someone who's insulin resistant. What do they look like bio chemically, and and the morphology, right? So they're hyperinsulinemia. They have elevated levels of glucose, they probably have some degree of obesity or outta positi. So what does that mean? Because clearly there fat cell is quite sensitive to insulin. If the fat cell ever became resistant to insulin. You could not reestablish fatty acids, and you would have an endless stream of policies exiting fatty acids from the fat cells you'd actually be quite lean. There's something going on in the muscle that clearly is resistant to the effect of insulin. But of course, there are both insulin dependent and insolent independent means by which we can dispose of. Glucose, and this is were coming back to what you said a moment ago. I actually wanted to ask you that question, which is that we'll park it. But the question was does met four men participate in the MP K driven insulin independent modality of glucose disposal. You're nodding. So I think that's a yes. And we'll come back to it. And then there's the liver, and this is the one to me that is the most complicated and the one I'd like to begin with. So before I ask you to elaborate on the specifically what is meant by insulin resistance in the liver. Am I complete moron for not understanding this? No, can I make a little bit more interesting even because I need to bring it to aging. Yes. I would love to talk about the Abe's. But let me just put up front. I don't I'm not sure that that the beaches property of forming a really the aging properties of mid for me. Okay. This is my vocation, but let me go back to insulin resistant because in in nineteen. Ninety-seven is science paper appeared that made the best day of my life and the worst day of my life. Okay. Wow. What was the paper? The paper was taking inimitable. Okay. Primitive model? Decreasing the insulin sensitivity, this is known as the Duff to model, and when you do that the Nemet owed accumulates fete in their intestinal sales. So they are becoming visceral bee's and they leave several times longer. So why is it might the best day in my life because you could with one genetic manipulation extends lifespan significantly that meant going from hope actually from nothing froze, the cynthia's paper would know that's the Gary roof game. But at the same time, Cindy, either adopt sixteen Tom Johnson has had the age one model. There are several papers that came in all of them said, hey, we can change a lifespan. And the exemple was always ancient since the end this mutation to be clear between Daf two sixteen and the dietary manipulations there are several permutations of that see elegance model, but just to make sure I know which paper were talking about this was only attenuation of Taft to nothing to death sixteen and nothing tonight. Terry, right, right..

hyperinsulinemia Uman FINA BCC Duff obesity Taft Cindy Terry Tom Johnson forty percent five years
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

02:15 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"But I'm I'm happy to be corrected if that biases incorrect. But, but yeah, I've always thought that frankly, so many of the drugs that we're really interested in now as we look back from aging perspective, whether p metformin rapamycin, so many of the negative side effects that people typically associated with those drugs are very difficult to isolate from the patients in whom those drugs have historically been given. And so it's nice to hear that that Malla is now being generally recognized. As an alternative of viewpoint to that. You know, metformin is to me an interesting drug from a diabetic standpoint. Because and I don't I don't know that this was appreciated in the eighties. In fact, I would suspect it was not because there's really two macro strategies for improving type two diabetes. You can obviously the highest goal is to control glucose levels. So to to regulate the degree of glucose in the blood, but you can do that through at the highest level two ways. You could increase insulin either exaggeratedly or through increase, insulin production pharmacologically, or you could reduce glucose, and of course, metformin falls into the latter category of that or increasing muscle insulin sensitivity for to enhance glucose disposal. Today. It's generally regarded that while both strategies will have an equal benefit on the micro vascular the glucose lowering by insulin lowering. So the less glucose production strategy has a superior effect on the macro pass catcher. And therefore metformin would be a better alternative to for example, drug. That's going to increase insulin. Production of the pancreas was appreciated at the time. Meaning when you were doing this in the late eighties. How potentially beneficial this drug was well adept time in the United States. It was all about insulin resistance, you know, people Jerry riven rows DeFrantz Zo, the people at the NIH Ron con where all discovering the insulin receptor discovering, insulin resistance discovering this association of insulin resistant with the Bullock syndrome. So it was all we all had the bias that the major problem with type two diabetes, insulin resistance..

metformin diabetes Malla NIH United States Bullock
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:42 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"And we've done these animal, and it was done these sales, and you're trying to show what is the major mechanism of action you you would have failed. So what I showed in Newman's is that. Admit forming targets if glucose production or the insulin sensitivity of liver, and that's the major mechanism of action. Unlike for example, Sufa Nina RIA that increasing Suissa creation right or TC dis increase the incident sensitivity in the muscle more than in the levers. So this was the mechanism that you could pick to the FDA, but it's really not the interstellar mechanism of mid for me. So at the time was it understood what metformin activity was on complex one of the mitochondria. Now, not really this came later. I I don't know what year, but he came later came when the seahorses essays were developed to show really which might Connery in which possibly of more might to Conrad you have changes. Maybe for the listener explain what a seahorse ASA is seahorse essays an essay too. To look at my Takao drill action. Whether you extract my country, our even tissues, it really shows some relationship between oxygen consumption in relationship to philosophy and it's very sensitive to look at some of the effects of drugs that are interferon might contra action or decrease might con- relativity in the indirect calorie Matry of the might occur riot right indirect because it's a provocative test, Johnny. So yes, metformin was discovered from a plant as well. Correct rights. It's a French lily firstly, obviously in this was discovered been forties or fifties. Correct. The first thing that happened. The was a drug by the name of informing a cousin of mid for me, which apparently is much more potent. It's much more potent. Because unlike mitt formity dozen need it transported to get into. The sales on the other hand it was associated with a lot of luck tick ac- doses in it was considered unsafe. Eventually and then mid forming was a safer part with much less of electric those side effects. What is the mechanism by which metformin 'cause like the doses because in all the use I've seen of metformin clinically. I've never seen a case of it. Which is not to say, it doesn't happen. I'm sure it does in you could stack risks by taking someone with renal insufficiency giving them contrast in tons of metformin, but in medical school. This was like the board question you got asked every single test. What you have to worry about lactic acidosis, what's the putative mechanism by which that happens? So first of all, I would tell you that in my study in the eighties every patient that we gave its forming headed increasing lactic 'Seat from what to what Miller within the. Normal range. So if it's too was the cutoff the cutoff. So it was you know, between went from wine one point five towards the two. And sometimes even went over the two, but it wasn't really anything associated with the does. There was no change in ph. Now now, no onion gap not to anything like that any probably has to do. I I don't know that I can tell you for sure, but it has to do with what happens when complex swan part of the bully effect when complex one is in heated, but there's lots of speculation, and I don't really care to comment on on that. But I think what became clear there is all we call it chronologies it Malla, it's mid forming associated lock tickets those. In other words, we moved away from it forming causing guts to this association because it. It's if anywhere described more in people that have kidney failures or have heart attacks or something and had locked dozen wear on with forming too. And that was kind of this association, but it's not clear to me that they're truly people who developed lactic acidosis from informing that these just because of Mott forming and not associated with something else. I'm glad to hear you say that sort of generally been my bias..

metformin mechanism of action lactic acidosis Newman Sufa Nina RIA Malla FDA renal insufficiency interferon Connery Conrad Johnny Miller
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

03:50 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"And so my first part of my life was metabolism. But then I started doing what I really was interested in this is aging in the biology of aging, and I remember reading a quote once from you that said may be paraphrasing. But metformin is the reason I came to the United States will in a weight was, but this is life in retrospect, right? I wasn't really expecting. I was done with mid forming nineteen eighty eight that was down with forming Antilles started again about three four years ago while I can't wait to talk about metformin because they're probably I'm trying to think if I think four or five eggs molecules, which is just the terminology used to describe anything that you ingest or take that comes outside the body. So I would include drugs supplements hormones anything in there. But when you lump. All of these things together. If I were to say, what are the three or four of these that I'm asked about the most frequently from patients, or frankly, anybody if I met at a party, and I let it slide what I do for a living. The first question is should I be taking metformin, and there's usually a handful of others that they wanna know about IB taking nicotinamide right beside. They usually don't say that usually say should I be taking any or something to that effect? So it's wonderful that we will speak today because few people can speak about metformin the way you can. And so I'm really looking forward to that. But before we got on that path. I do still want to kind of understand a little bit more about your journey and your interest in chronology, did you know from day one when you entered the field of medicine that this was the area that you want to study. Yes, I was interested in aging from the time. I was pretty much thirteen and spend weakens with my grandfather who was telling me his life story and. He's life story wasn't easy. And he did let's physical things, and he dried this woman any did this and that and I'm looking at the man who was then sixty eight years old that walk slowly, he's obese white hair. Any just didn't look like somebody who did everything he told me to do. And you know, they say that children heavy machine -ation, but most kids don't see their Crin parents as what they will be right. They see them as I don't know how they got there. And this really stuck with me. And I started to be interested in the biology of aging when I was for example, when I did my residency I always was interested in how not what's the age of the patient, but doesn't look older or younger than his age. I kind of realizing to Italy that there's. Chronological age and biological age. And won't what is this differences between the biological and chronological age in a course is the physician it looked like endocrine is a good place to start because you knew that there's a lot of the chronology Neiji, and you assumed that hormones are going down or some are going up, but if you could fix that maybe you could fix a lot of aging now everything happening my life was fascinating from the biology of aging replacing the hormones wasn't really part of. But we'll get to going to the hormone thread. The most obvious example of changes in hormones with aging. Of course, occur in women where you know, they have this very abrupt change in one of their undercurrent systems this androgen system. Did you think about it? Even more broadly than that, for example, like what was happening in firearm hormone, and what was happening in fuel partitioning hormones and other things like that. Oh, absolutely..

metformin United States Crin nicotinamide Italy sixty eight years three four years
"barzilai" Discussed on The Peter Attia Drive

The Peter Attia Drive

04:08 min | 3 years ago

"barzilai" Discussed on The Peter Attia Drive

"Drive and happy new year to everyone took a week off as you probably noticed. So hopefully, everybody's ready to jump back into this fun stuff. My guest this week is near Barzilai. And if you're at all into the space of longevity, he'll be no stranger to you near is the founding director of the institute for aging research, the Nathan shock center of excellence and based biology at Auburn Stein, he's completed two fellowships one in metabolism. At yale. The other in endocrinology molecular biology at Cornell, he directs the longevity genes project, and in my estimate near is probably the most knowledgeable person ever on the genetics of longevity. And we talk a ton about that during this episode. He also is leading the effort to test metformin in a prospective clinical trial for non diabetics with respect to aging, and this is referred to as the tame trial. We. Get into that obviously in detail here and also will use a lot of the data for that in the show notes. This is in many ways, I think near is probably one of the most insightful people when it comes to understanding the clinical benefits of metformin. And we talk about that a ton. We also talk about insulin resistance. I can't resist the urge no pun intended. I guess to get into sort of a detailed discussion on what I are is with sort of people who are really deep in the space. We talk a lot about I Jeff and growth hormone. And I gotta tell you. This is a topic that you've probably heard me waffle on a little bit because I'm still really kind of on the fence about this relationship of I G F G H centenarian data point in one direction. I think the EPA Miala g outside of centenarians point in a different direction. And of course, none of this really speaks to the question. I get asked constantly, which is do you think administration of growth hormone is beneficial from a lifespan or health span perspective, or do you think it's harmful and truthfully? I've always leaned towards the. Harmful side, but we get into this in detail in near offers. Some great insights certainly for me. I was really helped by this process. We do go back and talk about the centenarians. And because I'm in the midst is some of, you know, writing this book, I'm knee deep on health literature. And so it was really great to kind of clarify a few things that I think even if you're not steeped in this stuff what you'll find very interesting. And of course, we talk about all my other favorite topics like Ataf Aji, caloric restriction. We even get into a little bit of the stuff around any D And nicotinamide riboside and things like that. So overall, I think this is a bit of a technical episode. But not that technical we certainly done more technical stuff. The show notes will be valuable as always especially for show of this nature. So with nothing else to add please welcome to the show near Barzilai. In your. How are you? I'm terrific. Are you? I'm good. I can't believe not only did you make it down here on time. But you made it down here ahead of me at my own place. Nice to stay on. Yeah. This is this. I don't know how these these days is this weather, so unpleasant. But yeah, you beat me here. I if I was a bit of a bit of sun pleasant for you because you're in California, most of the time. Yeah. I think that's part of it. But you're from Israel. So this has to be unpleasant for you to Israel was too warm for me. I'm okay, got it. Speaking of which so you were born in Israel, you spent how long were you in? Did you serve military time? There ESI served military time, I was in nursing and medical student. I went to the technique medical school. I went into DASA hospital for residency, which I finished and only then I came to the United States that was a teal with Ralph diff'rent Zo doing 'em topples. Actually, I was looking at the mechanism of action of mid forming a nineteen eighty-seven before it was approved for using the United States. There's a. Deputies connection to that later. And then I went to Cornell for an endocrine, fella sheep, and then I was recruited to Einstein..

Ataf Aji Barzilai growth hormone Israel metformin United States Auburn Stein Cornell yale founding director Ralph diff'rent Zo mechanism of action Nathan California EPA Jeff nicotinamide
British Eurovision entry SuRie rushed by stage invader

5843 Show

01:18 min | 3 years ago

British Eurovision entry SuRie rushed by stage invader

"Winner of the eurovision song contest musical representatives from more than forty european countries squared off in portugal for these sixty third eurovision song contest votes came in from all over europe an estimated two hundred million viewers saw israel's entry netto barzilai be crowned champion for their song toy which carries a timely theme after winning netted said backstage i celebrate myself cyprus finished second israel's first winstons nine hundred ninety eight means it will host next year's contest brian clark abc news this is abc news komo aaa traffic we're getting a lot of traffic congestion going into the city of course that's part of the revive i five project and we're seeing heavy traffic northward between i five west seattle bridge and all the way down the number of lanes over the weekend and it looks as though we have a fairly lengthy backup in quilt senior one zero one southbound between fish hatchery road mount walker road an accident blocking a lane and in seattle we have an accident lake city way and eric place northeast your next report nine fourteen i'm mike conkland on komo news hi.

Israel Brian Clark West Seattle Bridge Seattle Mike Conkland Portugal Europe ABC
Eurovision song contest held in Lisbon, Portugal; Israel's Netta Barzilai takes top honors

NPR News Now

01:25 min | 3 years ago

Eurovision song contest held in Lisbon, Portugal; Israel's Netta Barzilai takes top honors

"To agree to show up in court researchers say more than four hundred thousand americans are stuck in jail every day because they can't pay bail for npr news i'm amy kylie in atlanta a new lava fisher has opened up on hawaii's big island in the vicinity of geothermal energy plant the us geological survey said that brings the total number of fissures to sixteen president trump on friday made federal aid available by declaring a major disaster on the big island the hawaiian volcano observatory reports the fisher opened up about a mile northeast of the last fisher and east of the puna geothermal venture plant this is npr news israel has won the eurovision song contest one of the world's most popular televised competitions beating out twenty five other countries entrance allison robert's reports from lisbon where this year's competition drew tens of thousands of fans from across europe and beyond the year these in some contest drills at global tv audience about two two hundred million from joining don'ts music to heavy metal that was a bit of everything in this year's grand final portugal has the competition for the first time having won last year many acts book packed with special effects including fireworks.

Amy Kylie Hawaii President Trump Israel Allison Robert Lisbon NPR Atlanta Europe