Podcasts about ADB

Send us Fan MailThis episode, Jez is joined by Mitch from ADB magazine for our first live podcast recording and it was at the Finke street party before the race.We interviewed - Ryan BranfordBen GrabhamDani FootPete BedfordClubbyTrent GilesStu from the Six27 race teamCampbell Hall and Brock Ritchie from HTr racing team.Support the show

Dr. Deb Muth 00:00:09 Hi there, how are you? Bob Miller 00:00:10 Excellent! Pedaling as fast as humanly possible, but doing okay. Dr. Deb Muth 00:00:14 Good, good. Well, I’m looking forward to our conversation today. This should be amazing. Bob Miller 00:00:20 Yeah, it should be a lot of fun. Dr. Deb Muth 00:00:22 Yeah, anything that’s off-limits for you in, our conversation? Bob Miller 00:00:28 No. Dr. Deb Muth 00:00:29 Okay, anything you want me to make sure we cover for you? Bob Miller 00:00:33 Well, I mean, is it okay if we put a little plug-in for our software? Dr. Deb Muth 00:00:35 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:38 Hey, can we… can we do a screen share? Yes, we can. Yeah, because I want to show you some maps, and… Dr. Deb Muth 00:00:43 Okay. Things like that, yeah, so… Perfect. So just let me know when you want to do screen share. Bob Miller 00:00:48 Okay. Dr. Deb Muth 00:00:49 And yeah, feel free to plug your software wherever you want to. Bob Miller 00:00:53 Okay, well, good. Let me pull up a, a slide for that, and give me one second, I just want to shut the door to my office to get the noise down. Dr. Deb Muth 00:01:01 No worries. Bob Miller 00:01:16 And, how should I refer to you? Dr. Debb? Dr. Muth, what do you like? Dr. Deb Muth 00:01:18 Dr. Deb is great, or Deb, either way, I’m pretty informal, so… Bob Miller 00:01:22 Yeah, and… Bob is fine for me. Okay. Yeah. Yeah, there you go. Why people feel like they need this, son. Special name, it’s like, seriously. Dr. Deb Muth 00:01:33 Right? I agree. Bob Miller 00:01:35 When I work with my clients, it’s like, Dr. Millison, just, just bop, just, just bop. Dr. Deb Muth 00:01:41 Yep, that’s how I am, too. Just call me Deb, it’s good. Dr. Deb Muth 00:01:44 They feel a little awkward with that, you know? They’re not used to that, but… Bob Miller 00:01:48 Alright. And you’re a naturopath, medical doctor. Dr. Deb Muth 00:01:52 A nastropathic doctor and a nurse practitioner. Oh, nice. Yeah, so I got the best of both worlds, right? Bob Miller 00:01:58 Yeah, damn. Okay. Alright, so here we go… There we go. Alright, so I got that ready, and then I will do a, I will do a screen share. I think you’re gonna really, appreciate what we’ve come up with. We’ve come up with the concept of, Cellular CPR. Dr. Deb Muth 00:02:23 Oh, nice! Bob Miller 00:02:24 And that is, construct the cell membrane, Protect the cell membrane. And restore it if it’s damaged. Dr. Deb Muth 00:02:32 Love that. Bob Miller 00:02:34 I love that. Yeah, so that’s what we’re focusing on, and then how, You know, we want to get to the point that, you know, most people think of genetics, they think of, like, 23andMe or Ancestry. Dr. Deb Muth 00:02:44 Yeah. Bob Miller 00:02:45 And then you have the professional geneticists who are looking at, you know, odd things that could create a disease. We’re looking at functional genomics. Dr. Deb Muth 00:02:54 Which is so much better. Bob Miller 00:02:56 Yeah. Are you familiar with what we do here, or… Dr. Deb Muth 00:02:58 A little bit, a little bit. So, it’ll be new to me, too, so I’m excited. Bob Miller 00:03:03 And how much time do we have? Dr. Deb Muth 00:03:04 We have an hour, give or take a little bit on either side. Do you have a hard stop anywhere? Bob Miller 00:03:10 No, no, I put a, I moved my clients around, and I don’t have anybody till, 3.30, so we’re good. Okay. Dr. Deb Muth 00:03:16 Perfect. Alright. Bob Miller 00:03:18 It’s like we’re getting started early as well, so… Dr. Deb Muth 00:03:19 Yeah, we’re getting started a little bit early, so that’s good. Bob Miller 00:03:22 Yeah, I just got my office cleaned up, so… Dr. Deb Muth 00:03:23 Okay, good. All right, are you all set to get started? Bob Miller 00:03:28 I’m good to go, my friend. Dr. Deb Muth 00:03:29 I’m gonna just record a little intro and a little bit of a, hook for people, and then we’ll get started. I’ll ask you to kind of tell us a little bit about yourself, and then we’ll just take this conversation wherever it’s supposed to go. Bob Miller 00:03:39 Okay, you got it. Dr. Deb Muth 00:03:40 Alright, sounds good. So what if the reason you’re not healing isn’t your diet, your supplements, or your labs, but it’s actually your genes? Dr. Bob Miller is uncovering how genetic variants, when combined with modern toxins, explain why some of us stay sick no matter what we try. Today, we’re talking genetic pathways, detox blocks, and the new science every wellness warrior needs to know. Welcome back to Let’s Talk Wellness Now, the show where we uncover the root causes of chronic illness, exploring cutting-edge regenerative medicine, and empower you to heal from the inside out. I’m Dr. Deb, your medical detective, and today, our guest, Dr. Bob Miller, is a true pioneer in functional genomics. He’s a board-certified traditional naturopath and the founder of Neutrogenetic Research Institute. And he’s the leading groundbreaking research on how genetic variants influence chronic illness, inflammation, and detoxification. His work has been recognized on international stages, uncovering links between genetic expression and conditions like Lyme disease, mast cell activation, or MCAS, and mitochondrial dysfunction. I’m so excited to talk to Dr. Bob today. He is gonna reveal some things that even I don’t know about, so I’m excited to learn alongside of you guys. So… Dr. Bob, let’s get started. Tell us a little bit about yourself, and kind of how you got on this journey. Bob Miller 00:05:04 Well, that’s, that’s interesting. I was sort of like a mid-career coming to the natural health field, because in my early 30s, I found myself with a severe case of ulcerative colitis. Bob Miller 00:05:15 And I was in the hospital for 21 days. probably within hours of death, pleading to death. And they told me I’ve got one option, and that is cut out the colon and wear a bag. Didn’t sound like a lot of fun. Dr. Deb Muth 00:05:27 Not an option I would want. Bob Miller 00:05:29 So, you know, the medical folks wasn’t real happy with me, but I said, yeah, I’d like to explore some alternative things.Never thinking that I’d get into this field, and then I just, you know, worked with some herbalists and things that I found absolutely fascinating. So, that’s how I got into this around 30 years ago. And, haven’t looked back since, and just having a… having a blast as we now move into how our genetics impacts things. So, that’s what we’re gonna… that’s what we’re gonna talk about today. Dr. Deb Muth 00:05:58 I’m excited to talk about this genetic thing. When you started over 30 years ago, what kind of patience and problems first inspired you to dig deeper into that root cause healing and kind of get into the genetic piece of it? Bob Miller 00:06:10 Sure. Well, you know, as a… now, I’m in a part of the country called Lancaster County, Pennsylvania, where there’s a lot of Amish and Mennonite, and they gravitate towards these things.So, this is their first thing to do, and that doesn’t work, then they’ll go other routes. So, you know, back then, we just saw typical, you know, a little tired, constipation. You know, a little bit of fatigue, arthritis, those kind of things. But things have changed dramatically over the years, as people are now getting more chronically sick. You know, it’s worse than it’s ever been. And what we’re finding is the, the culprits Primarily is mold exposure and Lyme disease. When people get those two together, they’re just… it’s an inflammatory cascade that nobody can seem to unravel. So that’s where we spend a lot of our time. And we’re also spending a lot of time looking at mental health, like ADD, ADHD. And, we give… this year I’ll be speaking at three autism conferences. And we can dig into that a little bit as to why we think we’re seeing such a dramatic increase. And aside from autism, that used to be 1 out of 1,000, now it’s 1 out of 33, or 23. You know, we’re also seeing dramatic increases in ADD, ADHD. People are stressed out. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. Dr. Deb Muth 00:07:37 This should be a fun visit. We can cover lots of topics. I am so excited. So, you founded Nutri Genetic Research Institute in 2015. What did you hope to accomplish, and what kind of surprised you in your findings so far about that? Bob Miller 00:07:51 Well, you know, let’s back up at what, you know, genetics is used for. Everybody’s familiar with 23andMe and Ancestry that, you know, tells you where your ancestors came from. Then you have your professional geneticists. I mean, these are people with a degree in genetics. And they’ll look for, you know, very odd sort of things that are prone to relate to a disease. So there are disease-related genetics. Well, in functional, we don’t look at either of those. We look at For example, how you’re breaking down your fats and utilizing them. How you’re recycling your glutathione. How you might be handling your iron. And none of those are disease-causing on their own.And none of those are disease-causing on their own. But when they pile up on you, and then combine that with environmental factors, that’s when things start to go south on us. So, that’s what we’re doing, we’re looking at patterns. And our first foray into this was, we did studies on Lyme disease. And our first foray into this was, we did studies on Lyme disease. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. Others have a little more struggle, and then others are struggling terribly for years. So there’s an old adage of genetics loads the gun, environment pulls the trigger. Dr. Deb Muth 00:09:14 Yeah, that is so true, and I think when we’re talking about Lyme and mold and things like that, we forget sometimes that our genetics can predispose us to be more sensitive to those things, and if we have genetic pathways where we don’t clear things properly, it’s harder for us to get them out of the body. And then you add on that whole rain barrel effect that we’ve always used as a functional medicine term, right? If the barrel’s half full, you’re okay. If it’s full, and now it’s spilling over, it’s a bigger problem. Have you guys found, too, that some of these environmental things actually are changing the genetics of people, or how they’re processing their own genetics? Bob Miller 00:09:53 Well, let’s go back to, Genetics 101. But we’ll go back a little bit further. So, what an interesting mechanism, what a miracle the body is. Bob Miller 00:10:03 Fats, carbohydrates, proteins, drink water, breathe air, expose the sunlight, and somehow everything gets made. I mean, when you just step back and think about that, it’s like, It’s pretty darn amazing. Dr. Deb Muth 00:10:15 I always tell women, you know, the fact that we get pregnant and we have healthy pregnancies and births is a miracle, because if we had to try to control that, that wouldn’t work so well. Bob Miller 00:10:25 Right. Well, that’s another miracle. These microscopic sperm and egg, human being, 9 months later, it’s like. But even inside of us. We are making our hair, our skin, our nails, our blood vessels, our ATP, our energy, it’s all being created. Well, that gets created by enzymes. So, enzymes take one substance, combine it with something else, and make something new. Then another enzyme comes along and does the same thing. Your DNA is the instructions on how to make the enzymes. So, when we are conceived. If it’s a, if it’s a female, of course, it’s the XX, the two chromosomes. You know, we’ve… everybody’s seen those… the genetics that… Listed pair. So, if it’s a female, the father donated the X enzyme. And the mother has no choice but to give the eggs, so that’s female. If the father donates the Y, you have a male that’s in chromosome number 1. Then 2 through 23 is the rest of the instructions on how to make enzymes. So, what can happen? We can get what are called SNPs, single nucleotide polymorphisms. And SNPs just mean that the instructions to make the enzyme’s not quite as good. So, if one parent gives a SNP on the making of an enzyme, The enzyme’s fine. It works. But, general rule of thumb, It may only work at 70-80% of efficiency. Now, a good analogy is think of an 8-cylinder and a 6-cylinder car. If parents give you good information, that’s like having an 8-cylinder car. If one parent gives you that snip, it’s like having a 6-cylinder car. Now, is a 6-cylinder car a fine car? Sure. It’ll get you from point A to point B, but it’s just going to have the power of an 8-cylinder. Then if both parents give you a SNP on the same enzyme, it may be 30-40%, and that’s like having a 4-cylinder car. Sits in the driveway, looks the same, puts gas in it, everything. But if you’ve got a 4-cylinder car. Probably not a good idea to go cross-country pulling a trailer behind you up and down mountains. Dr. Deb Muth 00:12:29 This is true. Bob Miller 00:12:32 So… We can get an 8-cylinder, 6-cylinder, or 4-cylinder enzyme. Now, if it’s not under a lot of stress, if that 4-cylinder car is just taking you to the bank and the grocery store. It’s just as good as an 8-cylinder car. But if you gotta pull that trailer, and there’s a lot of stress on it, being mountains, it’s gonna struggle. Now, there’s one other little caveat to this, and that is some genetic mutations are gain-of-function. They actually work faster. Now, we have enzymes that do all kinds of things. We have enzymes that make and recycle our antioxidants, but we also have enzymes that make inflammation. No, that’s a good thing, because if we get a virus or bacteria, if you didn’t make inflammation to kill it, well, we’d all die of infection. So, you know, we tend to think of free radicals as bad, antioxidants as good. They both play an important role. But interestingly, some of the major enzymes that make inflammation, they can be overactive. They can be turbocharged. And when they’re stimulated by environmental toxins, they overreact. Bob Miller 00:13:40 And therein lies the problem. When they overreact, we have a problem. Bob Miller 00:13:46 So, if we have genes that overreact when stimulated. And then the enzymes that take care of inflammation are underactive. Then you’re gonna be more inflamed. You know, the majority of people that, you know, come for functional medicine Or naturopathic help, or… Inflammation that they can’t seem to get under control. Dr. Deb Muth 00:14:06 Right. Bob Miller 00:14:07 And we will be, you know, during this hour, we’re going to look at some of the pathways that make that happen. So, what we can do then, we can’t change our genetics. When you’re conceived, that’s the hand you’re dealt. When your life would be over, if someone would take some tissue and measure, it’d be exactly the same as conception. Does it change. Bob Miller 00:14:28 The enzyme’s ability to do its job may be compromised. Because remember I said there’s a, the enzyme takes a cofactor. So an enzyme takes substance A, cofactor, make substance B. Well, if that cofactor’s not there, the enzyme’s not going to work either. So, you could have an 8-cylinder car, and if there’s no gas in it, it’s not going anywhere. So… It’s the strength of the enzyme, it’s the cofactor to do the A to B conversion. And that’s what we’re going to get into. So, many people say, well, where did these SNPs come from? Nobody knows for sure. Sometimes they’re what’s just called de novo, when the sperm and egg go together, the instructions get mixed up a little bit. We do believe a lot of it came from a long time ago, when we were almost wiped out by sexually transmitted diseases. And those STDs were altering the genes when the conception, in other words, when the sperm went into the egg, the STDs were interfering. And causing the problem, so… I often joke, if you want to blame somebody. Blame your great-great-great-great-great-great-great-grandparents for, being a bit promiscuous, so… Dr. Deb Muth 00:15:31 Yeah, for being… having a little too much fun, right? Bob Miller 00:15:35 So, we don’t know for sure, but, you know, there are some that, But most of the SNPs that we get inherit from our parents. So, if you look at a child. And you look at the SNPs. 99.9% of the time, it came from one of the parents. Dr. Deb Muth 00:15:50 In identical twins, do they have the exact same identical makeup? Bob Miller 00:15:54 Yep, Dr. Deb Muth 00:15:56 But not in fraternal twins, correct? Bob Miller 00:15:59 No, no, those could be different, Jeff. Dr. Deb Muth 00:16:00 It could be different because they have different sacs, they’re not sharing that same genetic makeup. Bob Miller 00:16:04 Yeah, so keep in mind, both your mother and your father have, you know, the two And so you get one from one parent, one from another. Dr. Deb Muth 00:16:13 So… Bob Miller 00:16:14 Interesting situation. I had, 3, 3 boys. And, we were looking at an enzyme related to breaking down oxalates. Now, the mother and father each had one SNP, and that’s called heterozygous. Three boys, and they all come together, they’re Amish boys, they’re a lot of fun. And I looked at their genomes, and the one boy didn’t have any SNPs at all. And one had won. And the other one had two. Dr. Deb Muth 00:16:41 Interesting. Bob Miller 00:16:42 So, we don’t quite know how these things get handed off, but with the parents each having one, you could have a child with none, one, or two. So, the one, his ability to break down oxalates, which is fine. The other one was slightly impaired, and the other one was dramatically impaired. So, you can have 3 children, and it all depends what the parents have. Now, if a parent has a homozygous, or 2 copies. And the other parent has nothing. Every child will have one. Okay. If both parents are homozygous, that they both have two, Every child will have two. Dr. Deb Muth 00:17:19 too. Bob Miller 00:17:20 Yes, so that’s the way it works, but, you know, but it’s somewhat rare that both parents are homozygous on an enzyme, but it can happen. Dr. Deb Muth 00:17:27 Do we think that infections today, like Lyme disease or mold exposure, things like that, if the parent, the woman, primarily, I’m thinking, is pregnant, and she actively has these infections. Can those infections affect the genetics, kind of like a past sexual transmission did where we thought back in the day? Bob Miller 00:17:47 Yeah, I… I mean, I’m not that much of a geneticist to answer that for sure, but my thought would be no, that at conception, the pattern’s made. Dr. Deb Muth 00:17:55 Okay. And then that’s… that’s the hand you’re dealt. Bob Miller 00:17:58 Yeah. So, I tell people we have good news and bad news. The good news is we can compensate for the weakness. The bad news is we can compensate for the weakness. Dr. Deb Muth 00:18:09 That is so very true. Bob Miller 00:18:11 Yeah, we can’t, because I often get asked, so we’ll do some things now, and we’ll check my genes again, and they’ll be better. It’s like, nope. Dr. Deb Muth 00:18:18 Oh, – – Bob Miller 00:18:19 You gotta play the hands you’re dealt, so… Dr. Deb Muth 00:18:21 That’s right. Bob Miller 00:18:22 You can test your genetics… if you’re looking at the same enzyme, you can test it every year. It’s not gonna change. It’s like the blueprint. Dr. Deb Muth 00:18:30 It’s good and bad, right? It’s the one test you only have to do once in your lifetime. Bob Miller 00:18:34 No, unless, you know, like, our. Dr. Deb Muth 00:18:36 All the time. Bob Miller 00:18:37 Yeah, now our test looks at, called the Functional Genomic Analysis Test of your genomic Resource. We look at 220,000 steps. Dr. Deb Muth 00:18:46 Wow, that’s a lot. Bob Miller 00:18:47 That’s not all of them. Dr. Deb Muth 00:18:49 Right. Bob Miller 00:18:50 So, maybe in the next year, we’re gonna come out with our third version of the chip. And then, if someone wants to get those new things that weren’t on it, they’d have to repeat. But whatever we measured is gonna stay the same. Dr. Deb Muth 00:19:03 That’s a lot of SNPs to look at. Bob Miller 00:19:05 Keeps us busy. Dr. Deb Muth 00:19:06 But there’s still, but there’s still SNPs that we. Bob Miller 00:19:09 That we’d like to have that we don’t have, so… Bob Miller 00:19:11 We started out with version 1 on our genetic test, then we worked with version 2, and we’re already compiling a list of what version 3 would look like. So if somebody has our version 2, And we’re saying, you know what, it’d be nice if we could see these, well, then you’d repeat, but it won’t change what you already know, so… Dr. Deb Muth 00:19:29 Got it, got it. So, when you started out, and you started looking at the research of Lyme disease and chronic infections, which detox pathways are most important for people who struggle with those conditions? Bob Miller 00:19:43 Okay. You know what might make sense as we do a screen share, and I’ll actually show you the pathway. Does that make sense? Bob Miller 00:19:48 Alright, so… let’s see if I… let me just press the share… Dr. Deb Muth 00:19:52 Yep, you should just be able to press share. Bob Miller 00:19:54 And… number 2. Okay. Are we seeing the screen there? Bob Miller 00:20:01 Okay. Dr. Deb Muth 00:20:02 So, this is a map that we made. Bob Miller 00:20:05 And by the way, this is not… All-inclusive of all the things we look at, but we believe this is a core issue. So, where we’re going to start here, there’s something called the microglia. And the microglia are glial cells. They’re in the brain and the central nervous system. And they’re very interesting little creatures, because most of the time, and this is just a drawing of what they sort of look like. Most of the time, they’re in what’s called the M2 anti-inflammatory mood. What that means, these little guys pick up dirt, debris, Recycle them. Turns on an enzyme called interleukin-10 that’s anti-inflammatory. And just kind of does general housekeeping. And just kind of does general housekeeping. However, when a trigger comes along. However, when a trigger comes along. They… it’s the same glial cell, but it moves over to a very pro-inflammatory enzyme. A pro-inflammatory glial cell. And it triggers these 3 enzymes, Actually, these four. That are pro-inflammatory. Tumor necrosis vector alpha, Interleukin-6. NF Kappa B, Inos. Now, these create inflammation. So you might think, well, why is that good? Well, if you have some foreign invader, virus, bacteria coming in, parasite. If you didn’t have these guys coming to the rescue, you would just die of infection. So, these guys are your friend unless they’re your worst enemy. Because TNFA, and we’ll show you when we actually do a demo account, TNFA can be overactive. So, in other words, it over-responds. Interleukin-6 can be overactive. And if Kappa-B can be overactive. The INOS, and I’ll explain each of these as we go through a demo, can be overactive. Now, what that means is, you’re very good at killing virus and bacteria. But this is where autoimmune disease comes in, and just inflammatory conditions. Now, this is just speculation, but we think what happened is, as you know. Thousands of years ago, we didn’t have refrigeration, we didn’t have sewer, we didn’t have pure water, and we didn’t have antibiotics. So, if you made it to 40, you were an old-timer, because everybody was dying of infection. So, what we believe happened is, by what’s called natural selection, Having these overactive. A thousand years ago was to your advantage. Dr. Deb Muth 00:22:31 Hmm. Bob Miller 00:22:32 But now… We have pure water, we have refrigeration, we have sewers, we have antibiotics. But now we have environmental factors that are stimulating them. Now it’s to our disadvantage. And we’ll talk about that a little bit as it relates to the hemochromatosis genes and maybe the G6PD. Dr. Deb Muth 00:22:48 Yep. Bob Miller 00:22:49 Now, why are we becoming so inflamed? Let’s look at the triggers. Now, one of my, favorite expressions is. I was born all the way back in 1954. Dr. Deb Muth 00:23:01 And it was a different world back then. Bob Miller 00:23:05 These are some of the triggers. And we’ll get into these, but right now, high fructose corn syrup, And the high-fat diet. High fructose corn syrup only came about in 1968. So now we’re being exposed to high fructose corn syrup. Then… we didn’t have these, these viruses like COVID. Dr. Deb Muth 00:23:26 Yeah. Bob Miller 00:23:27 Now, there’s now pretty strong evidence that COVID Was actually, you know, made as a gain of function. It’s debated, and I’m not taking an opinion on it, but there’s some people who believe Lyme disease was also a part of experimentation. Dr. Deb Muth 00:23:40 Go. Bob Miller 00:23:41 Then we have molds, and it appears as though mold is getting stronger. you know, 20 years ago, when I was seeing folks, mold wasn’t on the radar. I would say 7 out of the 10 folks we speak to today have mold problems. Yeah, 20 years ago, we talked more about mold allergy being an issue versus mold toxicity being an issue. Right. So… I know some folks are, you know, speculating what’s happening, but one of the theories out there is that EMF is strengthening mold. I don’t know if you ever heard that theory, and I don’t… Dr. Deb Muth 00:24:13 I have. Bob Miller 00:24:14 I’m not claiming it’s true, but it’s an interesting theory. Then even, you know, your black mold from water-damaged buildings. Then our air pollution is getting worse. We’re getting more toxic metals. Dr. Deb Muth 00:24:26 You know, if we have a… Bob Miller 00:24:27 You know, we’re gonna look back someday and say, what were we thinking, smearing aluminum into our armpits? The, what were we doing putting mercury in our teeth? Then, you know, glyphosate. When I was a kid, there was no glyphosate. So, all of these herbicides and pesticides. Polychlorinated biphenols, And then EMF. So, we love our cell phones, you know, and I think unless you, or in the middle of the desert, or down in a cave, you’re being exposed to EMF somewhere. So, you know, we have our cell phones with us, we have, We have Wi-Fi, the towers are everywhere. And we don’t know long-term, but we may find that this can… this creates some inflammation. And I don’t know if you get any folks, but do you have any folks that have… are they EMF sensitive? Dr. Deb Muth 00:25:16 Oh yeah, we have a whole bunch of them. Bob Miller 00:25:18 Yeah, and then if you have any TBIs, So, plenty of things here. that will stimulate into the microglia, M1. Now, you could say, well. We’re all pretty much exposed to the same thing. Why do some people get hit harder than others? So here’s where we’re gonna start. There’s an enzyme called Nrf2 and RF2. And Nrf2 is the enzyme that senses when there’s inflammation. And turns on hundreds of anti-inflammatory enzymes. We’ll show when we do the demo, you can have genetic weakness on NERF2. And NERF2 inhibits and slows down microglia M1. supports M2. Now, if it’s not complicated enough, there’s an enzyme called KEEP1. And KEEP1 inhibits NRF2. And you can actually have gain of function on keep 1, that makes Keap 1 stronger. So… A lot of the people who land on my doorstep So… A lot of the people who land on my doorstep Both parents gave a mutation on KEEP1, making it overactive. Both parents gave a mutation on KEEP1, making it overactive. Dr. Deb Muth 00:26:31 Hmm. Dr. Deb Muth 00:26:31 Hmm. Bob Miller 00:26:32 Suppressing Nrf2, nerve 2 might be weak. So, nobody’s putting the brakes on, M1. And by the same token, Nerve 2 supports M2. Then there’s a process called mTOR and autophagy. mTOR stands for mammalian tard of rapamycin, the growth of new cells. And then autophagy, taking our dead cells and recycling them. We need a balance between the two of them. If we didn’t have mTOR, the sperm and the egg would never become the baby, the baby would never become the adult, we wouldn’t make new cells. But our cells are constantly, you know, the old cells dying off. Autophagy is where we take that debris from the cell and recycle it, just like a farmer Plows the crop under at the end of the year. The dead plant then becomes the fuel for the spring, your dead cell becomes the fuel for the spring, and that’s autophagy. So we’re gonna look back someday and say, what were we thinking? We give our animals growth hormones so they get fatter faster. Oh my. So, we consume those animals, and inventory runs faster. Now, for anybody who’s, You know, maybe above 40, 45 years old. Think back when you were 12, and what did girls look like? They were primarily flat-chested little girls. Now they look like 16-year-olds. Because environmentally, we’re jacking up mTOR. So, mTOR stimulates microglia M1, suppresses microglia M2. Probably 80% of the folks we visit with. This is the part of the problem. NRF2 is weak. mTOR is strong. Environmental factors come along. And this guy gets carried away. He doesn’t do that burst and move back. Stays here. We’re calling that How environmental factors create a locked-in, pro-inflammatory. and neurotoxic phenotype. In other words, once it starts, it just keeps… Feeding upon itself. Alright, so what happens now when microglia is overactive. it triggers these 3 enzymes, TNFA, N of kappa B, And interleukin-6. Each one of these can have genetics that make them run stronger. Then it stimulates an enzyme called NLRP3, Which makes what are called inflammasomes. Now, guess what inflammasomes can be? Your best friend or your worst enemy? Because they will, if you’ve got, again, a virus or bacteria, or possibly even some bad cells in the body. They will zap them. Well, that’s good. Unless it’s overactive. Unless it’s overactive. And then what it does, through interleukin-1 beta, makes excess glutamate. And then what it does, through interleukin-1 beta, makes excess glutamate. Anxiety, gut inflammation, OCD, ADD, autism. And, you know, glutamate, we’ll talk about that a little bit, but glutamate makes you intelligent, highly motivated go-getter. but can also be excitatory. And then, look what it does. Let’s see, do I have the drawing tool here? Yes, I do. Okay. So, it comes down through here, Makes the glutamate. Comes back up through here. through the ADORA 2A enzyme, Then we’ve got a feedback loop that feeds upon itself. Then, through interleukin-18, we make histamine. and mast cells. And then through histamine receptor site number 1, we come back and spin it. And now you’ve just got this spinning feedback loop. So, the glutamate will make you anxious, the histamine will give you allergies and make you anxious. And you’re allergic to everything, and you’re feeling horrible. Now, it doesn’t end there, Dr. Dad. It then goes on to make something called gast dermins that creates pyroptosis, where it actually starts punching a hole in the cell membrane. And you’re only going to be as healthy as your cells are. Just a little background. You know, we’re made up of trillions of cells, and each one of them has what’s called a lipid bilayer, made from lipids, which comes from fats. And you’re only going to be as healthy as those membranes are. So that’s why we coined an interesting phrase. Cellular CPR. Construct the cell. Protect the cell. And restore the cell membrane. And we believe that’s going to be revolutionary in the functional medicine world. So… It’s not hard to figure out that if you start punching holes in the cell membrane, that’s not a good thing, okay? Bob Miller 00:31:22 Now… There’s an interesting molecule called NAD. Thicotide adenoside dinucleotide. And anybody who’s in the, you know, listening to the health podcasts and things, they’re… They’re, they’re learning about NAD. And I’m going to show you a chart later, all the good things that NAD does, but For the most part, it helps what’s called sirtuins. And sirtuins are quite interesting. If anybody’s looking at longevity. The sirtuins is where they’re looking at.Because sirtuins turn on good things. Turn off bad things. And I’ll show some charts on that later. So for right here, this sirtuin uses NAD, to slow down NF-kappa-B. CERT 2 uses NAD to slow down an ORP3. So, if we’ve got genetic weakness on these, or we don’t have enough NAD, We don’t hold this pathway back. Make sense? Dr. Deb Muth 00:32:24 Yeah, makes perfect sense. Bob Miller 00:32:25 Now, I’ll show this a little bit later. So, people are like, oh, well, I’m gonna start taking some NAD. Dr. Deb Muth 00:32:31 Right. Bob Miller 00:32:32 And there’s functional doctors who give NAD intravenous. It was just this morning, I was talking to a woman who said, Oh my gosh. I went and got intravenous NAD, and it took me a month to recover from that. Dr. Deb Muth 00:32:45 Hmm. Bob Miller 00:32:46 what happens is, and I’ll show this in a little more detail, there’s an enzyme called CD38, that’s stimulated by NF-kappa-B. And it takes NAD, To make intracellular calcium. that stimulates NLRP3 and actually makes things worse. So, if we have this guy upregulated, and I’ll show a chart what does that. taking NAD will make you worse. Again, when I go into the software, I’ll show you that whole pathway, so… I would encourage people, you know, just don’t go out and start taking massive amounts of NAD, you know, stick your toe in the water, see how you do. Because everything you’ve heard about, how good it is, is true, unless this guy says, oh, thank you very much, let me make more inflammation. Now, this might be part of our innate immune system, that if we have some pathogen that’s gonna kill us. By golly, we want that to happen. But if this is happening by environmental factors, Then it’s detrimental. So the immune system that protected us a thousand years ago now might be turning on us because of the environmental factors that we showed earlier. All right. Then there’s an enzyme called PARP that’s NAD-dependent, and that actually repairs strain breaks in your DNA. Now, the next thing that happens… is there’s an enzyme called NADPH oxidase that gets stimulated. and something called INOS. Now, I’m sure most people know about nitric oxide. It’s a gas that dilates your blood vessels. That’s why sometimes they’ll even give people drugs, nitroglycerin, to boost their nitric oxide. That’s why people are doing beetroots and other things to boost their nitric oxide. But there’s an OS3 enzyme that makes the nitric oxide that’s good for blood flow. But there’s an INOS That makes nitric oxide to kill pathogens. probably might be the third or fourth time I’ve said this. That’s a good thing, unless it isn’t. So, if it’s killing some pathogen, great. It was just misfiring. it combines… With superoxide that’s made by this enzyme, and makes something called peroxynitrite, which is one nasty free radical that chews you up and spits you out. So, the NOx enzyme, NADPH oxidase, uses NADPH, To make this free radical called superoxide. If we have time, we’ll get into it. NADPH is what your body needs to recycle your antioxidants.So, I coined the phrase, the NADPH steel. Where the NOX enzyme takes this very important NADPH, And rather than being useful, makes superoxide. Now, again, is that fine if you’ve got some bacteria to kill? Of course. But if it’s just chronically running, it’s just making all this chronic inflammation. Then it makes something called hydrogen peroxide. And we need to clear hydrogen peroxide by 3 enzymes, catalase, thyroid reduction. And glutathione peroxidase. If we have genetic issues on here, or we don’t have the cofactors. There’s something called the Fenton reaction, discovered in 1895 by Dr. Fenton. Where hydrogen peroxide combines with iron to make what are called hydroxyl radicals. And guess what they do? They create lipid peroxides, That damages your cell membranes. Now, again, the body’s pretty darn amazing. We have glutathione, And here’s where your body’s taking glutathione and recycling it. But look who’s needed to recycle it. NADPH. So, if this guy up here is chewing it up, We don’t recycle our glutathione. And then an enzyme called glufon peroxidase 4, Takes this damaged lipid and repairs it. So, here we’ve got this protecting, we want to protect it by not having this happen. But then we also need this guy to do the restoration. So, there’s a lot that can go wrong in here, Dr. Deb. Dr. Deb Muth 00:37:07 There’s a lot that could go wrong. And I can imagine some of my listeners are thinking that lipid peroxidase, is that the same thing as what they’re thinking of when we talk about lipids and cholesterol? Is that the same process that’s happening there? Bob Miller 00:37:22 Well, no, no, the lipids can be used to make cholesterol, but here we’re talking about where they’re going to build the cell membrane. And they’re being… and they’re being, destroyed. If anybody would like to see a visual representation of this, just go on YouTube. And type in, ferrooptosis Animation. cool little video, it’s about 3 minutes long, and it shows the lipids coming over, being oxidized, and now GPX4 fixes them, so… YouTube, Pharaoptosis Animation, cute little video. It’s just that really… Shows vividly what we’re… what we’re talking about here. Now, this is… Dr. Deb Muth 00:37:59 And so this is very common, too. Like, a lot of people do hydrogen peroxide IVs. Dr. Deb Muth 00:38:04 And so, if somebody doesn’t know their genetics, they could have a problem with doing those, just like they could doing the NADHIVs, correct? Bob Miller 00:38:13 Sure, yeah, yeah, yeah. So, I’ve talked to so many, you know, of course, the hydrogen peroxide kills pathogens. I mean, that’s what it does. So… but I’ve spoken to so many people that said. I had one client that said they’ve never been the same after having one hydrogen peroxide infusion. Dr. Deb Muth 00:38:30 Interesting. Bob Miller 00:38:31 Yeah. So… it can be… I see why people use it, because it. Bob Miller 00:38:36 pathogens, But on the other hand. And now’s a good time to speak about… I don’t have it on here, but there’s a, there’s an enzyme called the HFE gene. And that is what causes you to absorb iron. And there’s mutations in it that cause something called hemochromatosis. Were you overabsorb iron? Now, true hemochromatosis is when both parents give you a mutation. But there’s now growing evidence even a heterozygous can cause a little bit more iron absorption, not to the human chromatosis point, but overabsorption. So, if you overabsorb iron, And you have too much hydrogen peroxide that’s not cleared, All kinds of inflammation. Now, what’s happened is sometimes this inflammation Will damage the red blood cells. And some well-meaning doctor says, oh, you need some iron. And they take iron and it makes it worse. So, can’t tell you how many people I’ve said, you’ve got the overabsorption of iron, and they say, well, that can’t be right, because I’m low in iron. Well, that could be because it’s being chewed up here. Dr. Deb Muth 00:39:40 Sure. GPX1 and TXN turn it into, to water. The, catalase turns it into water and oxygen. Dr. Deb Muth 00:39:58 Now, I see a lot of my clients who have mutations or SNPs on that GPX gene, on that glutathione gene. And they really struggle to clear a lot of their toxins. Bob Miller 00:40:12 Sure. Dr. Deb Muth 00:40:14 Yeah, absolutely. Well, GPX4. Bob Miller 00:40:18 is what, repairs, but you can see GPX1 Is what uses glutathione. To turn hydrogen peroxide. So, but it all depends upon having enough glutathione. Dr. Deb Muth 00:40:30 Yeah. Bob Miller 00:40:31 Well, guess who controls making a glutathione? Dr. Deb Muth 00:40:34 Nerf 2. Bob Miller 00:40:37 So, if you have a keep one weakness, or strength to two… I’m sorry, keep one is too strong. Nrf2 is too weak. You don’t make glutathione. So, when a lot of people do that, it’s like, well, I’m gonna take glutathione. Dr. Deb Muth 00:40:51 Right. Bob Miller 00:40:52 And some do great, and some do poorly. You know, because… and I’ll show this on one of the other charts. You can see here that the, The glutathione has to be recycled. And if we don’t recycle it, it actually turns into superoxide free radical. So… NADPH are the cofactors, For taking the oxidi… here’s oxidized glutathione, here’s reduced. So, this is a good glutathione. After it does its job, you can see it becomes oxidized.We need to recycle it. Well, if we have weakness on the enzyme that does that, or a weakness in Nrf2, or not enough NADPH. The oxidized glutathione never gets recycled. So, I’ve talked to a lot of people who said, oh, glutathione made me so sick, and say, well. Dr. Deb Muth 00:41:43 Yeah. Bob Miller 00:41:44 You need it, but you need to recycle it. Dr. Deb Muth 00:41:46 Can you speak for just a brief moment, too, about MTHFR? That is a very popular gene, it’s all over social media as the major gene, but can you speak to a little bit about that, and how that fits into this whole process of things? Because it is just such a small piece. Dr. Deb Muth 00:42:04 understanding genetics. Bob Miller 00:42:06 Yeah, to be honest, it drives me nuts. Dr. Deb Muth 00:42:08 Me too. Bob Miller 00:42:11 Alright, so… You know, there are people on social media I won’t say what I think, I’ll be kind. But… But the, And, you know, they might mean well. But they talk about, if you have MTHFR and COMT and PEMT, that’s… oh my goodness, that’s horrible, and we’ll fix that for you, and you’ll be fine. Bob Miller 00:42:36 it just irritates me to no end. And it really could get anybody who’s doing this legitimately in trouble. I mean, I’m afraid someday, you know, there might be some cracking down on this kind of nonsense. Now, to answer your question about MTHFR. Dr. Deb Muth 00:42:51 I mean, it really is, but I’ll tell you what, why don’t we hold that thought until I go to another map and I can actually… Okay. Bob Miller 00:42:56 But the real… the cliff notes is the MTHFR puts a methyl group on your folate, which is needed, but it has gotten way, way, way too much attention. And people learn they have MTHFR, and they start taking a multivitamin with methylfolate, then they take a B vitamin with methylfolate. Dr. Deb Muth 00:43:13 And they’re pushing it too hard. Bob Miller 00:43:15 Yeah. So I can’t tell you how many people I’ve helped by saying, stop it. Dr. Deb Muth 00:43:20 Yeah, take less of it. Bob Miller 00:43:21 Take less of it, yeah. So, yeah. Yeah, there’s a… If somebody, say, ranked the enzymes at their level of importance, MTHFR might be 40 or 50 on a scale of 100, you know. Keep one Nerf two. big deals. Dr. Deb Muth 00:43:40 deals. Bob Miller 00:43:41 NQO1 that I didn’t even talk about yet, NQO1, takes your, NA… your NAD goes into NADH, To make electrons for the electron transport chain. you need NQ01 to bring that back. If that’s not working, and I’ll show you on the NAD map how disastrous that can be. Now, the next piece is here, and I think You know, if you talk to any school teachers and say, if you’ve taught for more than 10 years, how are the kids today? Every one of them says, more ADD, ADHD, more autism. Just look at human beings, we’ve never been so agitated. You know, everybody, and it might be a social media thing, but people take a position on something, and if anybody doesn’t share that position, they view them as the enemy. Dr. Deb Muth 00:44:29 And it’s kind of scary what’s happening to us. Bob Miller 00:44:33 So, we can’t agree to disagree anymore. We see anybody who has a differing opinion as the enemy. And, you know, there was… there’s people that didn’t have Christmas dinners together, because they had political differences, like… Dr. Deb Muth 00:44:44 Excuse me. Bob Miller 00:44:45 can’t you put your political differences aside to have Christmas together, you know? Dr. Deb Muth 00:44:49 Right? Bob Miller 00:44:50 become that, you know, no matter what your position is, and I’m not saying anyone’s right or wrong, I’m just saying. You know, in the old days, they used to say that the Republicans and Democrats in Congress would argue policy and then go have dinner together. And now everybody’s all up in arms, angry. Dr. Deb Muth 00:45:05 Yeah. Bob Miller 00:45:06 So… There’s likely multiple reasons for that. But let me show you one of them. That, you know, to what degree this is… very important, we don’t know, but I think We’re beginning to believe this is very important. So, there’s something… there’s a neurotransmitter called GABA. And God buys the don’t worry, relax, be happy. Chill. Okay. Dr. Deb Muth 00:45:31 Nobody has enough of that anymore. Bob Miller 00:45:33 Well, yeah, you’ll be surprised what I’m gonna show you. So, let me see if I can find a, Let me see if I can find the right slide here. Let me look for it here. So, there’s something called a GABA receptor site. And here you can see… This is a neuron, and this is where you, The neuron normally is excitatory. However, there’s normally low chloride in the neuron. Dr. Deb Muth 00:46:09 Hmm. Bob Miller 00:46:10 So, GABA itself is neither relaxing. For excitatory, all GABA does, it opens up what’s called a chloride channel. And then chloride, which has a negative charge, will flow into the neuron. Follow me there? Dr. Deb Muth 00:46:26 Yep. Bob Miller 00:46:27 And as it does, it changes this from a positive charge to a negative charge, And it’s relaxing. and inhibitory. Dr. Deb Muth 00:46:34 Hmm. Bob Miller 00:46:36 Now, on the other hand, there’s enzymes called NKCC1, That will push chloride in. and KCC2 that will bring chlor… oops and bring chloride out. And then there’s a sodium channel. And, sodium has a positive charge. And glutamate will push that in. So, as long as this is happening. And GABA says, receptor sites, open, chloride goes in, Chill. However, If NKCC1 Pushes extra chloride in. KCC2 doesn’t pull it out. and GABA hits the receptor site, the GABA comes flowing out, Sodium comes in, And now it’s excitatory. So Gabba didn’t change. GABA just opened the receptor site, that’s all it does. Dr. Deb Muth 00:47:33 Yeah. Bob Miller 00:47:34 But it’s the chloride balance that’s going to determine whether this is relaxing or not. Now, these are the things that go along with when they lose that KCC2 or gain NKCC1. Pain and sensitivity, burning electrical, neuropathic pain. Normal touch hurts. Sound and light sensitivity. Tinnitus can flare. Headaches and migraines. Seizure tendency. Body jolts. Spasticity, cramps, stiffness, startle reflex. Trouble falling asleep, non-restorative sleep. Anxiety, stress, reactivity, that’s what we have now. Hyperarousal, panic-like surges, irritability, racing thoughts. Brain fog, slowed processing, working memory slip-ups. Mental fatigue. Episodes of racing hearts, sweaty palms, guts on edge. Those are all the things that happen when this GABA switch occurs. Now, here’s what happens, and this is what I’m going to be presenting at an autism conference. When you have a newborn, they need that NKCC dominant to develop. By early childhood, it should… or, sorry, early adulthood. we should move over to the KCC dominant, that’s the taking the chloride out. Nice-looking 25-year-old boys, functioning very well. However, when we get microglia M1 upregulated. Because of environmental toxins, processed foods, Tylenol, aluminum. they stay in NKCC1 dominant, and there’s ADD, ADHD, Autism, the whole spectrum. because… They’ve not moved over to the… They’ve not moved over to the KCC2. And again, this is caused by… Environmental factors. Stimulating the microglia. And then, interleukin-1, interleukin-18 weakens KCC2, interleukin-1 beta, Strengthens NKCC1. high chloride. We open up the chloride channel, In Rebell Excitatory. So, I think when, When the pediatricians get ahold of this, they’re going to be very excited to know that This could be why we’re seeing such a rise, and not just autism, but ADD, ADHD, anxiety, the whole shit mess. Dr. Deb Muth 00:49:58 thing. Bob Miller 00:49:59 Yeah, so… and you can see NF-kappa-B stimulates that. These stimulate it, and I think that’s why everyone’s getting so anxious. Now, there’s a little bit more to it, and we’ll get into this when we look at some of the maps, but… The, the glutamate, Which is excitatory. will stimulate the NMDA receptor, make more glutamate, And glutamate will inhibit KCC2. And then we also need an astrocyte To, take both ammonia And glutamate, and… Turn them back into glutamine. And I’m going to talk to you a little bit about arachidenic acid, and if we have too much arachidenic acid. or TNFA is upregulated, that doesn’t happen. Ammonia goes up, and there may be multiple reasons for this, but this is a reason why some of the autistic kids do flapping. Dr. Deb Muth 00:50:49 Hmm. Bob Miller 00:50:50 Because they’re not clearing their ammonia. And you can tell if somebody has high ammonia by… they get that old person smell, you know. Dr. Deb Muth 00:51:00 Yup. Bob Miller 00:51:01 your vehicle cycle’s not taking out the, the ammonia. Now, last pathway here. There’s growing interest in mast cell activation. So, back here, we talked about peroxynitride. And that will stimulate mast cells, and those are white blood cells that are your best friend, unless they’re your worst enemy. Then it’ll make histamine. And there’s enzymes called histidine decarboxylase that’ll make more. Dr. Deb Muth 00:51:28 I’m sure everybody’s heard of DAO, the enzyme that degrades histamine. Yep. Bob Miller 00:51:31 We can have genetic weakness, we don’t make that. There’s an enzyme called histamine and methyltransferase, That, That breaks down the histamine. Then if we don’t do that, it’ll get stuck in the histamine receptor site. And then it’ll make something called, renin. Which will cause angiotensinogen to turn into angiotensin. One, that turns into angiotensin II,And that’s where people make aldosterone, where they’ll get the, The swollen ankles and high blood pressure. But interestingly, there’s an enzyme called ACE2, that takes this guy and turns it into angiotensin 1-7, Which is anti-inflammatory and also inhibits… TNFA. Now, you can have weakness on ACE2, But… and anybody’s saying, that sounds familiar? Dr. Deb Muth 00:52:25 That’s where COVID comes in, using ACE2. Bob Miller 00:52:28 And now we just found there’s literature that if you get COVID long enough, it can actually make ACE2 not be able to work as well. So look what it does. It comes down here, stimulates the NADPH oxidase, More superoxide. More peroxynitrite. And we’re on a cycle here. We’ve actually named this the Home Cycle Hypothesis, the proposed feed-forward loop. That just keeps feeding on itself. All being caused by… Primarily, The environmental factors. But hitting those who have genetic weakness the hardest. That’s why. Dr. Deb Muth 00:53:08 To the people. Bob Miller 00:53:09 Don’t live in a moldy house. One person is sick as can be, and the other person says, well, you must be imagining things, because I don’t feel anything. Dr. Deb Muth Yeah. Same thing with long haul, right? Two people can both get sick, one gets sick and never seems to recover, and somebody else gets sick, and they have absolutely no problems with it at all. Bob Miller 00:53:30 Sure. Well, think about it, if you get COVID, and ACE2 is weak, and some of this other stuff is going on. This thing just starts feeding upon itself. Dr. Deb Muth 00:53:38 Keep creating more inflammation, more complications, nothing’s calming down. Bob Miller 00:53:43 Yeah. Now, you, you ask about, MTHFR. So, this is the, this is the, the software called Functional Genomic Analysis. There’s a demo report we have. So, let’s talk a little bit about, MTHFR. So, we actually have a map called a methylation map. Now, what happens is, when you do your saliva test, you, you know, you spit, you put some saliva. in a collection kit, goes to a lab, takes out the DNA data, sends it to the computer, and now you can actually see it visually. Okay. So, it’s gonna take a second for this, data to load up, it’s, and each of these Circles, each of these ovals, is an enzyme. And the data gets loaded up to see where it is. So, until it gets loaded up here, I didn’t preload this. There it goes. So… The primary thing about methylation is There’s a nasty substance called homocysteine that, if it’s too high, can really be detrimental. The body takes methylfolate, and combines with methyl B12, To bring this back up to methionine. And then through the MAT genes, we make SAMI, S-adml methionine. Which is involved in so many processes. Then after it does its thing, it turns back into homocysteine. And this thing needs to keep spinning around. That’s why, you know, it’s a good idea to keep homocysteine at, do you have a number that you’d like? 7, 8? What do you like for a number? Dr. Deb Muth 00:55:24 Yeah, I like mine below 7. Bob Miller 00:55:26 Yeah. So if the homocysteine goes too high. It, caused all kinds of problems. So, here’s where you ask about the MTHFR. So, here you can see on this individual. I click on MTHFR, and you can see it comes up here, here’s the C677. And you can see here where it says, variants. I’ll… I’ll draw in case somebody’s having a hard time seeing that. So, you can see there’s nothing in there. That means there’s no genetic mutations. If one parent would have given a mutation, there’d be a 1. If both parents did, there’d be a 2. Now, here’s why Yes, methylation is important, I’m not saying it isn’t important, but look at this MTHFRC677. In my software. Only 42.5% of the population does not have a mutation. 44.7% have won. 12.9 have 2. So, this isn’t some rare, oh my god, I’m gonna die… Kind of thing, yeah. Dr. Deb Muth 00:56:27 Right. Bob Miller 00:56:28 So, And then what happens is that, and again, I’m not dismissing methylation, I… we could do a whole show on methylation. Bob Miller 00:56:36 get it. But I think that what people are doing is they’re, they’re learning about MTHFR, they get it measured, they panic. They start taking massive amounts of methylfolate, which many times is to their detriment. Dr. Deb Muth 00:56:50 Well, it’s… and isn’t it true, too, with MTHFR, like, you have to also look at MTR, MTRR, and the more we stack up of those, the more complicated than MTHFR can be. It’s not… it’s not as simple as just saying MTHFR 677 versus 1298. It’s more complex than that, kind of like what you’ve already shown with some of the other things. There’s more to it than just that one little sliver. Bob Miller 00:57:17 Oh, sure, well, let’s take a look. So, remember I said there’s a cofactor? One of the cofactors is called FAD. Just a Bob Miller observation, that’s all. But when people have trouble with their riboflavin and they don’t have enough FAD, They’re doing much worse than people who have just a C677. So, right here, you could have perfect C677th. And if you don’t have the cofactor, it’s not gonna work, okay? Dr. Deb Muth 00:57:48 And as you said, there’s an MTR enzyme. Bob Miller 00:57:51 that takes methylfolate and methyl B12, to spin it around. So, here on this individual. here’s your… here’s your B vitamins, or I’m sorry, your B12s. There’s an enzyme called TCN1 that takes it from the stomach into the blood. Then there’s other enzymes that take it from the blood into the tissue. And if you’re having trouble here. Well, then you’re not going to have this working, so… Even if you don’t have MTHFR, And you have MTR, like this, no, I’m sorry, this person doesn’t. But they have the MTRR, and then they don’t have enough B12, this isn’t gonna work, aside from that. And then there’s a middle pathway. And then there’s enzymes called the MAT1. they take the methionine to the salmon. If that’s not working, we stick… we get stuck in methionine. So, it’s, it’s not just an MTHFR. And then, one of the things that people forget about. is through these CBS enzymes and CTH, We make cysteine, which is needed to make glutathione. The master antioxidant. So, it really is that… I call it the, The 3D chess game played underwater. Dr. Deb Muth 00:59:07 It really is. I mean, I see people who have CVS, COMT, glutathione, MGHFR genes. And some of them function just fine. Like, they have Like, I look at this person and I’m like, oh my gosh, I don’t know how they’re functioning because they’re double mutated on so many pathways, but yet they don’t have a lot of symptoms, they don’t have a lot of complications. Somehow their body has figured out a way to adapt to what it has so it can stay alive and it can function at a high functioning level. Bob Miller 00:59:36 Yeah, and they may be, you know, eating right? Yeah. Staying out of a moldy house. reducing stress. So, it’s diet, it’s stress, it’s genetics, environmental factors. So, yeah, we can’t just say somebody’s gonna be good or somebody’s gonna be bad. You know, some people get scared, oh, I got all these, it’s like, well… Bob Miller 00:59:56 Are you living in a moldy house? You know, and if you live in a moldy house and your glucuronidation pathway doesn’t do well, or if you’re, you know, a smoker, or you’re constantly eating junk food, I mean, all. Bob Miller 01:00:07 things come together. Although, you know, when we focus on genetics, we’re well aware that this is just a piece of it. You know, you could have identical twins, Genetically, and if one… Is exposed to mold and smokes and drinks and stressed out. They’re gonna be a whole lot sicker than their sibling. Bob Miller 01:00:28 Yep. Dr. Deb Muth 01:00:29 Yeah, it’s that concept of taking twins, and one gets raced with one family, and one gets raced with another family, and they don’t have the same… problems that… that each other have, you know? It’s a very unique situation, we don’t think about that enough. Bob Miller 01:00:44 Alright, so again, genetics loads the gun, environment pulls the trigger. So, if you’ve got a loaded gun, but you don’t have the triggers, you’re okay. Dr. Deb Muth 01:00:53 Yeah. Bob Miller 01:00:54 Yeah. So, remember I said I was going to talk about NAD? So, here’s NAD, and what it does, it turns into NADH. And what NADH does, it, Comes down this pathway, what’s called the electron transport chain. And that makes your ATP, that’s your energy. So, if this wasn’t working, we wouldn’t be alive, because we wouldn’t have energy. So it donates an electron, that’s why it’s called electron transport chain. So, we need NAD, To make this, to make the energy. But remember I said that NQ01, this would probably be, like, on my top 10 list of… Bob Miller 01:01:36 Much more important than MTHFR. This one takes NADH back to NAD. If we’re stuck over here, We’re low in this NAD+, But what happens is, NQO1 also provides CoQ10. And CoQ10 Is what’s needed for the electron transport chain to flow. So if we get too many electrons up here. And they don’t turn them into energy. They make a nasty free radical called superoxide. Okay. Now, NAD plus also makes NADPH, And that is needed. Remember I said we need to recycle our antioxidants. So, if we have a problem with FAD from riboflavin. Yeah, we don’t have enough NADPH, Glutathione’s not getting recycled, and you’re gonna be inflamed. And you take glutathione, you’ll feel worse. There’s another enzyme called thimoredoxin. Same thing, needs NADPH and FAD. And same way with your nitric oxide, there’s an enzyme called NOS3, That makes the nitric oxide that dilates your blood vessels. And if we don’t have enough NADPH or fat, You’re gonna make superoxide. Rather than nitric oxide. Now, remember

This is a recap of the top 10 posts on Hacker News on June 05, 2026. This podcast was generated by wondercraft.ai (00:30): Changing how we develop LadybirdOriginal post: https://news.ycombinator.com/item?id=48409191&utm_source=wondercraft_ai(01:59): Gov.uk has replaced Stripe with Dutch provider AdyenOriginal post: https://news.ycombinator.com/item?id=48415217&utm_source=wondercraft_ai(03:29): C++: The DocumentaryOriginal post: https://news.ycombinator.com/item?id=48408016&utm_source=wondercraft_ai(04:59): Tracing a powerful GNSS interference source over EuropeOriginal post: https://news.ycombinator.com/item?id=48409664&utm_source=wondercraft_ai(06:29): Astronauts told to return to ISS after sheltering over air leak repairsOriginal post: https://news.ycombinator.com/item?id=48413464&utm_source=wondercraft_ai(07:59): pg_durable: Microsoft open sources in-database durable executionOriginal post: https://news.ycombinator.com/item?id=48414367&utm_source=wondercraft_ai(09:29): Did Claude increase bugs in rsync?Original post: https://news.ycombinator.com/item?id=48411635&utm_source=wondercraft_ai(10:59): Gemma 4 QAT models: Optimizing compression for mobile and laptop efficiencyOriginal post: https://news.ycombinator.com/item?id=48414653&utm_source=wondercraft_ai(12:29): New method turns ocean water into drinking water, without wasteOriginal post: https://news.ycombinator.com/item?id=48413500&utm_source=wondercraft_ai(13:59): Meta enables ADB on deprecated Portal devices [video]Original post: https://news.ycombinator.com/item?id=48406640&utm_source=wondercraft_aiThis is a third-party project, independent from HN and YC. Text and audio generated using AI, by wondercraft.ai. Create your own studio quality podcast with text as the only input in seconds at app.wondercraft.ai. Issues or feedback? We'd love to hear from you: team@wondercraft.ai

In this episode, Asian Development Bank (ADB) President Masato Kanda discusses the economic impact of the Middle East conflict on Asia and the Pacific, ADB's response, and the need for countries to strengthen resilience against future shocks.   Host: Brad W. Setser, Whitney Shepardson Senior Fellow, Council on Foreign Relations   Guests: Masato Kanda, President, Asian Development Bank   Want more comprehensive analysis of global news and events sent straight to your inbox? Subscribe to CFR's Daily News Brief newsletter. To keep tabs on all CFR events, visit cfr.org/event. To watch this event, please visit it on our YouTube channel: A Conversation With President Masato Kanda of the Asian Development Bank

EDITORIAL: ​PH should take advantage of new ADB critical minerals facility | May 14, 2026Check out our Streaming Channel: https://streaming.manilatimes.net/Subscribe to The Manila Times Channel - https://tmt.ph/YTSubscribeVisit our website at [https://www.manilatimes.net](https://www.manilatimes.net/)Follow us:Facebook - https://tmt.ph/facebookInstagram - https://tmt.ph/instagramTwitter - https://tmt.ph/twitterDailyMotion - https://tmt.ph/dailymotionSubscribe to our Digital Edition - https://tmt.ph/digitalCheck out our Podcasts:Spotify - https://tmt.ph/spotifyApple Podcasts - https://tmt.ph/applepodcastsAmazon Music - https://tmt.ph/amazonmusicDeezer: https://tmt.ph/deezerStitcher: https://tmt.ph/stitcherTune In: https://tmt.ph/tunein#TheManilaTimes#VoiceOfTheTimes Hosted on Acast. See acast.com/privacy for more information.

- Tổng Bí thư, Chủ tịch nước Tô Lâm lên đường thăm cấp Nhà nước tới Ấn Độ theo lời mời của Thủ tướng Narendra Modi.Phó Thủ tướng Lê Tiến Châu chủ trì cuộc họp với 1 số bộ, ngành về chính sách Luật phổ biến giáo dục pháp luật.- Nga và Ucraina đưa ra các tuyên bố ngừng bắn đơn phương, giữa lúc các cuộc không kích vẫn diễn ra ác liệt.- Ngân hàng Phát triển Châu Á (ADB) cắt giảm dự báo tăng trưởng cho khu vực châu Á - Thái Bình Dương còn 4,7% trong năm nay.- Thương vong tăng lên hơn 80 người, Chủ tịch Trung Quốc yêu cầu xử lý nghiêm vụ nổ nhà máy sản xuất pháo hoa.

EDITORIAL: Retain Kanda as ADB president | Apr. 29, 2026Check out our Streaming Channel: https://streaming.manilatimes.net/Subscribe to The Manila Times Channel - https://tmt.ph/YTSubscribeVisit our website at [https://www.manilatimes.net](https://www.manilatimes.net/)Follow us:Facebook - https://tmt.ph/facebookInstagram - https://tmt.ph/instagramTwitter - https://tmt.ph/twitterDailyMotion - https://tmt.ph/dailymotionSubscribe to our Digital Edition - https://tmt.ph/digitalCheck out our Podcasts:Spotify - https://tmt.ph/spotifyApple Podcasts - https://tmt.ph/applepodcastsAmazon Music - https://tmt.ph/amazonmusicDeezer: https://tmt.ph/deezerStitcher: https://tmt.ph/stitcherTune In: https://tmt.ph/tunein#TheManilaTimes#VoiceOfTheTimes Hosted on Acast. See acast.com/privacy for more information.

In Pacific Waves today: Typhoon Sinlaku slowly weakening - US weather service Guam; Solomons PM ordered to face motion of no-confidence; ADB releases latest economic forecast for the Pacific. Go to this episode on rnz.co.nz for more details

In this episode, our guest is Pratish Halady, Regional Head for Private Sector Development (Southeast Asia) at the Asian Development Bank (ADB). He shares how ADB is bringing together green finance and private sector investment to accelerate the region's energy transition. We dive into real-world examples—from EV charging infrastructure and geothermal development to blended finance and policy reform—showing how markets are created and scaled. The conversation also explores energy security, electrification, and the role of regional initiatives like the ASEAN Power Grid in building a more resilient, low-carbon future. Connect with Sohail Hasnie: Facebook @sohailhasnie X (Twitter) @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie YouTube @energypreneurs

Running Oracle Database@AWS is most effective when you have full visibility and control over your environment.   In this episode, hosts Lois Houston and Nikita Abraham are joined by Rashmi Panda, who explains how to monitor performance, track key metrics, and catch issues before they become problems. Later, Samvit Mishra shares key best practices for securing, optimizing, and maintaining a resilient Oracle Database@AWS deployment.   Oracle Database@AWS Architect Professional: https://mylearn.oracle.com/ou/course/oracle-databaseaws-architect-professional/155574 Oracle University Learning Community: https://education.oracle.com/ou-community LinkedIn: https://www.linkedin.com/showcase/oracle-university/ X: https://x.com/Oracle_Edu   Special thanks to Arijit Ghosh, Anna Hulkower, Kris-Ann Nansen, Radhika Banka, and the OU Studio Team for helping us create this episode. ------------------------------------------------------ Episode Transcript: 00:00 Welcome to the Oracle University Podcast, the first stop on your cloud journey. During this series of informative podcasts, we'll bring you foundational training on the most popular Oracle technologies. Let's get started! 00:26 Nikita: Welcome to the Oracle University Podcast! I'm Nikita Abraham, Team Lead: Editorial Services with Oracle University, and with me is Lois Houston, Director of Communications and Adoption with Customer Success Services  Lois: Hello again! Last week's discussion was all about how Oracle Database@AWS stays secure and available. Today, we're joined by two experts from Oracle University. First, we'll hear from Rashmi Panda, Senior Principal Database Instructor, who will tell you how to monitor and log Oracle Database@AWS so your environment stays healthy and reliable. Nikita: And then we're bringing in Samvit Mishra, Senior Manager, CSS OU Cloud Delivery, who will break down the best practices that help you secure and strengthen your Oracle Database@AWS deployment. Let's start with you, Rashmi. Is there a service that allows you to monitor the different AWS resources in real time? Rashmi: Amazon CloudWatch is the cloud-native AWS monitoring service that can monitor the different AWS resources in real time. It allows you to collect the resource metrics and create customized dashboards, and even take action when certain criteria is met. Integration of Oracle Database@AWS with Amazon CloudWatch enables monitoring the metrics of the different database resources that are provisioned in Oracle Database@AWS. Amazon CloudWatch collects raw data and processes it to produce near real-time metrics data. Metrics collected for the resources are retained for 15 months. This facilitates analyzing the historical data to understand and compare the performance, trends, and utilization of the database service resources at different time intervals. You can set up alarms that continuously monitor the resource metrics for breach of user-defined thresholds and configure alert notification or take automated action in response to that metric threshold being reached. 02:19 Lois: What monitoring features stand out the most in Amazon CloudWatch? Rashmi: With Amazon CloudWatch, you can monitor Exadata VM Cluster, container database, and Autonomous database resources in Oracle Database@AWS. Oracle Database@AWS reports metrics data specific to the resource in AWS/ODB namespace of Amazon CloudWatch. Metrics can be collected only when the database resource is an available state in Oracle Database@AWS. Each of the resource types have their own metrics defined in AWS/ODB namespace, for which the metrics data get collected.  02:54 Nikita: Rashmi, can you take us through a few metrics? Rashmi: At Exadata database VM Cluster, there is CPU utilization, memory utilization, swap space storage file system utilization metric. Then there is load average on the server, what is the node status, and the number of allocated CPUs, et cetera. Then for container database, there is CPU utilization, storage utilization, block changes, parse count, execute count, user calls, which are important elements that can provide metrics data on database load. And for Autonomous Database metrics data include DB time, CPU utilization, logins, IOPS and IO throughput, RedoSize, parse, execute, transaction count, and few others. 03:32 Nikita: Once you've collected these metrics and analyzed database performance, what tools or services can you use to automate responses or handle specific events in your Oracle Database@AWS environment? Rashmi: Then there is Amazon EventBridge, which can monitor events from AWS services and respond automatically with certain actions that may be defined. You can monitor events from Oracle Database@AWS in EventBridge, which sends events data continuously to EventBridge at real time. Eventbridge forwards these events data to target AWS Lambda and Amazon Simple Notification Service to perform any actions on occurrence of certain events. Oracle Database@AWS events are structured messages that indicate changes in the life cycle of the database service resource. Eventbridge can filter events based on your defined rules, process them, and deliver to one or more targets. Event Bus is the router that receives the events, optionally transform them, and then delivers the events to the targets. Events from Oracle Database@AWS can be generated by two means: they can be generated from Oracle Database@AWS in AWS, and they can also be generated directly from OCI and received by EventBridge in AWS. You can monitor Exadata Database and Autonomous Database resource events. Ensure that the Exadata infrastructure status is an available state. You can configure how the events are handled for these resources. You can define rules in EventBridge to filter the events of interest and the target, who is going to receive and process those events. You can filter events based on a pattern depending on the event type, and apply this pattern using Amazon EventBridge put-rule API, with the default event bus to route only those matching events to targets. 05:13 Lois: And what about events that AWS itself generates? Rashmi: Events that are generated in AWS for the Oracle Database@AWS resources are delivered to the default event bus of your AWS account. These events that are generated in AWS for Oracle Database@AWS resources include lifecycle changes of the ODB network. The different network events are successful creation or failure of the creation of the ODB network, and successful deletion or failure in deletion of the ODB network. When you subscribe to Oracle Database@AWS, then an event bus with prefix aws.partner/odb is created in your AWS account. All events generated in OCI for the Oracle Database@AWS resources are then received in this event bus. When you are creating filter pattern using Amazon EventBridge put-rule API, you must set the event bus name to this event bus. Make sure you do not delete this event bus. Events generated in OCI and received into event bus are extensive. They include events of Oracle Exadata infrastructure, VM Cluster, container, and pluggable databases. 06:14 Lois: If you want to look back at what's happened in your environment, like who made the changes or accessed resources, what's the best AWS service for logging and auditing all that activity? Rashmi: Amazon CloudTrail is a logging service in AWS that records the different actions taken by a user or roles, or an AWS service. Oracle Database@AWS is integrated with Amazon Cloud Trail. This enables logging of all the different events on Oracle Database@AWS resources.  Amazon Cloud Trail captures all the API calls to Oracle Database@AWS as events. These API calls include calls from the Oracle Database@AWS console, and code calls to Oracle Database@AWS API operations. These log files are delivered to Amazon S3 bucket that you specify. These logs determine the identity of the caller who made the call request to Oracle Database@AWS, their IP from which the call originated, the time of the call, and some additional details.  CloudTrail event history stores immutable record of the past 90 days of management events in an AWS region. You can view, search, and download these records from CloudTrail Event History. You can access CloudTrail when you create an AWS account that automatically gives you the access to CloudTrail. Event history. If you would like to retain the logs for a longer period of time beyond 90 days, you can create CloudTrail trails or CloudTrail Lake event data store.  Management events in AWS provide information about management operations that are performed on the resources in your AWS account. Management operations are also called control plane operations. Thus, the control plane operations in Oracle Database@AWS are logged as management events in CloudTrail logs.  07:59 Are you a MyLearn subscriber? If so, you're automatically a member of the Oracle University Learning Community! Join millions of learners, attend exclusive live events, and connect directly with Oracle subject matter experts. Enjoy the latest news, join challenges, and share your ideas. Don't miss out! Become an active member today by visiting mylearn.oracle.com. 08:25 Nikita: Welcome back! Samvit, let's talk best practices. What should teams keep in mind when they're setting up and securing their Oracle Database@AWS environment?  Samvit: Use IAM roles and policies with least privilege to manage Oracle Database@AWS resources. This ensures only authorized users can provision or modify DB resources, reducing the risk of accidental or malicious changes.  Oracle Data Safe monitors database activity, user risk, and sensitive data, while AWS CloudTrail records all AWS API calls. Together, they give full visibility across the database and cloud layers. Autonomous Database supports Oracle Database Vault for enforcing separation of duties. Exadata Database Service can integrate with Audit Vault and Database Firewall to prevent privileged users from bypassing security controls. Enable multifactor authentication for AWS IAM users managing Oracle Database@AWS. This adds a strong second layer of protection against stolen credentials.  Always deploy your Oracle Database@AWS in private subnets without public IPs. Use AWS security groups and NACLs to strictly limit inbound and outbound traffic, allowing access only from trusted applications. Exadata Database Service supports integration with Oracle Vault for key lifecycle management. And in case of Autonomous Database, the transparent data encryption keys are automatically managed. But you can bring your own keys with OCI Vault. Key rotation ensures compliance and reduces risk of key compromise. Oracle Database@AWS enforces encrypted connections by default. Ensure clients connect with TLS 1.2 or 1.3 to protect data in transit from interception or tampering.  Use Oracle Data Safe's user assessment features to detect dormant users or excessive privileges. Disable unused accounts and rightsize permissions to reduce insider threats and security gap. Export database audit logs to Oracle Data Safe Audit Vault or AWS S3 with object lock for immutability. This prevents lock tampering and ensures audit evidence is preserved for compliance.  11:25 Lois: OK, that covers security. Do you have any tips for making sure your Oracle Database@AWS setup is reliable and resilient? Samvit: Start with clear recovery objectives. Define how much downtime and data loss each workload can tolerate. These targets drive your HADR architecture and backup strategy.  Implement business continuity measures to deliver maximum uptime for your databases. As a best practice, you must configure disaster recovery environment for your critical databases so that, in the event of any disaster affecting the primary database, applications can be immediately failed over to the DR environment, ensuring least application downtime and zero or minimal data loss. With Oracle Database@AWS, you can automate the creation and management of DR environment for your database services using different deployment capabilities. You can opt to configure either cross-availability zone DR in the same region or configure cross-region DR. Since cross-availability zone can only provide site failure protection, you must also configure a cross-region DR to protect against regional failure. A DR plan is only effective if tested. Regular failover and switchover drills validate that people, processes, and systems can recover as designed.  For Exadata Database, Autonomous Recovery Service provides automated backup validation, recovery guarantees, and protection against accidental data loss or corruption.  Oracle-managed backups are fully managed by OCI. When you create your Oracle Exadata Database, you can enable automatic backups by choosing Enable Automatic Backups in the OCI Console. When you do that, you can select Amazon S3 or OCI Object Storage or Autonomous Recovery Service as the backup destination. Don't just take backups. You also need to test them. Regularly restore backups into non-production environment to validate integrity and recovery time.  Plan beyond just the database. Map application and middleware dependencies to ensure end-to-end business resilience. A database failover is useless if dependent apps can't reconnect. 14:09 Nikita: Another area of interest is performance and cost. What practices help teams balance the two? Samvit: Autonomous Database automatically scales CPU and storage as workloads grow. This ensures performance during peaks while avoiding overprovisioning. So you should enable ADB auto-scaling.  Monitor CPU, memory, and IO metrics with AWS CloudWatch to rightsize your compute. Scale up or down based on actual utilization instead of static provisioning. Autonomous databases continuously evaluate and creates indexes automatically. This improves query performance without requiring manual tuning.  Use connection pooling in your applications to optimize database connections. Minimizing round-trip reduces latency and improves throughput. Apply AWS tags to database and related resources for cost allocation and chargeback. Tagging also helps with governance and cost visibility.  Choose between bring your own license and license-included models for Oracle Database@AWS. The right model depends on your existing license portfolio and cost strategy. Not all workloads need long backup retention. Adjust retention policies based on business needs to balance compliance with storage costs.  Exadata Database supports Oracle multitenant with pluggable databases. Consolidating databases reduces infrastructure footprint and licensing costs. Performance tuning isn't just technical. Align metrics with business KPIs. correlating DB performance to user experience and revenue impact helps prioritize optimizations.  16:20 Lois: Before we wrap up, Samvit, let's look at operational efficiency. What advice do you have for making day-to-day operations more efficient? Samvit: Use infrastructure as code tools like Terraform or AWS CloudFormation to automate provisioning. This ensures consistent, repeatable deployments with minimal manual errors.  For Autonomous Database, enable auto-start/stop to optimize costs by running databases only when needed. This is ideal for dev test or seasonal workloads. Exadata Database Service provides fleet maintenance to patch multiple systems consistently. This reduces downtime and simplifies lifecycle management.  Integrate AWS CloudWatch for performance monitoring and EventBridge for event-driven automation. This helps detect issues early and trigger automated workflows. Oracle Data Safe provides ready-to-use audit and compliance reports. Use these to streamline governance and reduce the effort of manual compliance tracking.  For Autonomous databases, Performance Hub simplifies monitoring while Exadata users benefit from AWR and ASH reports. Together, they give deep insights into performance trends. Automated tagging policies and change management workflows help maintain governance. They ensure resources are tracked properly and changes are auditable.  Monitor storage consumption and growth patterns using AWS CloudWatch and the ADB Console. Proactive tracking helps avoid capacity issues and unexpected costs. Send CloudTrail logs into EventBridge to trigger automated incident responses. This shortens response time and builds operational resilience.  18:36 Nikita: Samvit and Rashmi, thanks for spending time with us today. Your insights always help bring the bigger picture into focus. Lois: They definitely do. And if you'd like to go deeper into everything we covered, head over to mylearn.oracle.com and look up the Oracle Database@AWS Architect Professional course. Until next time, this is Lois Houston… Nikita: And Nikita Abraham, signing off! 19:03 That's all for this episode of the Oracle University Podcast. If you enjoyed listening, please click Subscribe to get all the latest episodes. We'd also love it if you would take a moment to rate and review us on your podcast app. See you again on the next episode of the Oracle University Podcast.

Andrew Mountbatten-Windsor yog Askiv tsev neeg huab tais thawj tug neeg raug txhom, tsoom fwv Albanese rov qab qhia tias yuav tsis pab IS tej poj niam me nyuam rov qab los rau Australia, NSW ib tug nom MP cov kev tib Pauline Hanson tej lus tawm tswv yim tsis nyiam neeg Muslim, hau xeev Victoria raug tsub nias kom txheeb tej lus iab liam tias CFMEU lwg noj lwg haus lub xeev no tej nyiaj se txog $AUD 15 billion, NSW cov kev txheeb txog kev ruaj ntseg rau tej tsev kho mob uas kho tej neeg mob hlwb/puas hlwb, Trump ceeb toom tias Iran tsuas muaj sij hawm 10 hnub sib khom txog nws cov hauj lwm nuclear, tsab ntawv peb uas hawv yuav tua neeg Muslim ntawm lub tsev teev hawm Lakemba Mosque, ntau caum tus neeg tas sim neej ntawm Nigeria ib lub chaw khawb txhuas, muaj kev cej luam tshiab tias xeev Northern Territory tej chaw pab tej neeg puas cev siv tej tswv yim tsub nias tej neeg puas cev kom lawv tau txais txiaj ntsim, neeg Muslim ntawm Gaza lub koom txoos Ramadan, ADB tej nyiaj $USD 42 million pab Nplog yug tsiaj ua luam, tus coj Thaib pab nom Klatham qhia tias nws npaj txhij yuav qhia qhov tseeb seb nws puas muaj cai ua ib tug nom tseem ceeb ntawm Thaib tus tsoom fwv koom tswj.

In our upcoming episode of You And The Law Podcast, join me on Thursday, January 29, 2026, at 6 PM CST, 7 PM EST, with my guests, Monty Bynum, founder and CEO of ADB training, Lieutenant Sean M. Carroll (Ret), and the Author of A.I.O. Leadership for Law Enforcement. In this episode, we'll explore how poor leadership choices ripple through law enforcement agencies, the legal consequences that follow, and why training at the top is just as important, if not more than, training on the street. Because when leadership fails, the law doesn't look away.

IOM warns of deepening needs as millions of people return to Sudan WHO: India on alert with two cases of Nipah virus in JanuaryFAO's new 100 million initiative with ADB plans to strengthen food security for around one million Afghans 

Pat Conroy hais tias neeg Muslim Australians yog ib co zejzog neeg tseem ceeb rau Australia, Australia tus qub thawj pwm tsav dhau los tau hais kom tsim ib co accreditation process los txheeb tej xibfwb uas pheej teev txog cov kev ntseeg Islam, kab mob Nipha virus ntawm India, nqe kub (Gold price), India thiab Eu cov kev lagluam, cov kev yuam ua txij nkawm, tej koom txoos nco txog tej xwm txheej holocaust, tej huab cua kub sov ntau hnub sib law liag ntawm qab teb hnub tuaj Australia, Fabkis tsab cai txwv social media, neeg txum tim cov kev aws av, Meskas cov ICE agents thiab xeev Minnesota thiab Philadelphia, Cob tsib tej pej xeem laus neeg, ADB tej nyiaj pab txhim kho Nplog, Thaib cov kev nrhiav suab xaiv tsa.

Inleder med en sammanfattning av helgens ganska innehållsrika jakter (11.10) Ung jaktterriertik som husse funderar på att kastrera. Men finns det någon risk att de jaktliga egenskaperna försämras om kastrerar innan hon ”lärt sig” att jaga? (15.20) Lyssnare som undrar om vi är på gång att skaffa ännu en hund och i så fall vad och varför? Och varför har vi bara tikar. Plus en liten diskussion kring hur en gammal hund i familjen klarar av att det kommer en valp. (26.30) Ung laika som kan förfölja långt, men ofta lämnar bakspåret och tar upp nytt vilt på väg tillbaka. Vad göra? (31.25) Samma laika har ”tagit” några vildsvin, storlek 20– 30 kg, själv. Finns det något annat än munkorg som hjälper? (36.30) 4-månaders ADB-tik som morrar och hugger när man ska ta hennes klöv. (39.15) Advokat ”Taxerik” är åter behjälplig med svar på frågor om vapen- och ammunitionsförvaring. (44.00) Hur är det med den åldrade hundens sinnen. Syn och hörsel verkar ju svikta först, men vad vet man om det viktiga luktsinnet? (44.55) Hundgodiset vil lottade ut i förra avsnittet – finns det att köpa i Sverige? (46.10) Tips för att jaga in en spets – i detta fall en östlaika. (50.40) Ytterligare en fråga om resursförsvar. I detta fall en basset som morrade/bet när husse närmade sig den skjutna haren. (57.10) Hur kan det skilja så mycket i kostnad mellan att kastrera en tik och operera den för livmodersinflammation – man gör väl i princip samma sak? (1.00.10) Ung jaktlabrador som får krampanfall pga en neurologisk sjukdom. Törs man släppa honom på jakt, bl a efter vildsvin, eller bör man ”skola om” honom till eftersökshund?

Victoria tus neeg ua lagluam luam yeeb txhaum cai raug txhom ntawm teb chaws Iraq, rooj plaub uas hais seb puas pub Marine le Pen ua nom, tus neeg Iran uas raug teem txim tuag vim rwg npoj tawm tsam tsoom fwv, tus coj ntawm Bondi Beach thiab tej kev pab cuam rau tej neeg raug neeg phem tua, tej lus cav tias hauv xeev Malinauskas cov raug liam tias hais lus ua rau Randa Abdel-Fattah poob ntsej muag, cov kev thov kho tsab cai hate speech thiab gun laws, Pentagon yuav siv cov AI Grok, ADB tej nyiaj pab txhim kho Nplog tej nroog, Cambodia ib tug nom raug liam tias raus tes rau Thaib tej laj fai kum xeeb.

Send us a textCheck us out at:  https://www.cisspcybertraining.com/Get access to 360 FREE CISSP Questions:  https://www.cisspcybertraining.com/offers/dzHKVcDB/checkoutGet access to my FREE CISSP Self-Study Essentials Videos:  https://www.cisspcybertraining.com/offers/KzBKKouvYour TV, camera, or even a smart bird feeder can be a beachhead for attackers. We dive into the Kimwolf botnet and expose how low-cost IoT turns into residential proxies that scan, DDoS, and quietly pivot across your home or enterprise network. From weak defaults and exposed ADB to shady apps, we call out the telltale signs and the simple architecture changes that shut the door: dedicated IoT VLANs, strict egress controls, and logging that actually sees what leaves your network.Then we switch gears into CISSP Domain 7.1 and break down what a defensible investigation looks like when the alarms go off. Evidence collection starts with a mindset: don't touch originals, document everything, and assume you'll need to defend the process in court. We cover IOCE-aligned practices, creating bit-for-bit copies with hashes, and when to engage a forensic retainer so you are not building a plan mid-incident. Memory captures, media recovery, network telemetry, and software analysis all play a role in reconstructing the timeline and proving what happened.Legal readiness sits at the core. We talk about involving counsel early, understanding insurer-approved panels, and mapping out rules of engagement for interviews and device access in your IR policy and onboarding. We clarify evidence authorities—voluntary surrender, subpoenas, and search warrants—plus the three evidence types and how chain of custody preserves admissibility. By the end, you'll have a clear blueprint: segment IoT, monitor outbound traffic, and run investigations that survive scrutiny.If this helped sharpen your security playbook, subscribe, share with your team, and leave a quick review to help others find the show.Gain exclusive access to 360 FREE CISSP Practice Questions at FreeCISSPQuestions.com and have them delivered directly to your inbox! Don't miss this valuable opportunity to strengthen your CISSP exam preparation and boost your chances of certification success. Join now and start your journey toward CISSP mastery today!

Assurances obligatoires, garanties clés, nouvelles attentes des pros… Quentin Boyer décrypte les besoins du marché immobilier en France, au micro de Baptiste Julien Blandet.Quentin Boyer est l'invité de ce nouvel épisode de Mon Podcast Immo. Au micro de Baptiste Julien Blandet, il détaille le rôle d'Assur'Agent, courtier spécialisé en immobilier, et la manière dont les agents, syndics, ADB ou mandataires peuvent proposer facilement une quinzaine de garanties à leurs clients tout en percevant jusqu'à 50 % de rétrocommissions.Dans un marché immobilier en France sous tension, les besoins évoluent. Garantie revente pour rassurer les acquéreurs, GLI, PNO ou MRH pour les bailleurs, protection juridique pour les copropriétés, et même dépôt de garantie revisité pour alléger la charge des locataires : les usages se diversifient. « Il faut donner de la visibilité et rassurer l'acquéreur », insiste-t-il.Les syndics, eux, cherchent désormais des solutions pour anticiper les litiges, tandis que les marchands de biens sollicitent des contrats de RCP très spécifiques. Grâce à son partenariat avec Nous Assurons et 90 compagnies, Assur'Agent développe des produits sur-mesure pour répondre à ces demandes. « La beauté de l'assurance, c'est qu'il n'y a pas de limite », résume Quentin Boyer.Une plongée claire et concrète dans la mécanique des garanties et les attentes d'un secteur en pleine mutation.

Top Indian Stock Market News for Dec 11, 2025! Catch the US Fed 25bps rate cut, the massive EMS stock crash (Kaynes, Dixon), Adani Enterprises rights issue update, and SpaceX's potential $30Bn IPO. Plus: India-US trade deal & ADB upgrades India GDP forecast (7.2% for FY26). Don't miss these key market drivers!Link for Investing Ebooks: https://shorturl.at/gM97lHow to Use Artificial Intelligence for Investing - Combo of 5 ebooks00:00 Start00:51 US Fed Rate Cut03:25 SpaceX Plans $30Bn IPO05:16 India-US Trade Deal update08:09 ADB Raises India's FY26 GDP Forecast09:49 Indian Markets overview11:34 Adani Enterprises Rights Issue Oversubscribed13:10 EMS Stocks Crash Led by Kaynes15:50 Hindustan Zinc Surges on Silver Prices16:32 Swiggy's ₹10,000 Crores QIP

In this episode, our guest is Curtis S. Chin, former U.S. Ambassador to the Asian Development Bank and current Asia Fellow at the Milken Institute. With deep experience spanning diplomacy, finance, and sustainable development, Curtis shares insights on Asia's energy future, the balance of access and innovation, and why responsible development must focus on "People, Planet, and Partnership." He reflects on his days at the ADB, the need for localized energy solutions like micro-hydro and solar, and why maintenance—not just installation—is critical for long-term success. The conversation also dives into AI's growing role, the risks of misinformation, the widening digital divide, and how social and AI literacy are becoming vital skills. Curtis also touches on entrepreneurship, sharing case studies from clean tech to creative economies, while encouraging a broader, more inclusive definition of prosperity—one that includes investing in children, health, education, and community-level impact. Please join to find more. Connect with Sohail Hasnie: Facebook @sohailhasnie X (Twitter) @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie YouTube @energypreneurs Instagram @energypreneurs Tiktok @energypreneurs Spotify Video @energypreneurs

Edouard Sakakini est l'invité de ce nouvel épisode de Mon Podcast Immo. Au micro d'Ariane Artinian, il revient le rachat d'Inch par Septeo ADB et les ambitions technologiques qui l'accompagnent. Enjeu central : accélérer la modernisation des logiciels métiers utilisés par les administrateurs de biens et les syndics, dans un marché immobilier en pleine tension opérationnelle.Avec 2 200 clients et des outils historiques « très puissants », Septeo veut franchir un cap grâce aux innovations développées par Inch et la suite Lobby. « À deux, on sera plus forts pour écrire l'avenir », explique-t-il, rappelant les exigences technologiques croissantes du secteur. Ticketing avancé, gestion dématérialisée des immeubles, communication simplifiée, comptabilité syndic modernisée : la nouvelle offre promet des gains de productivité importants.L'IA sera au cœur de la feuille de route. Déjà intégrée dans Inch et Bellman — email sorting, chatbots, OCR, imputations comptables — elle arrivera aussi dans les logiciels existants de Septeo ADB. « On doit aider nos clients avec des outils qui apportent vraiment de l'automatisation », souligne-t-il. Une stratégie détaillée sera dévoilée en mars lors d'une grande réunion clients.Animé par Ariane Artinian, journaliste et fondatrice du média MySweetImmo

Việt Nam đặt mục tiêu tăng trưởng năm 2026 đạt 10% trở lên “để tạo đà, tạo lực, tạo thế cho tăng trưởng hai con số trong những năm tiếp theo, GDP đầu người đạt 5.500 đô la” (1). Đây là hai trong số 15 chỉ tiêu về kinh tế-xã hội trong kế hoạch dự kiến năm 2026 để đạt hai mục tiêu 100 năm đã đề ra : Đến năm 2030 trở thành nước đang phát triển có công nghiệp hiện đại, thu nhập trung bình cao; đến năm 2045 trở thành nước phát triển, thu nhập cao. Ngày 19/10/2025, thủ tướng Phạm Minh Chính thừa nhận mục tiêu tăng trưởng GDP hai con số những năm tới là không dễ đạt được, nhưng không thể không làm. Chính phủ duy trì mức tăng trưởng 8% cho năm 2025 (thấp hơn so với dự báo hồi đầu năm) nhờ vào việc “nền kinh tế Việt Nam đã chứng minh được khả năng phục hồi bất chấp những cú sốc bên ngoài”. Tuy nhiên, các định chế tài chính, ngân hàng quốc tế đưa ra mức thẩm định thấp hơn : từ 6,5% đến 6,7%. Chính phủ xác định phải thay đổi mô hình kinh tế, hiện vẫn dựa vào gia công, nhập khẩu và mô hình tăng trưởng, chủ yếu đến từ vốn, lao động (2). Tuy nhiên, những thay đổi này liệu có thể mang lại kết quả ngay năm 2026 để góp phần cho mục tiêu tăng trưởng 10% ? Tăng trưởng của Việt Nam vẫn phụ thuộc rất lớn vào xuất khẩu, đặc biệt là thị trường Mỹ, mức thuế hải quan 20% áp dụng đối với hàng hóa của Việt Nam, cũng như những xáo trộn trên thế giới do thuế đối ứng của Mỹ, sẽ tiếp tục tác động như thế nào đến hoạt động xuất khẩu của Việt Nam năm 2026 ? Ông Hubert Testard, chuyên gia về châu Á và các thách thức kinh tế quốc tế, tổng biên tập báo mạng Asialyst chuyên về châu Á, chia sẻ một số nhận định với RFI Tiếng Việt. RFI : Chính phủ Việt Nam đưa ra dự báo tăng trưởng GDP năm 2025 là 8%. Vào tháng 9, Ngân hàng Phát triển châu Á (ADB) đưa ra dự báo là khoảng 6,7%, còn Ngân hàng Thế giới là 6,6%, Quỹ Tiền tệ Quốc tế là 6,5%. Có thể thấy sự khác biệt rất rõ giữa những mức dự báo này. Liệu chúng ta có thể lạc quan về dự báo được chính phủ Việt Nam đưa ra không ? Hubert Testard : Đúng là có sự khác biệt giữa dự báo chính thức của chính phủ Việt Nam, khá là lạc quan cho năm 2025, và dự báo của các tổ chức quốc tế. Sự khác biệt này có thể là do những gì xuất hiện trong báo cáo của các tổ chức quốc tế thường dựa trên dữ liệu chậm hơn ngày công bố từ một đến hai tháng. Ví dụ, Quỹ Tiền Tệ Quốc Tế - IMF vừa công bố báo cáo thường niên vào ngày 15/10, nhưng dữ liệu đối với Việt Nam có lẽ là những dữ liệu dừng lại vào cuối tháng 8. Vấn đề ở chỗ là Việt Nam đã ghi nhận kết quả quý III rất tốt, với mức tăng trưởng hơn 8% một chút. Và đó là lý do khiến chính phủ Việt Nam lạc quan về tăng trưởng cả năm. Nhưng chúng ta biết rằng quý IV sẽ ít khả quan hơn vì áp lực từ thuế quan của Mỹ. Xuất khẩu của Việt Nam sang Hoa Kỳ trong quý I đã rất tốt vì các nhà xuất khẩu lường trước được những vấn đề này và do đó, xuất khẩu của Việt Nam sang Mỹ đã tăng gần 30% trong nửa đầu năm. Nhưng rõ ràng, giờ đây mọi chuyện không thể như cũ được nữa và sẽ có tác động trong quý IV. Đọc thêmMỹ-Việt công bố tuyên bố chung về thỏa thuận khung thương mại, Hà Nội vẫn chịu mức thuế quan 20% Nhưng vì kết quả quý III rất tốt, tôi nghĩ rằng nhìn chung, kết quả cả năm sẽ không chênh lệch quá nhiều so với dự báo của chính phủ. Tôi nghĩ con số này sẽ tốt hơn so với những gì Quỹ Tiền Tệ Quốc Tế hoặc Ngân Hàng Thế Giới dự báo trong số liệu chính thức hiện nay của họ. Theo tôi, kết quả sẽ đạt trên 7% trong năm nay. RFI : Ngày 20/10, thủ tướng Phạm Minh Chính nhấn mạnh “kinh tế Việt Nam khẳng định đủ sức chống chịu trước các cú sốc bên ngoài, tăng trưởng cao hàng đầu thế giới”. Liệu điều này có thể giúp đạt được mục tiêu tăng trưởng 10% cho năm 2026 ? Hubert Testard : Mức 10% vào năm 2026, trái lại, lại quá lạc quan, rất tham vọng. Và theo tôi, có lẽ không thể đạt được đối với Việt Nam, bởi vì bối cảnh quốc tế trong năm 2026 sẽ bớt thuận lợi hơn nhiều. Trước tiên là mức thuế quan trung bình 20% của Mỹ mà ai cũng biết, nhưng cũng phải kể đến nhiều mức thuế đặc biệt khác đối với ô tô, thép, nhôm. Gần đây, còn có một vấn đề khác đối với các nhà xuất khẩu thủy sản Việt Nam, với thông báo ngừng xuất khẩu một số mặt hàng vào năm 2026. Tất cả những điểm này sẽ có tác động nhất định. Ngoài ra, bối cảnh chung ở một số nước khác cũng không đặc biệt hơn. Nghĩa là, nhu cầu của Trung Quốc không mạnh lắm, châu Âu đang cố gắng hạn chế dòng hàng nhập khẩu từ châu Á, đặc biệt là từ Trung Quốc. Vì vậy, bối cảnh quốc tế sẽ kém thuận lợi hơn. Tất cả các tổ chức quốc tế đều dự đoán năm 2026 sẽ có mức tăng trưởng kém hơn một chút so với năm 2025. Vì vậy, việc đạt được 10% trong bối cảnh này, đối với tôi, là không được khả thi lắm. RFI : Ông vừa nhắc đến mức thuế 20% của Mỹ, khả năng thủy sản Việt Nam không được xuất khẩu sang Mỹ năm 2026… những biện pháp này có tác động đến GDP của Việt Nam không trong khi năm 2024, xuất khẩu sang Hoa Kỳ chiếm khoảng 30% GDP của Việt Nam ? Hubert Testard : Có, chắc chắn là có. Đã có những đánh giá về tác động này, nhưng chúng ta hãy chờ xem tác động thực sự như thế nào. Theo Quỹ Tiền Tệ Quốc tế - IMF, tác động của chủ nghĩa bảo hộ mậu dịch của Mỹ gây thiệt hại ít nhất là khoảng 0,5 đến 0,7% GDP cho Việt Nam. Đó là một cú sốc đáng kể và có thể bù đắp được nếu Việt Nam thúc đẩy nhiều hơn nhu cầu nội địa và đa dạng hóa trao đổi thương mại quốc tế. Tuy nhiên, đây vẫn là một cú sốc tiềm tàng khá mạnh. Chương trình Phát triển Liên Hiệp Quốc (UNDP) cũng ước tính xuất khẩu của Việt Nam sang Hoa Kỳ có thể giảm 20%. Tôi thấy con số này hơi quá. Nhưng rõ ràng là vẫn sẽ có một cú sốc rất lớn, cho nên Việt Nam sẽ phải bù đắp cú sốc này bằng nhiều biện pháp khác nhau trên thị trường nội địa cũng như đa dạng hóa trao đổi thương mại. Đọc thêmViệt Nam : “Bạn” hay “thù” trong chính sách đánh thuế của Trump ? RFI : Mô hình tăng trưởng của Việt Nam phụ thuộc vào tín dụng ngân hàng, đầu tư công và xuất khẩu, chủ yếu từ các nhà đầu tư nước ngoài. Liệu mô hình này có còn phù hợp trong tương lai ? Hubert Testard : Rõ ràng là phải thay đổi mô hình này. Đó là điều mà Tổ chức Hợp tác và Phát triển Kinh tế (OCDE) khuyến nghị trong báo cáo tháng 06/2025 về Việt Nam. Tổ chức này đưa ra một loạt đề xuất để mô hình tăng trưởng của Việt Nam tiến triển. Tôi nghĩ là trong bối cảnh nhu cầu quốc tế sẽ phức tạp, Việt Nam cần phát triển nhu cầu nội địa nhiều hơn hiện tại. Dù sao vẫn có một số điểm tích cực, ví dụ như tiền lương ở Việt Nam đang tăng nhanh hơn so với các nước ASEAN khác. Và đó là một cách tốt để hỗ trợ nhu cầu nội địa. Nhưng vẫn còn nhiều vấn đề khác, ví dụ, chi tiêu về xã hội rõ ràng là không đủ, đặc biệt là cho người cao tuổi. Cho nên lương hưu, đặc biệt là lương hưu tối thiểu, là một vấn đề. Ngoài ra, chi tiêu cho giáo dục, đặc biệt là giáo dục đại học, cũng không đủ. Chúng ta biết rằng kinh phí mà thanh niên Việt Nam phải trả để học đại học là quá cao, và khiến một bộ phận người trẻ không muốn hoặc không thể theo học. Đó là điều cần phải thay đổi bởi vì Việt Nam ngày càng cần một lực lượng lao động được đào tạo bài bản và có trình độ để đạt được tăng trưởng hiệu quả hơn và hướng tới các công nghệ khác. Đọc thêmĐể duy trì tăng trưởng cao, Việt Nam buộc phải thúc đẩy khu vực kinh tế tư nhân Ngoài ra, còn có một vấn đề tiềm ẩn khác đang bắt đầu nổi lên, đó là tình trạng lão hóa dân số. Hiện nay, những người trên 65 tuổi chiếm 15% dân số Việt Nam, còn khá thấp so với các quốc gia khác. Tuy nhiên, điều này sẽ thay đổi rất nhanh chóng và sẽ đạt hơn 30% vào năm 2050, đồng nghĩa với việc chi tiêu xã hội cho y tế và hưu trí sẽ tăng đáng kể. Như vậy, chính phủ cần tìm cách tài trợ cho chi tiêu xã hội và làm thay đổi phát triển mô hình xã hội Việt Nam. RFI : Gần đây thiệt hại do thiên tai gây ra ở Việt Nam cũng được đề cập. Theo đánh giá sơ bộ, thiệt hại này chiếm khoảng 2% GDP. Liệu đây có phải là một tác động cần được xem xét cho tăng trưởng ở Việt Nam ? Hubert Testard : Như chúng ta đã biết, biến đổi khí hậu vẫn đang tiếp tục gây ra những tác động, và Việt Nam nằm trong số những nước bị tác động nặng. Chị nhắc đến khoảng 2%, nhưng có khả năng con số này sẽ tăng lên trong những năm tới. Điều đó có nghĩa là, chúng ta không nên kỳ vọng vào việc các cú sốc khí hậu sẽ giảm đi, mà ngược lại sẽ gia tăng. Vì vậy, ở điểm này, Việt Nam cần đầu tư nhiều hơn để có thể ứng phó với những cú sốc trong tương lai. Ngoài ra còn có một khía cạnh khác, đó là quá trình chuyển đổi năng lượng của Việt Nam nhằm giảm phát khí thải gây hiệu ứng nhà kính. Đây cũng là một dự án đầu tư lớn được tiến hành tại Việt Nam. Có thể thấy là có nhiều dự án đã được khởi động, mọi việc tiến triển, nhưng vẫn còn rất xa mục tiêu được đặt ra cho năm 2050. Cho nên chính phủ Việt Nam vẫn còn rất nhiều việc phải làm. RFI Tiếng Việt xin chân thành cảm ơn chuyên gia Hubert Testard, tổng biên tập báo mạng Asialyst chuyên về châu Á.  (1) Quốc hội thảo luận mục tiêu tăng trưởng 2026 từ 10%, GDP đầu người đạt 5.500 USD 2/ Chính phủ đặt mục tiêu GDP năm 2026 tăng 10%

Việt Nam đặt mục tiêu tăng trưởng năm 2026 đạt 10% trở lên “để tạo đà, tạo lực, tạo thế cho tăng trưởng hai con số trong những năm tiếp theo, GDP đầu người đạt 5.500 đô la” (1). Đây là hai trong số 15 chỉ tiêu về kinh tế-xã hội trong kế hoạch dự kiến năm 2026 để đạt hai mục tiêu 100 năm đã đề ra : Đến năm 2030 trở thành nước đang phát triển có công nghiệp hiện đại, thu nhập trung bình cao; đến năm 2045 trở thành nước phát triển, thu nhập cao. Ngày 19/10/2025, thủ tướng Phạm Minh Chính thừa nhận mục tiêu tăng trưởng GDP hai con số những năm tới là không dễ đạt được, nhưng không thể không làm. Chính phủ duy trì mức tăng trưởng 8% cho năm 2025 (thấp hơn so với dự báo hồi đầu năm) nhờ vào việc “nền kinh tế Việt Nam đã chứng minh được khả năng phục hồi bất chấp những cú sốc bên ngoài”. Tuy nhiên, các định chế tài chính, ngân hàng quốc tế đưa ra mức thẩm định thấp hơn : từ 6,5% đến 6,7%. Chính phủ xác định phải thay đổi mô hình kinh tế, hiện vẫn dựa vào gia công, nhập khẩu và mô hình tăng trưởng, chủ yếu đến từ vốn, lao động (2). Tuy nhiên, những thay đổi này liệu có thể mang lại kết quả ngay năm 2026 để góp phần cho mục tiêu tăng trưởng 10% ? Tăng trưởng của Việt Nam vẫn phụ thuộc rất lớn vào xuất khẩu, đặc biệt là thị trường Mỹ, mức thuế hải quan 20% áp dụng đối với hàng hóa của Việt Nam, cũng như những xáo trộn trên thế giới do thuế đối ứng của Mỹ, sẽ tiếp tục tác động như thế nào đến hoạt động xuất khẩu của Việt Nam năm 2026 ? Ông Hubert Testard, chuyên gia về châu Á và các thách thức kinh tế quốc tế, tổng biên tập báo mạng Asialyst chuyên về châu Á, chia sẻ một số nhận định với RFI Tiếng Việt. RFI : Chính phủ Việt Nam đưa ra dự báo tăng trưởng GDP năm 2025 là 8%. Vào tháng 9, Ngân hàng Phát triển châu Á (ADB) đưa ra dự báo là khoảng 6,7%, còn Ngân hàng Thế giới là 6,6%, Quỹ Tiền tệ Quốc tế là 6,5%. Có thể thấy sự khác biệt rất rõ giữa những mức dự báo này. Liệu chúng ta có thể lạc quan về dự báo được chính phủ Việt Nam đưa ra không ? Hubert Testard : Đúng là có sự khác biệt giữa dự báo chính thức của chính phủ Việt Nam, khá là lạc quan cho năm 2025, và dự báo của các tổ chức quốc tế. Sự khác biệt này có thể là do những gì xuất hiện trong báo cáo của các tổ chức quốc tế thường dựa trên dữ liệu chậm hơn ngày công bố từ một đến hai tháng. Ví dụ, Quỹ Tiền Tệ Quốc Tế - IMF vừa công bố báo cáo thường niên vào ngày 15/10, nhưng dữ liệu đối với Việt Nam có lẽ là những dữ liệu dừng lại vào cuối tháng 8. Vấn đề ở chỗ là Việt Nam đã ghi nhận kết quả quý III rất tốt, với mức tăng trưởng hơn 8% một chút. Và đó là lý do khiến chính phủ Việt Nam lạc quan về tăng trưởng cả năm. Nhưng chúng ta biết rằng quý IV sẽ ít khả quan hơn vì áp lực từ thuế quan của Mỹ. Xuất khẩu của Việt Nam sang Hoa Kỳ trong quý I đã rất tốt vì các nhà xuất khẩu lường trước được những vấn đề này và do đó, xuất khẩu của Việt Nam sang Mỹ đã tăng gần 30% trong nửa đầu năm. Nhưng rõ ràng, giờ đây mọi chuyện không thể như cũ được nữa và sẽ có tác động trong quý IV. Đọc thêmMỹ-Việt công bố tuyên bố chung về thỏa thuận khung thương mại, Hà Nội vẫn chịu mức thuế quan 20% Nhưng vì kết quả quý III rất tốt, tôi nghĩ rằng nhìn chung, kết quả cả năm sẽ không chênh lệch quá nhiều so với dự báo của chính phủ. Tôi nghĩ con số này sẽ tốt hơn so với những gì Quỹ Tiền Tệ Quốc Tế hoặc Ngân Hàng Thế Giới dự báo trong số liệu chính thức hiện nay của họ. Theo tôi, kết quả sẽ đạt trên 7% trong năm nay. RFI : Ngày 20/10, thủ tướng Phạm Minh Chính nhấn mạnh “kinh tế Việt Nam khẳng định đủ sức chống chịu trước các cú sốc bên ngoài, tăng trưởng cao hàng đầu thế giới”. Liệu điều này có thể giúp đạt được mục tiêu tăng trưởng 10% cho năm 2026 ? Hubert Testard : Mức 10% vào năm 2026, trái lại, lại quá lạc quan, rất tham vọng. Và theo tôi, có lẽ không thể đạt được đối với Việt Nam, bởi vì bối cảnh quốc tế trong năm 2026 sẽ bớt thuận lợi hơn nhiều. Trước tiên là mức thuế quan trung bình 20% của Mỹ mà ai cũng biết, nhưng cũng phải kể đến nhiều mức thuế đặc biệt khác đối với ô tô, thép, nhôm. Gần đây, còn có một vấn đề khác đối với các nhà xuất khẩu thủy sản Việt Nam, với thông báo ngừng xuất khẩu một số mặt hàng vào năm 2026. Tất cả những điểm này sẽ có tác động nhất định. Ngoài ra, bối cảnh chung ở một số nước khác cũng không đặc biệt hơn. Nghĩa là, nhu cầu của Trung Quốc không mạnh lắm, châu Âu đang cố gắng hạn chế dòng hàng nhập khẩu từ châu Á, đặc biệt là từ Trung Quốc. Vì vậy, bối cảnh quốc tế sẽ kém thuận lợi hơn. Tất cả các tổ chức quốc tế đều dự đoán năm 2026 sẽ có mức tăng trưởng kém hơn một chút so với năm 2025. Vì vậy, việc đạt được 10% trong bối cảnh này, đối với tôi, là không được khả thi lắm. RFI : Ông vừa nhắc đến mức thuế 20% của Mỹ, khả năng thủy sản Việt Nam không được xuất khẩu sang Mỹ năm 2026… những biện pháp này có tác động đến GDP của Việt Nam không trong khi năm 2024, xuất khẩu sang Hoa Kỳ chiếm khoảng 30% GDP của Việt Nam ? Hubert Testard : Có, chắc chắn là có. Đã có những đánh giá về tác động này, nhưng chúng ta hãy chờ xem tác động thực sự như thế nào. Theo Quỹ Tiền Tệ Quốc tế - IMF, tác động của chủ nghĩa bảo hộ mậu dịch của Mỹ gây thiệt hại ít nhất là khoảng 0,5 đến 0,7% GDP cho Việt Nam. Đó là một cú sốc đáng kể và có thể bù đắp được nếu Việt Nam thúc đẩy nhiều hơn nhu cầu nội địa và đa dạng hóa trao đổi thương mại quốc tế. Tuy nhiên, đây vẫn là một cú sốc tiềm tàng khá mạnh. Chương trình Phát triển Liên Hiệp Quốc (UNDP) cũng ước tính xuất khẩu của Việt Nam sang Hoa Kỳ có thể giảm 20%. Tôi thấy con số này hơi quá. Nhưng rõ ràng là vẫn sẽ có một cú sốc rất lớn, cho nên Việt Nam sẽ phải bù đắp cú sốc này bằng nhiều biện pháp khác nhau trên thị trường nội địa cũng như đa dạng hóa trao đổi thương mại. Đọc thêmViệt Nam : “Bạn” hay “thù” trong chính sách đánh thuế của Trump ? RFI : Mô hình tăng trưởng của Việt Nam phụ thuộc vào tín dụng ngân hàng, đầu tư công và xuất khẩu, chủ yếu từ các nhà đầu tư nước ngoài. Liệu mô hình này có còn phù hợp trong tương lai ? Hubert Testard : Rõ ràng là phải thay đổi mô hình này. Đó là điều mà Tổ chức Hợp tác và Phát triển Kinh tế (OCDE) khuyến nghị trong báo cáo tháng 06/2025 về Việt Nam. Tổ chức này đưa ra một loạt đề xuất để mô hình tăng trưởng của Việt Nam tiến triển. Tôi nghĩ là trong bối cảnh nhu cầu quốc tế sẽ phức tạp, Việt Nam cần phát triển nhu cầu nội địa nhiều hơn hiện tại. Dù sao vẫn có một số điểm tích cực, ví dụ như tiền lương ở Việt Nam đang tăng nhanh hơn so với các nước ASEAN khác. Và đó là một cách tốt để hỗ trợ nhu cầu nội địa. Nhưng vẫn còn nhiều vấn đề khác, ví dụ, chi tiêu về xã hội rõ ràng là không đủ, đặc biệt là cho người cao tuổi. Cho nên lương hưu, đặc biệt là lương hưu tối thiểu, là một vấn đề. Ngoài ra, chi tiêu cho giáo dục, đặc biệt là giáo dục đại học, cũng không đủ. Chúng ta biết rằng kinh phí mà thanh niên Việt Nam phải trả để học đại học là quá cao, và khiến một bộ phận người trẻ không muốn hoặc không thể theo học. Đó là điều cần phải thay đổi bởi vì Việt Nam ngày càng cần một lực lượng lao động được đào tạo bài bản và có trình độ để đạt được tăng trưởng hiệu quả hơn và hướng tới các công nghệ khác. Đọc thêmĐể duy trì tăng trưởng cao, Việt Nam buộc phải thúc đẩy khu vực kinh tế tư nhân Ngoài ra, còn có một vấn đề tiềm ẩn khác đang bắt đầu nổi lên, đó là tình trạng lão hóa dân số. Hiện nay, những người trên 65 tuổi chiếm 15% dân số Việt Nam, còn khá thấp so với các quốc gia khác. Tuy nhiên, điều này sẽ thay đổi rất nhanh chóng và sẽ đạt hơn 30% vào năm 2050, đồng nghĩa với việc chi tiêu xã hội cho y tế và hưu trí sẽ tăng đáng kể. Như vậy, chính phủ cần tìm cách tài trợ cho chi tiêu xã hội và làm thay đổi phát triển mô hình xã hội Việt Nam. RFI : Gần đây thiệt hại do thiên tai gây ra ở Việt Nam cũng được đề cập. Theo đánh giá sơ bộ, thiệt hại này chiếm khoảng 2% GDP. Liệu đây có phải là một tác động cần được xem xét cho tăng trưởng ở Việt Nam ? Hubert Testard : Như chúng ta đã biết, biến đổi khí hậu vẫn đang tiếp tục gây ra những tác động, và Việt Nam nằm trong số những nước bị tác động nặng. Chị nhắc đến khoảng 2%, nhưng có khả năng con số này sẽ tăng lên trong những năm tới. Điều đó có nghĩa là, chúng ta không nên kỳ vọng vào việc các cú sốc khí hậu sẽ giảm đi, mà ngược lại sẽ gia tăng. Vì vậy, ở điểm này, Việt Nam cần đầu tư nhiều hơn để có thể ứng phó với những cú sốc trong tương lai. Ngoài ra còn có một khía cạnh khác, đó là quá trình chuyển đổi năng lượng của Việt Nam nhằm giảm phát khí thải gây hiệu ứng nhà kính. Đây cũng là một dự án đầu tư lớn được tiến hành tại Việt Nam. Có thể thấy là có nhiều dự án đã được khởi động, mọi việc tiến triển, nhưng vẫn còn rất xa mục tiêu được đặt ra cho năm 2050. Cho nên chính phủ Việt Nam vẫn còn rất nhiều việc phải làm. RFI Tiếng Việt xin chân thành cảm ơn chuyên gia Hubert Testard, tổng biên tập báo mạng Asialyst chuyên về châu Á.  (1) Quốc hội thảo luận mục tiêu tăng trưởng 2026 từ 10%, GDP đầu người đạt 5.500 USD 2/ Chính phủ đặt mục tiêu GDP năm 2026 tăng 10%

VOV1 - Từ đầu năm đến nay, nền kinh tế Việt Nam có nhiều dấu ấn nổi bật. Tăng trưởng GDP duy trì ở mức cao, lạm phát được kiểm soát, cán cân thương mại tiếp tục xuất siêu, trong khi môi trường đầu tư - kinh doanh được cải thiện rõ rệt.Mới đây, nhiều tổ chức quốc tế tiếp tục nâng dự báo tăng trưởng kinh tế năm nay của Việt Nam thêm 1-1,5%. Cụ thể, Standard Chartered đã nâng dự báo tăng trưởng của Việt Nam năm nay lên 7,5%, cao hơn mức 6,1% đưa ra cuối tháng 7. Ngân hàng Hồng kong và Thượng hải(HSBC) nâng từ 6,6% lên 7,9%; Ngân hàng United overseas(UOB) đưa lên 7,5% (trước là 6,9%); Ngân hàng phát triển Châu Á(ADB) lên 6,7%.Tuy nhiên, theo UOB, quý cuối năm nay được dự báo sẽ gặp nhiều thách thức trong bối cảnh căng thẳng thương mại và thuế quan. Do đó, để đạt được mục tiêu tăng trưởng cả năm 2025 từ 8,3–8,5%, quý IV sẽ cần đạt mức tăng trưởng rất cao từ 9,7 - 10,5%.Khách mời: PGS.TS Phạm Thế Anh-Trưởng Khoa Kinh tế học, ĐH Kinh tế quốc dân.

James and John discuss eBay finds: 1985 MacCollege binder, Macintosh TV, and 1989 Macintosh Pink OS binder. James opens up another bin of Apple stuff from his colleciton, and news includes a USB-to-ADB keyboard adapter and an archive of Mac programming books.   Join our Facebook page, follow us on X (Twitter), watch us on YouTube, and visit us at RetroMacCast.

The nights are drawing in for Europeans, and Elliot Williams is joined this week by Jenny List for an evening podcast looking at the past week in all things Hackaday. After reminding listeners of the upcoming Hackaday Supercon and Jawncon events, we take a moment to mark the sad passing of the prolific YouTuber, Robert Murray-Smith. Before diving into the real hacks, there are a couple of more general news stories with an effect on our community. First, the takeover of Arduino by Qualcomm, and what its effect is likely to be. We try to speculate as to where the Arduino platform might go from here, and even whether it remains the player it once was, in 2025. Then there's the decision by Google to restrict Android sideloading to only approved-developer APKs unless over ADB. It's an assault on a user's rights over their own hardware, as well as something of a blow to the open-source Android ecosystem. What will be our community's response? On more familiar territory we have custom LCDs, algorithmic art, and a discussion of non-stepper motors in 3D printing. Even the MakerBot Cupcake makes an appearance. Then there's a tiny RV, new creative use of an ESP32 peripheral, and the DVD logo screensaver, in hardware. We end the show with a look at why logic circuits use the voltages they do. It's a smorgasbord of hacks for your listening enjoyment.

In this episode, our guest is Yongping Zhai, former ADB energy leader and now Senior Advisor at Tencent, leading their carbon neutrality strategy. He shares his journey from early solar projects to driving green innovation in big tech—covering dramatic cost drops in renewables, the rise of AI in grid management, and why mindsets must shift for the energy transition to succeed. Yongping also discusses Tencent's role in supporting frontier technologies like direct air capture, long-duration storage, and carbon-to-product solutions, all aiming for net zero by 2030. Connect with Sohail Hasnie: Facebook @sohailhasnie X (Twitter) @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie YouTube @energypreneurs Instagram @energypreneurs Tiktok @energypreneurs Spotify Video @energypreneurs

In this episode, our guest is Daan Boom, former Knowledge Management Specialist at ADB, who shares how knowledge systems have evolved—from early platforms like K-Map and E-Star to today's AI-driven environments. He reflects on building a culture of learning within development institutions, his current work on climate resilience in Bangladesh, and how to stay intellectually and physically active in retirement. A thoughtful conversation on knowledge, AI, and lifelong engagement. Please join to find more. Connect with Sohail Hasnie: Facebook @sohailhasnie X (Twitter) @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie YouTube @energypreneurs Instagram @energypreneurs Tiktok @energypreneurs Spotify Video @energypreneurs

Selon Women in Games France, l'industrie du jeu vidéo ne comptait que 24% de femmes en 2023. Des chiffres étonnamment bas quand on sait que plus de la moitié des Françaises considèrent être des joueuses actives, d'après une enquête de l'IFOP de 2024. Il faut dire que les nombreux scandales misogynes et racistes qui ont éclaboussé l'industrie vidéoludique ont de quoi dissuader les programmeuses de jeux vidéo en devenir. Dernier exemple en date, le procès de trois anciens cadres d'Ubisoft qui comparaissaient au tribunal de Bobigny en juin 2025 pour des faits de harcèlement moral et sexuel et tentative d'agression sexuelle au sein de l'entreprise. Face à cette réalité, des collectifs et des gameuses s'activent pour faire bouger les lignes d'un secteur à la réputation viriliste. Elles militent pour une meilleure représentation des femmes et des personnes racisées dans les personnages, mais aussi pour davantage de mixité dans l'industrie. Qui sont ces femmes qui transforment le jeu vidéo ? Comment changer les codes d'un secteur façonné par des hommes ?  Avec : • Jennifer Lufau, fondatrice de l'association Afrogameuses et chroniqueuse à RFI. Sa chronique Bienvenue dans le game est diffusée chaque dimanche à 7h20 TU sur RFI et disponible en podcast.  • Elison Nioka, créatrice de contenu gaming, streameuse connue sous le nom Elixon7. • Farhanaz Kassee-Elahee, co-fondatrice et directrice créative et artistique du studio Purple Meadows.   En fin d'émission, la chronique Écouter le monde de Monica Fantini.   Programmation musicale : ► Wa wa wa  — ADB feat. Yujio ► Special — Olamide.

Selon Women in Games France, l'industrie du jeu vidéo ne comptait que 24% de femmes en 2023. Des chiffres étonnamment bas quand on sait que plus de la moitié des Françaises considèrent être des joueuses actives, d'après une enquête de l'IFOP de 2024. Il faut dire que les nombreux scandales misogynes et racistes qui ont éclaboussé l'industrie vidéoludique ont de quoi dissuader les programmeuses de jeux vidéo en devenir. Dernier exemple en date, le procès de trois anciens cadres d'Ubisoft qui comparaissaient au tribunal de Bobigny en juin 2025 pour des faits de harcèlement moral et sexuel et tentative d'agression sexuelle au sein de l'entreprise. Face à cette réalité, des collectifs et des gameuses s'activent pour faire bouger les lignes d'un secteur à la réputation viriliste. Elles militent pour une meilleure représentation des femmes et des personnes racisées dans les personnages, mais aussi pour davantage de mixité dans l'industrie. Qui sont ces femmes qui transforment le jeu vidéo ? Comment changer les codes d'un secteur façonné par des hommes ?  Avec : • Jennifer Lufau, fondatrice de l'association Afrogameuses et chroniqueuse à RFI. Sa chronique Bienvenue dans le game est diffusée chaque dimanche à 7h20 TU sur RFI et disponible en podcast.  • Elison Nioka, créatrice de contenu gaming, streameuse connue sous le nom Elixon7. • Farhanaz Kassee-Elahee, co-fondatrice et directrice créative et artistique du studio Purple Meadows.   En fin d'émission, la chronique Écouter le monde de Monica Fantini.   Programmation musicale : ► Wa wa wa  — ADB feat. Yujio ► Special — Olamide.

À l'occasion de la journée internationale de sensibilisation à l'albinisme qui se tient tous les 13 juin, nous parlons de cette maladie héréditaire caractérisée par une absence de pigmentation de la peau, des cheveux et des yeux. L'albinisme est une maladie présente partout à travers le monde, mais est plus fréquente en Afrique subsaharienne avec une prévalence qui varie entre 1 cas sur 5 000 à 1 cas sur 15 000 selon l'OMS. Souvent discriminées, les personnes atteintes d'albinisme peuvent avoir des handicaps, notamment visuels, et ont plus de risques de déclencher des cancers de la peau.  Dr Fanny Morice-Picard, dermatologue au Centre de référence maladies rares de la peau du CHU de Bordeaux et au Service de Dermatologie et Dermatologie Pédiatrique de ce même CHU Pr Mohamed Maciré Soumah, dermatologue-vénéréologue au CHU Donka de Conakry, praticien hospitalier, professeur d'université, enseignant-chercheur à la Faculté des Sciences et Techniques de la Santé de l'Université Gamal Abdel Nasser de Conakry, en Guinée Souradji Ouro-Yondou, directeur exécutif de l'Association Nationale des personnes atteintes d'albinisme au Togo (ANAT).   Programmation musicale :  ► Eu.clides - Ira para que ? ► ADB, Yujio - Wa wa wa.

À l'occasion de la journée internationale de sensibilisation à l'albinisme qui se tient tous les 13 juin, nous parlons de cette maladie héréditaire caractérisée par une absence de pigmentation de la peau, des cheveux et des yeux. L'albinisme est une maladie présente partout à travers le monde, mais est plus fréquente en Afrique subsaharienne avec une prévalence qui varie entre 1 cas sur 5 000 à 1 cas sur 15 000 selon l'OMS. Souvent discriminées, les personnes atteintes d'albinisme peuvent avoir des handicaps, notamment visuels, et ont plus de risques de déclencher des cancers de la peau.  Dr Fanny Morice-Picard, dermatologue au Centre de référence maladies rares de la peau du CHU de Bordeaux et au Service de Dermatologie et Dermatologie Pédiatrique de ce même CHU Pr Mohamed Maciré Soumah, dermatologue-vénéréologue au CHU Donka de Conakry, praticien hospitalier, professeur d'université, enseignant-chercheur à la Faculté des Sciences et Techniques de la Santé de l'Université Gamal Abdel Nasser de Conakry, en Guinée Souradji Ouro-Yondou, directeur exécutif de l'Association Nationale des personnes atteintes d'albinisme au Togo (ANAT).   Programmation musicale :  ► Eu.clides - Ira para que ? ► ADB, Yujio - Wa wa wa.

प्रधानमंत्री नरेंद्र मोदी और गृहमंत्री अमित शाह के बीच हुई अहम बैठक, PM मोदी 6 जून को जम्मू जाएंगे, CDS अनिल चौहान ने कहा भारत ने 48 घंटे की लड़ाई 8 घंटे में ही पूरी की, राहुल गांधी ने पीएम मोदी को घेरा, योगी का अग्निवीरों के लिए लिया बड़ा फैसला, कश्मीर के अनंतनाग जिले में VPN यूज पर रोक, ADB पाकिस्तान को देगा 800 मिलियन अमेरिकी डॉलर और आईपीएल का फाइनल मुकाबला जारी, सिर्फ 5 मिनट में सुनिए रात 9 बजे की बड़ी ख़बरें.

Food security is one of the most pressing issues faced by Asia and the Pacific, including the Philippines. Developing Asia accounts for more than half of the undernourished population in the world according to the Asian Development Bank (ADB).About 40% of the region's workforce are also employed in jobs related to agri-food systems.In this B-Side episode, BusinessWorld speaks with Pavit Ramachandran, ADB country director for the Philippines, in an interview on the sidelines of ADB's annual meeting in Milan, Italy.He shares the latest developments and initiatives by the multilateral bank to further improve and strengthen food systems in the Philippines and the overall region.Interview by Luisa JocsonAudio editing by Jayson Mariñas

Africa has been uniquely impacted by the economic rollercoaster of 2025, with the African Development Bank warning that tariffs could send "shockwaves" through the dozens of nations impacted, reducing trade and raising debt. The ADB aims to reduce poverty and living conditions for Africans across the continent, and its President Akinwumi Adesina joins Christiane from Abidjan.   Also on today's show: Author Daniel Kehlmann; journalist Karen Attiah  Learn more about your ad choices. Visit podcastchoices.com/adchoices

VOV1 - Trong thư gửi cô Amanda Nguyễn, Chủ tịch nước Lương Cường bày tỏ vui mừng và tự hào khi lần đầu tiên có một phụ nữ Việt Nam bay vào vũ trụ, khẳng định tài năng và trí tuệ của người Việt Nam tại Mỹ và trên thế giới.- Thủ tướng Phạm Minh Chính tiếp ông Scott Morris, Phó Chủ tịch Ngân hàng Phát triển châu Á (ADB) đang thăm, làm việc tại Việt Nam và dự Hội nghị thượng đỉnh Diễn đàn Đối tác vì Tăng trưởng xanh và Mục tiêu toàn cầu 2030 lần thứ tư - P4G.- Sáng nay, nhà ga T3 Cảng hàng không quốc tế Tân Sơn Nhất đón chuyến bay thương mại đầu tiên do Vietnam Airlines khai thác trên chặng TP.HCM – Vân Đồn.- Công an Thanh Hóa triệt phá đường dây sản xuất, buôn bán thuốc tân dược giả quy mô lớn, thu lợi gần 200 tỷ đồng.- Chủ tịch Trung Quốc Tập Cận Bình kêu gọi các quốc gia châu Á đoàn kết chống lại xung đột địa chính trị, chủ nghĩa đơn phương và chủ nghĩa bảo hộ.- Tổng thống Mỹ Donald Trump lần thứ 7 góp mặt trong top 100 người ảnh hưởng nhất thế giới năm 2025, theo bình chọn của Tạp chí Time.

This week on Tagata o te Moana: Pacific nations are disappointed and are trying to wrap their head around US tariffs; The ADB says economic growth in the Pacific is projected to moderate to 3.9 per cent in 2025 and 3.6 per cent in 2026; Bougainville, which is seeking independence, continues to face trauma that can be traced back to the eight years of civil war from 1989; A National Geographic rapid assessment expedition has found Tokelau's coral reefs appear to be recovering following coral bleaching.Go to this episode on rnz.co.nz for more details

미국, 상호관세 90일 유예 / 관세 유예에 미 증시 유가 폭등 / 중국에 125% '맞보복' 관세 / 한국 협상시간 벌어 / 트럼프 또 다시 패키지 언급 / 이재명 오늘 출마선언 / 오세훈 오는 13일 출마 선언 / 국민의힘, 다음달 3일 대선후보 선출 / 한덕수 지명은 위헌, 헌법소원·가처분신청 / 공수처 "한덕수 수사중 이완규도 수사대상" / 이완규 "한덕수 지명 존중" / '권한대행 헌법재판관 임명불가' 법사위 의결 / 국회의장 "대선과 동시 개헌 사실상 어려워" / 박성재 법무 탄핵 선고 / ADB 올해 한국경제 1.5% 성장 하향 전망 /2021년 한국 공공사회복지 지출 OECD 하위권See omnystudio.com/listener for privacy information.

In Pacific Waves today: ADB projects moderate growth for Pacific economies; Guam's tariff exemption unlikely to be permanent - ex delegate; Tokelau navigates its trifecta of issues. Go to this episode on rnz.co.nz for more details

VOV1 - Tổng Bí thư Tô Lâm chủ trì buổi gặp mặt với đại diện các cựu chiến binh, cựu Thanh niên xung phong, dân quân tự vệ tham gia cuộc kháng chiến chống Mỹ cứu nước tại Hà Nội, nhân dịp kỷ niệm 50 năm giải phóng hoàn toàn miền Nam thống nhất Đất nước.-Thủ tướng Phạm Minh Chính chủ trì lễ đón, hội đàm với Thủ tướng Vương quốc Tây Ban Nha.-Ngân hàng Phát triển châu Á ADB dự báo Việt Nam có mức tăng trưởng tích cực nhất khu vực Đông Nam Á trong năm nay và năm tới.Hai bệnh viện ở Quảng Ninh hoàn thành hai ca ghép tạng từ người hiến tạng chết não, đánh dấu bước tiến mới của bệnh viện tuyến tỉnh.- Căng thẳng thương mại toàn cầu đã đẩy lên nấc thang mới, khi Trung Quốc khẳng định sẵn sàng trả đũa với mức thuế mới lên tới 104% mà Mỹ dự kiến áp đặt đối với hàng hóa nước này từ đêm nay. Còn Liên minh châu Âu chính thức công bố danh sách các sản phẩm của Mỹ sẽ bị áp thuế quan trả đũa. - Ít nhất 79 người thiệt mạng và hơn 150 người bị thương trong vụ sập trần một câu lạc bộ đêm ở Cộng hòa Dominica, trong khi ít nhất 20 người thiệt mạng trong vụ cháy tại viện dưỡng lão ở thành phố Thừa Đức, tỉnh Hà Bắc, Trung Quốc.

VOV1 - Sau khi tạm lắng dịu được vài ngày, không khí căng thẳng tại thủ đô Seoul của Hàn Quốc đã quay trở lại với các cuộc biểu tình rầm rộ của phe ủng hộ Tổng thống vừa bị phế truất.- Tổng Bí thư Tô Lâm gặp mặt đại diện các cựu chiến binh, cựu Thanh niên xung phong, dân quân tự vệ tham gia cuộc kháng chiến chống Mỹ cứu nước, khẳng định công tác “đền ơn đáp nghĩa” là một trong những nhiệm vụ chính trị hàng đầu.- Thủ tướng Phạm Minh Chính hội đàm; lãnh đạo Đảng, nhà nước tiếp, hội kiến Thủ tướng Vương quốc Tây Ban Nha Pedro Sánchez thăm chính thức Việt Nam.- Ngân hàng Phát triển châu Á ADB cập nhật tình hình kinh tế Việt Nam đạt mức tăng trưởng tích cực nhất khu vực Đông Nam Á.- Sau 1 năm thực hiện Đề án “Phát triển bền vững một triệu héc-ta lúa chuyên canh chất lượng cao, phát thải thấp gắn với tăng trưởng xanh vùng ĐBSCL” cho thấy lợi ích rõ rệt cả về kinh tế lẫn môi trường.- Khai trương “Cổng thông tin tiếp nhận và công bố các sản phẩm, giải pháp khoa học, công nghệ, đổi mới sáng tạo và chuyển đổi số”. - Thuế đối ứng của Mỹ bắt đầu có hiệu lực, trong đó Trung Quốc chịu mức thuế cao lên tới 104%.

In this episode, our guest is Woochong Um, Chief Executive Officer of the Global Energy Alliance for People and Planet (GEAPP). With a distinguished career spanning more than 30 years in international development, Woochong shares his journey from senior leadership at the Asian Development Bank to now spearheading one of the world's most ambitious efforts to end energy poverty and combat climate change. He discusses GEAPP's mission to bring clean, affordable energy to 1 billion people by 2030, reduce carbon emissions, and generate millions of green jobs across Africa, Asia, Latin America, and the Caribbean. Woochong also reflects on the role of public-private-philanthropic partnerships, flexible capital, and local innovation in scaling climate solutions—highlighting transformative projects in Rajasthan, Haiti, Indonesia, and beyond. From off-grid solar and battery storage to digital grid management and electric mobility, this conversation offers insight into what it takes to deliver a just, inclusive energy transition in emerging markets. Please join to find more. Connect with Sohail Hasnie: Facebook @sohailhasnie X (Twitter) @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie YouTube @energypreneurs Instagram @energypreneurs Tiktok @energypreneurs Spotify Video @energypreneurs

In this episode of Energypreneurs, our guest is Jaimes Kolantharaj, Principal Energy Specialist at the Asian Development Bank (ADB). Jaimes shares insights on renewable energy projects in South Asia, highlighting ADB's role in shifting investments from government funding to private sector-driven initiatives. He discusses solar and battery storage deployment in the Maldives, electric ferries for sustainable transport, and policy trends in India, Sri Lanka, Nepal, and Bhutan. The conversation also explores the impact of AI, digitalisation, and energy-efficient solutions, particularly in agriculture and electric mobility. Jaimes offers valuable advice to young entrepreneurs entering the renewable energy, emphasising the need for innovation and digital solutions in an evolving energy landscape.   Connect with Sohail Hasnie: Facebook @sohailhasnie X (Twitter) @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie YouTube @energypreneurs Instagram @energypreneurs Tiktok @energypreneurs Spotify Video @energypreneurs

Today's recipe is Cozy Country Gravy.Here are the links to some of the items I talked about in this episode: #adBéchamel SauceMedium Sauce PanFlat WhiskLiquid Measuring CupFine Mesh SieveLarge BowlAll New Chicken CookbookThis episode was also published in April, 2023.Here's the Recipe Of The Day page with all of our recipe links.If you want to make sure that you always find out what today's recipe is, do one or all of the following:Subscribe to the Podcast,Join the ROTD Facebook Group hereHave a great day! -Christine xo

AI is not just for tech experts—it's a powerful tool for every leader. In AI Unleashed, Reddy Mallidi shares a practical playbook for executives and managers to harness AI for efficiency, innovation, and ethical success. Discover how to turn AI into a business advantage.00:39- About Reddy MallidiReddy is an AI strategist and a Chief Operating Officer.He's the author of a book titled AI Unleashed: A Leader's Playbook to Master AI for Business Excellence.He was earlier with Intel, ADB, and Autodesk. 

In this episode, Alfredo Baño Leal, an energy expert with the Asian Development Bank (ADB), discusses Uzbekistan's evolving energy sector. The conversation highlights the country's transition from gas dependency to renewable energy, with recent policy reforms driving energy efficiency and reducing waste. With over 1-2 GW of rooftop solar already installed and a target of 40% renewable capacity by 2030, Uzbekistan is rapidly reshaping its power grid. Alfredo shares insights into the challenges of modernising the grid, the growing adoption of electric vehicles, and how distributed generation is becoming a cost-effective alternative for rural electrification. He also discusses Uzbekistan's push toward clean energy investments, including the development of local solar manufacturing and a new BYD electric vehicle assembly plant. The episode closes with a look at Uzbekistan's cultural richness, its emerging role as an energy leader in Central Asia, and why it's a fascinating place to visit. Connect with Sohail Hasnie: Facebook @sohailhasnie X (Twitter) @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie YouTube @energypreneurs Instagram @energypreneurs Tiktok @energypreneurs Spotify Video @energypreneurs

In this episode, Tor and Romain chat with Leland and Chuck from the Compose team about performance -- recent optimizations, upcoming optimizations, and challenges. Leland: @intelligibabble.bsky.social Chuck: @chuckjaz.bsky.social Tor: @tornorbye.bsky.social Romain: @romainguy, @romainguy.dev, romainguy@androiddev.social Catch videos on YouTube → https://goo.gle/adb-podcast   Subscribe to Android Developers  → https://goo.gle/AndroidDevs  #Featured #Compose #AndroidDevelopersBackstage   

In this episode, our guest is Sonia Chand Sandhu, with extensive experience in project development, and knowledge work on livable cities, environment, and climate adaptation. Sonia shares her journey in sustainable development, highlighting innovative environment management, urban planning, evaluation, and capacity-building approaches. She discusses the importance of knowledge management in development projects, the role of AI in evaluation, and how strategic investments in climate adaptation can shape future cities. All opinions and views expressed are solely her own and do not reflect those of her organization.   Connect with Sohail Hasnie: Facebook @sohailhasnie Twitter @shasnie LinkedIn @shasnie ADB Blog Sohail Hasnie

ท่องเที่ยว ส่งออก และ FDI ดันกัมพูชา GDP โตแรงแซงไทย คาดปีนี้โต 5.6% ด้าน ADB ประเมินไทย-เมียนมามีแนวโน้มเติบโตลดลงจากความไม่แน่นอนภายในประเทศและการเมือง รายละเอียดเป็นอย่างไร เจาะสายสัมพันธ์ โดนัลด์ ทรัมป์ เอื้อประโยชน์อาณาจักรธุรกิจ อีลอน มัสก์ แค่ไหน พูดคุยกับ รศ. ดร.สมชาย ภคภาสน์วิวัฒน์ นักวิชาการอิสระด้านเศรษฐศาสตร์และการเมือง

Over the last decade, we have been getting news updates, social media highlights, and WhatsApp forwards about India being the “fastest growing economy” in the world. IMF, World Bank, and ADB have confirmed this. The question is, in the face of demonetisation, GST, and the drastic shift of focus to the organised sector from the unorganised one, is this data a true reflection of India's economic reality?  Today, Neon talks about these facts with Professor Arun Kumar, a renowned author of economic titles and an Economic Professor at JNU.Watch the episode to know more!Timestamps0:00 - Introduction0:14 - Introducing Economist Arun Kumar0:40 - Current scenario of India's Economy1:25 - South East Asian countries' growth from 1947 as compared to India?3:31 - Proof of India's failure in education system 5:20 - How can India develop education & health?8:48 - Does India really have “TOO MANY” billionaires & why is it a concern?  9:24 - The journey from becoming a “developing” nation to a “developed nation.”10:51 - The “Bottom-Up Approach” - What's that? 14:00 - Growing chasm between high-earning & low-earning category?15:22 - Is the current budget failing to fund labour-intensive sectors?17:03 - What's the unorganised sector in India?17:47 - What are the Micro, Small & Medium Sectors in India?18:33 - Robot uprising vs human employment! 21:03 - What are the 4 types of unemployment in India?23:27 - 60k jobs and 47 lakhs applicants ?27:20 - Is GDP a proxy of the organised sector for the unorganised sector?30:03 - Demonetisations hits the unorganised sector32:12 - Is IMF, World Bank & ADB's version of India's fastest economic growth true?34:25 - Black economy = Digging holes & filing holes40:40 - India should have been 8X its current economy - how & why did we fail?42:31 - Are we really a 3.6 trillion dollar economy?51:11 - How can we help the unorganised sector generate more income? 1:01:48 - Bottom economy = 40% of the Goverment's vote bank & yet not the focus of development & growth? Why?1:05:26 - Why does the government want to help the organised sector?1:11:38 - How will India transform into a “developed” nation or double the GDP per capita?___________________________________Hi, I am your host Siddhartha! I have been an entrepreneur from 2012-2017 building two products AddoDoc and Babygogo. After selling my company to SHEROES, I and my partner Nansi decided to start up again. But we felt unequipped in our skillset in 2018 to build a large company. We had known 0-1 journeys from our startups but lacked the experience of building 1-10 journeys. Hence was born The Neon Show (Earlier 100x Entrepreneur) to learn from founders and investors, the mindset to scale yourself and your company. This quest still keeps us excited even after 5 years and doing 200+ episodes. We welcome you to our journey to understand what goes behind building a super successful company. Every episode is done with a very selfish motive, that I and Nansi should come out as a better entrepreneur and professional after absorbing the learnings. __________________________________Visit our Website: https://neon.fund/Follow us on Instagram: https://www.instagram.com/theneonshoww/Follow us on Twitter: https://twitter.com/TheNeonShowwFollow us on LinkedIn: https://www.linkedin.com/company/beneon/__________________________________Sponsor Shout OutLooking to build a differentiated tech startup with a 10X better solution? Prime is the high conviction, high support investor you need. With its fourth fund of $120M, Prime actively works with star teams to accelerate building great companies.To know more, visit https://primevp.in/