Podcasts about seizure

Here are the news stories we covered in thi weeks show: Macky: Border Force secures its largest ever cannabis seizure - GOV.UK  Smee: Legalized Cannabis Does Not Increase Consumption - Neuroscience News  Dr.Margaret:  Scientists found a cannabis compound that relieves pain without the high | ScienceDaily  John: Supreme Court rules government can't restrict gun rights for casual drug use This week we discuss the UK's largest-ever cannabis seizure, examining what it means for enforcement efforts and whether major busts like this have any lasting impact on the cannabis market. We also look at new research suggesting that cannabis legalisation does not lead to increased consumption rates, adding another piece of evidence to an increasingly debated topic. Dr. Margaret brings exciting medical news as researchers identify a cannabis-derived compound that may provide pain relief without the intoxicating effects typically associated with THC, potentially opening the door to new treatment options. Meanwhile, John covers a significant Supreme Court ruling in the United States involving constitutional rights, drug use, and the limits of government restrictions. Another packed episode featuring cannabis science, policy, law, and the stories making headlines around the world.

Welcome to the Tapt News podcast. A snapshot of the latest stories, including: ** The largest cocaine seizure in Australia ** Auction data triggers fresh tax criticism ** And One Nation leader granted security wish The biggest news stories delivered three times a day with reports from across Australia and overseas. Subscribe now to make it part of your daily news diet.See omnystudio.com/listener for privacy information.

I break down the Treasury's claim that it seized $1B of Iran's "crypto" and explain why this was actually Tether, not Bitcoin – and why that distinction matters. I digs into how stablecoins, ETFs, and exchanges recreate the same centralized, confiscable banking system, contrasted with true Bitcoin self-custody. When you consider Iran, Russia, and Afghanistan as case studies, it is clear that every other reserve asset becomes politicized. The writing is on the wall for centralised finance, and the world will be forced onto Bitcoin because it is the only neutral money that simply keeps working. Affiliate Links Become sovereign, hold your keys, be censorship resistant with the Bitbox hardware wallet. Get 5% off everything in the store with code GUY (Link: https://bitbox.swiss/) Get 10% off the best Bitcoin board game in the world, HODLUP! Or any of the other great games from The Free Market Kids! Use code GUY10 at checkout for 10% off your cart! (Link: https://www.freemarketkids.com/collections/games-1) Host Links ⁠Guy on Nostr ⁠(Link: http://tinyurl.com/2xc96ney) ⁠Guy on X ⁠(Link: https://twitter.com/theguyswann) Guy on Instagram (Link: https://www.instagram.com/theguyswann) Guy on TikTok (Link: https://www.tiktok.com/@theguyswann) Guy on YouTube (Link: https://www.youtube.com/@theguyswann) ⁠Bitcoin Audible on X⁠ (Link: https://twitter.com/BitcoinAudible) The Guy Swann Network Broadcast Room on Keet (Link: https://tinyurl.com/3na6v839)

Gregory Copley addresses the crisis in the UK Ministry of Defense, marked by high-level resignations and budget cuts. He describes the Royal Marines' seizure of a Russian "shadow fleet" tanker and a Russian warship firing warning shots at a yacht. Copley argues years of neglect have degraded British naval power. (9)

On this month's Film Seizure: Now Playing, the guys talk a lot of the most recent flicks that are getting a lot of attention lately, including Backrooms, Obsession, Masters of the Universe, and The Mandalorian and Grogu. Episodes release on Wednesday at www.filmseizure.com "Beyond My Years" by Matt LaBarber LaBarber The Album Available at https://mattlabarber.bandcamp.com/album/labarber-the-album Copyright 2020 Like what we do? Buy us a coffee! www.ko-fi.com/filmseizure Follow us on Facebook: www.facebook.com/filmseizure/ Follow us on BlueSky: https://bsky.app/profile/filmseizure.bsky.social Follow us on Mastodon: https://universeodon.com/@filmseizure Follow us on Instagram: www.instagram.com/filmseizure/ You can now find us on YouTube as well! The Film Seizure Channel can be found here: https://www.youtube.com/c/FilmSeizure

Laura Clery built an empire being the funniest person on the internet — 26 million followers, three books, a character (Pamela Pupkin) people quote back to her in the street. What most of that audience never hears is the rest of it. Tyler sits down with Laura — both of them in recovery — for the unfiltered version: getting sober at 25, a marriage that started in the rooms and turned into an FBI-involved thriller (the subject of her new book), raising a brilliant autistic son as a single mom, and the 600-pound refrigerator that nearly killed her two weeks before this taping. In this episode: Why coffee is 'the one drug I have left' — and what 14 years sober actually looks like From Downers Grove to LA at 17: the flea-bitten couch, the Spanish cell-phone commercial, and the first viral video everyone stole Building 26 million followers (and buying two houses) on Facebook before anyone thought it could pay Meeting her husband 59 days sober — and the day a text from a contact named 'Absolutely No Way' blew the marriage open The relapse, the rehab, the second chance — and the second relapse that ended everything The account-hack, the restraining order, and the 'thriller' her publisher couldn't believe was real Single-parenting a level-3 autistic son who 'elopes' — air tags, triple locks, and Augie Health The night a 600-pound fridge pinned her with her kids home — and the 911 call that almost got hung up on How she actually got sober: 90 meetings in 90 days, a sponsor, and a prayer she still says The 3 signs you might have a problem (and the one that involves Tijuana) Guest: Laura Clery — comedian, content creator, and New York Times bestselling author. Her third book, What Doesn't Kill You Makes You Hotter, is out July 14. Follow @lauraclery Host: Tyler Ramsey — Punk Rock Sober. 0:00 — The Queen of the Internet Walks In 1:24 — “Coffee's the One Drug I Have Left” 2:37 — The Book That Reads Like a Thriller 4:43 — The Worst Drug of Choice (and a Chaotic House) 9:57 — “I Wrote to Lorne Michaels When I Was 11” 12:01 — Broke in Westwood: The Flea Couch and the First Yes 14:06 — The Viral Video Everyone Stole But Her 17:12 — Atheist to “I Believe in a Higher Power” 21:17 — “He Might Never Speak”: A Diagnosis at Two 24:51 — “I Didn't Have a Plan B. Either It Works or I Die.” 25:42 — Meeting Stephen 59 Days Sober 28:48 — Tijuana With a Random Irish Guy 30:51 — “You Look Like ----. You're One of Us.” 31:56 — Love or Fear: A Course in Miracles 37:13 — Single Mom, Autism, and a Son Who “Elopes” 40:01 — Air Tags, Triple Locks, and Augie Health 49:43 — The Text From “Absolutely No Way” 51:51 — Driving to Malibu to Catch Him 55:58 — The Seizure, the Rehab, the Second Chance 57:23 — The Relapse That Ended Everything 59:04 — The Cult That Called Her Satan 1:00:13 — Why She'll Never Marry Again 1:05:32 — A 600-Pound Fridge and Ten Minutes to Live 1:08:37 — “If You Don't Calm Down, I'll Hang Up” 1:10:24 — Teaching a 5-Year-Old to Unlock the Door 1:11:15 — “You're Made of Steel”: The Trauma Center 1:16:13 — Tyler's Relapse on the Way to Africa 1:17:56 — Three Things to Do If You Want Help 1:19:09 — Three Signs You Might Have a Problem If you or someone you know is struggling with substance use, the SAMHSA National Helpline is free, confidential, and 24/7: 1-800-662-4357. In a crisis, call or text 988. #PunkRockSober #LauraClery #Sobriety #Recovery #Addiction #Comedy #ContentCreator #AutismParent #Resilience #WhatDoesntKillYou

Richard Epstein critiques the construction of the Obama Center in Chicago, lamenting the destruction of 800 historical trees and the seizure of public land. He describes the project's design as a "monstrosity" with a flawed traffic plan and expresses concern over the foundation's lack of financial transparency and endowment. (4)1904 BAGHDAD

Gregg Carlstrom, Middle East Correspondent for The Economist

Exclusion of evidence and habeas corpus? Who needs us? It's a Dallin Oaks episode and we go over two law review articles (pub. 1966 & 70) he wrote focusing on the rights of criminals. How we handle evidence consistent with the constitution is a complicated issue and Hoaks has a hot take. Plus, he thinks habeas corpus has gotten a bit out of hand with how many death row convicts it was helping. Then we dive through 2 more chapters from Pure in Heart about Spirituality and Worship. The hot takes here are akin to moldy soup in the back of the fridge. We round out with happy civil engineering news from California!   Show Notes:  Studying the Exclusionary Rule in Search and Seizure https://chicagounbound.uchicago.edu/cgi/viewcontent.cgi?article=3650&context=uclrev Search and Seizure laws and SCOTUS rulings https://www.uscourts.gov/about-federal-courts/educational-resources/about-educational-outreach/activity-resources/what-does-fourth-amendment-mean https://www.justia.com/criminal/procedure/search-and-seizure-rules/ https://constitution.congress.gov/browse/essay/amdt4-7-1/ALDE_00000805/ Legal History in the High Court–Habeas Corpus (1966) https://repository.law.umich.edu/cgi/viewcontent.cgi?article=5483&context=mlr Bushel's Case https://en.wikipedia.org/wiki/Bushel%27s_Case   Sword of Laman: Pure In Heart, by Dallin H. Oaks    Happy News: https://www.goodgoodgood.co/articles/california-wildlife-crossing-biggest-annenberg    Email: glassboxpodcast@gmail.com  Patreon: https://www.patreon.com/GlassBoxPod  Patreon page for documentary: https://www.patreon.com/SeerStonedProductions BlueSky: @glassboxpodcast.bsky.social  Other BlueSky: @bryceblankenagel.bsky.social and @shannongrover.bsky.social  Instagram: https://www.instagram.com/glassboxpodcast/  Merch store: https://www.redbubble.com/people/exmoapparel/shop Or find the merch store by clicking on "Store" here: https://glassboxpodcast.com/index.html One time Paypal donation: bryceblankenagel@gmail.com  Venmo: @Shannon-Grover-10  

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

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Last time we spoke about the first phase of the One Hundred Regiment Offensive. On 20 August 1940, forces launched the Zhengtai Campaign, part of the "Hundred Regiments Offensive," aiming to disrupt Japan's transport network and thus weaken its "cage-and-strongpoint" defense. Orders from the Eighth Route Army split tasks: the Jin-Cha-Ji Military Region attacked the eastern Zheng–Tai line, the 129th Division struck the western section , and the 120th Division hit the Tongpu Railway and the Fen–Li Highway. Success was to be judged by the damage inflicted on the Zheng–Tai line. Preparations were conducted under strict secrecy: reconnaissance teams mapped Japanese strongholds with help from villagers; communities stockpiled grain, ammunition, and tools, and trained for demolition, including heating and bending rails. At night, units infiltrated stations and villages, seized positions, and destroyed bridges, power lines, roads, and mines across multiple columns; rain slowed movement and shaped the fighting. By early September, the Zheng–Tai line and related transport routes were severed, isolating strongpoints and hindering reinforcement.    #203 The One Hundred Regiment Offensive Phase Two Welcome to the Fall and Rise of China Podcast, I am your dutiful host Craig Watson. But, before we start I want to also remind you this podcast is only made possible through the efforts of Kings and Generals over at Youtube. Perhaps you want to learn more about the history of Asia? Kings and Generals have an assortment of episodes on history of asia and much more  so go give them a look over on Youtube. So please subscribe to Kings and Generals over at Youtube and to continue helping us produce this content please check out www.patreon.com/kingsandgenerals. If you are still hungry for some more history related content, over on my channel, the Pacific War Channel where I cover the history of China and Japan from the 19th century until the end of the Pacific War. During the second phase, the Hundred Regiments Offensive stopped being a single burst of action and became a sustained attempt to keep the Japanese occupation system off-balance. More regiments entered the fighting until, by the scale of commitment on the map, 104 regiments were involved. This matters because it changes what the campaign was: not merely a set of raids, but an effort to broaden pressure so that the enemy could not concentrate everything in one place at one time. Years later, Peng Dehuai—the commander closely associated with the Hundred Regiments offensive—described how the entry of these units felt as "spontaneous." That word can sound mysterious, so it helps to interpret it in operational terms. "Spontaneous" here does not mean unplanned chaos; it means that once the offensive logic took hold—once units saw that Japanese movement and control were being disrupted—local commanders and regiments felt empowered to join the fight without always waiting for the Eighth Route Army headquarters to issue fresh, detailed instructions for each smaller step. In other words, the campaign became something like an expanding network: local success and shared strategic perception fed into more participation across regions. Strategically, the campaign was guided by political and military guidance issued on September 10, 1940 by the Central Committee of the Chinese Communist Party. That instruction tied current operations to the earlier political-military framework of the July 7 Declaration and the July 7 Decision. The instruction argued that the moment mattered: it called for focusing "main efforts" on striking the Japanese army during a period when unity was being strengthened. It specifically urged that, based on the experience of the North China Hundred Regiments Offensive, Communist forces should organize one or more planned large-scale offensive operations in Shandong and Central China. In North China, the instruction pushed for expansion into Japanese army areas that had not yet been attacked—because the battlefield effect of the campaign was not only measured in immediate battlefield outcomes, but in reducing enemy-occupied space, enlarging base areas, breaking through blockade lines, and improving combat effectiveness. That last phrase—"Striking the enemy and attacking our allies is the general policy of military operations at present"—was the harsh shorthand for the operational reality: the campaign had to prevent Japanese occupation from appearing stable and manageable. If the occupation system could treat insurgency as "localized trouble," it would recover quickly. If, instead, occupation became dangerous in multiple places at once—requiring constant defense, constant movement, constant reinforcement—then the Japanese would be forced into a defensive posture that undermined their ability to exploit control. On September 16, 1940, the headquarters issued the second phase plan with a clear aim: expand results from the first phase. The headquarters explained the second phase would continue with an emphasis on disrupting Japanese transportation and destroying some strongholds that had penetrated deep into the base areas. This reveals the campaign's real "background and stakes": the offensive wasn't built around capturing territory in the traditional sense alone. It was built around breaking the system that makes occupation work. In the enemy's logic, occupation relies on movement: soldiers need to move, supplies need to be shipped, and reinforcement must be routed quickly to where trouble appears. Transportation infrastructure—roads, railways, bridges, power lines—forms the skeleton of control. Strongholds and outposts are the organs that occupy space, but they depend on that skeleton. If transportation becomes unreliable, strongholds become isolated islands. If strongholds become isolated, the Japanese must decide between (1) defending each island and spreading themselves thin, or (2) leaving some islands to contain the rest—either way, control weakens. Strongpoints—whether forts, fortified villages, gatehouses, or road blocks—also function as a "cage-and-silkworm" system: they are placed so Japanese forces can consolidate inside them, while routes outside are controlled or denied. In that model, even a small disruption can trigger a major ripple effect. When highways or key segments of rail are repeatedly broken, Japanese units cannot move "cleanly." They must detour, slow down, repair under threat, or escort repairs with larger forces than they prefer. Every extra hour spent repairing is an hour not spent consolidating. Every detour is a chance for ambush or for further sabotage. The second phase sought to exploit that dependency deliberately. That strategic framing explains why, even as the campaign broadened, different regions emphasized different battles. The Jin-Cha-Ji Military Region mainly fought the Lai-Ling Campaign, the 129th Division mainly fought the Yu-Liao Campaign, and the 120th Division focused on attacking the Tong-Pu Railway. They were not separate stories. They were different methods of attacking the same underlying vulnerability: the occupier's ability to move, reinforce, and coordinate. In Jin-Cha-Ji's sector, the stakes were especially sharp around Laiyuan and Lingqiu. The Japanese forces stationed in Mongolia had occupied those areas and penetrated deeply into the northwestern parts of the Jin-Cha-Ji Border Region. Japanese strength around these positions included elements of the 2nd Independent Mixed Brigade and the 26th Division, totaling more than 1,500 men, plus more than 1,000 puppet troops. The presence of puppet forces mattered not only for manpower, but because puppet troops supported the occupier's local control apparatus: they served as locally sourced enforcers, scouts, guards, and "administration-adjacent" security. Removing or weakening them was part of disrupting occupation credibility and local stability. Because the Japanese had been attacked in the first phase, they did not respond by retreating into passivity. They increased troops at each stronghold. Laiyuan City alone was reinforced to around 500 men, and the Japanese strengthened fortifications and stockpiled food and ammunition. This meant the defenders were preparing for a second round: not a sudden surprise raid, but a sustained threat that would test their ability to endure isolation and keep their network intact. Under these conditions, the Jin-Cha-Ji leadership decided to mobilize forces for the Lai-Ling Campaign, beginning at 22:00 on September 22, 1940. Here the background and stakes show up in the campaign's timing and tactics. The objective was not to "beat the defenders in open battle" only; it was to attack in ways that would prevent consolidation. By pushing on county areas and surrounding strongholds immediately, the attackers aimed to force the defenders into reactive mode—closing gates, shifting forces into defensive positions, and preparing for fights that would consume time and ammunition. The right wing launched a fierce attack on Laiyuan County and surrounding strongholds. After a night of hard fighting, the east, west, and south gates were taken, and the Japanese troops retreated into the city. Taking gates matters because it compresses space. It turns a wider defensive perimeter into a narrower, more concentrated posture. It also creates a psychological and operational trap: defenders who retreat into the city may survive longer as a fortified concentration, but their ability to conduct aggressive movement outside their walls—and their ability to receive reinforcements through many approaches—becomes more limited. In the night of September 23, the 2nd Regiment, supported by a battalion of the 1st Regiment and artillery, attacked Sanjia Village, described as an important enemy stronghold on the Laiyuan–Yixian highway, roughly 10 kilometers east of Laiyuan City. Highways are not just routes; they are corridors that connect strongholds to each other and to supply lines. By capturing a stronghold on a highway, the campaign attempted to break a portion of the corridor network feeding the city. The attackers annihilated most of the enemy and captured the village. At the same time, the 3rd Regiment attacked Dongtuanbao, northeast of Laiyuan City, and by the night of September 24, they had taken surrounding fortifications and forced remaining enemies into only a few houses inside the village. Then, on September 25, the enemy burned weapons, supplies, and food stored at the stronghold, preparing for a breakout. That detail reveals a key stake of stronghold warfare: if defenders believe they cannot hold and cannot escape, they may destroy supplies rather than let attackers seize them intact. It's a grim tactical psychology—destroying stores can deny the enemy immediate benefit, even if it reduces defenders' chances of future endurance. When the attackers launched another fierce assault and the remaining defenders, with no hope of escape, threw themselves into the flames and perished, the event underscored the "closed-options" nature of the battle: the stronghold system was being compressed until breakout became impossible. On September 26, other right-wing units, together with the 9th Regiment of the Pingxi Military Sub-district, captured 13 strongholds including Taohuabao, Bailebao, Jijiazhuang, Xinzhuang, Beikou, Xiabeitou, Baishikou, Zhongzhuang, Wangxidong, Liujiazui, Zhangjiayu, Beishifo, and Jinjiajing. Capturing strongholds in clusters has a strategic function. It doesn't just remove personnel; it interrupts local control geography. It makes it harder for defenders inside the city to extend influence outward and harder for them to create new safe points for movement. But the Japanese did what well-prepared occupiers can do: reinforce at the most important time and the most important place. On the second day after the start, Japanese reinforcement began from Zhangjiakou and other locations. Roads had not been completely destroyed, so the Japanese could advance rapidly. This becomes a major background lesson of the second phase. The first phase had demonstrated the power of sabotage to disrupt Japanese movement. But by the time second-phase campaigns began, the Japanese were not ignorant—they were learning. Where sabotage had fully severed roads, reinforcement could be delayed or routed into danger. Where sabotage remained incomplete, reinforcement could arrive quickly, changing the battle's character from attack-dominant to defense-dominant. By noon on September 28, over 3,000 Japanese and puppet troops arrived in Laiyuan City by car, supported by 20 tanks and 4 aircraft. This mechanized support was not just "extra firepower." It was a statement about how the Japanese aimed to retain control: tanks and aircraft increase defenders' ability to resist assault and keep morale from collapsing. Under these conditions, the right wing found it difficult to launch a favorable offensive. So the Jin-Cha-Ji leadership shifted offensive focus to the Lingqiu area, rather than forcing the original plan to continue against reinforced mechanized defense. The first step was to eliminate enemy strongholds between Lingqiu and Hunyuan. The second step was to seize enemy strongholds along a line from southeast of Daying to Shentangbao, and in mountainous areas north of Daying and Shahe. This shift highlights a core strategic principle: when a target becomes too fortified, the offensive can still succeed by moving the pressure elsewhere—aiming to break the enemy's network of strongpoints and keep forcing them to respond across space. On October 2, the headquarters ordered the main force of the right wing to concentrate in the area east and southeast of Laiyuan. Part of the force was assigned to monitor and contain the enemy in Laiyuan, while the 1st and 2nd Regiments were placed under the left wing's command and joined the left wing in combat. This reallocation reflects operational adaptability. If a city becomes a fortress, smaller units may be better employed as containment—tying down defenders—while the main effort moves to seize other stronghold lines where the Japanese might still be vulnerable. The fighting continued with tactical attacks that show how strongpoint warfare unfolded in the field. On the night of October 8, the 1st Battalion of the 1st Regiment launched an attack on the 2nd Regiment while a portion of the Japanese army in Nanpotou was attacking it. The attackers broke into enemy lines, annihilated most of the enemy, and drove the rest off. At the same time, the 1st Battalion of the 6th Regiment captured Qiangfengling, and the Japanese forces in Qingciyao fled in panic. The campaign also included actions such as attacks on Jinfengdian by the 3rd Battalion of the 6th Regiment on the night of September 9, and mention that the 26th Regiment entered Huangtai Temple on the night of October 8 while attacking between Lingqiu and Guangling. By understanding the background and stakes, you can see what these actions were really doing. They weren't random. They were repeated attempts to keep dismantling the enemy's ability to maintain a functioning strongpoint chain. Each captured stronghold reduces the enemy's ability to create secure corridors. Each panic-driven retreat increases their time burden and may cause breakdown in communication between local nodes. Even when the battle remains fierce and deadly, these changes in tempo can accumulate into operational outcomes. The Lai-Ling Campaign lasted 18 days, producing concrete results: killing and wounding over 1,000 Japanese and puppet troops, capturing 49 Japanese and 237 puppet troops, and leaving 1,419 casualties for the Eighth Route Army. The losses show the campaign was not a "clean victory." It was expensive. But the operational logic—disrupting a strengthened occupation zone, capturing strongholds, and forcing enemy reinforcements to concentrate—was consistent with the second phase's broader mission. Support for Lai-Ling came from the Jizhong Military Region through the Renqiu–Hejian–Dacheng–Suning Campaign from October 1 to October 20, simultaneously sabotaging the Cangshi, Deshi, Beining, and Jinpu railways. This is where "background and stakes" become especially clear. The Japanese, even when they defend in one area, have to move elsewhere to respond. When you attack multiple transportation lines and strongpoint zones at once, you prevent the enemy from solving one problem cleanly before moving to the next. You make the enemy chase multiple fires. After the Hundred Regiments Offensive began, Japanese forces in Jizhong moved west to reinforce in some cases, but most were tied down on important transportation lines. That relative weakening meant defenses in Jizhong's interior became weaker—creating space where a larger contest could occur. Jizhong decided to deploy 10 battalions totaling more than 8,500 men from the 18th, 23rd, and 30th Regiments across left wing, center, and right wing roles, fighting in the area. The plan was not only to attack; it was to manipulate where the Japanese had to respond. The two wing units would contain and draw Japanese forces away from the central Renhe Dasu zone, and then the central unit would break into that central area to open the situation. In other words: wings would pull; center would punch. The Renhe Dasu battle began on October 1, 1940. On the left wing, the 18th Regiment entered an area east of the Zhulong River and west of Hejian and Renqiu, capturing Lianjiazhuang, Dongguxian, and Liangcun between October 2 and October 6. By the night of October 7, Japanese troops at strongholds including Yuhuangmiao, Fenglebao, and Liushansi fled in panic—another reminder that once stronghold cohesion fractures, the enemy's ability to endure a second phase of pressure drops. On the right wing, the 30th Regiment operated with four battalions east of Dacheng and east of the Ziya River, capturing a series of strongholds including Liminju, Dengzhuangzi, Shigeju, Xiliuzhuang, Zangzhuangzi, and Chencun, while engaging in road-breaking and ditch digging. These actions show the campaign's "method," not just its target. Even when the opponent could be fought directly, sabotage and engineering measures could amplify the damage by reducing mobility and forcing time-consuming repairs. The central unit, the 23rd Regiment, had two battalions crossing the Hutuo River northward. On October 1, it ambushed more than 100 Japanese troops coming from Shangjialin to seize grain, killing more than 90 and capturing all their weapons. On October 9, it ambushed the enemy from Liugezhuang to Litan at Baimatang, annihilating 20 Japanese and puppet troops. These ambushes illustrate a second background principle: occupiers need sustenance and extraction operations, and those operations follow routes and patterns. By striking troops during foraging or supply-related movement, the offensive attacks not only the army but also the logic that keeps occupation armies fed and maintained. From October 15 to October 20, the second stage of those operations targeted the east and west banks of the Ziya River, leaving only a small force in the central Renhe River Great Suppression area. On the night of October 19, the central force captured Banjiehe and destroyed a bridge over the nearby Guyang River. On the night of October 16, the left wing captured Daqudi and the Renqiu Shimen Bridge, and on October 18 it captured the stronghold at Wangpan. A note in the operational description also indicates that the right wing faced a serious enemy situation and could not take major action during one segment—another reminder that even a planned operation cannot control all battlefield variables. What matters is whether the operation still meets its strategic purpose, not whether every segment goes perfectly. In the Battle of Renhe Dasu, Japanese and puppet losses were heavy: 805 killed or wounded, and 3 Japanese and 326 puppet troops captured. The campaign took 29 strongholds. The Jizhong Military Region suffered 573 casualties. Strategically, this battle contained enemy forces and effectively supported the Battle of Lai-Ling. Again, support here is not just "help in the same region," but redistribution of pressure: by forcing the enemy to allocate troops to Jizhong, Japanese defenders around Lai-Ling face more difficulty maintaining overall operational coherence. While Jin-Cha-Ji and Jizhong fought around Laiyuan and Lingqiu, a deeper pressure developed in the Taihang base region—through the Yuliao (Yu-Liao) Campaign, fought mainly by the 129th Division. The background stakes in the Yu-Liao theater were the highway route from Yangquan through Pingding, Heshun, Liaoxian to Yushe, described as the deepest penetration route through which the Japanese penetrated the Taihang base area. The Japanese tried to extend this road southwestward and connect it with the Baijin Railway through Wuxiang, aiming to split the Dahang area and deploy forces flexibly along the Zhengtai and Baijin lines. This was about strategic mobility and operational geometry. A road connection isn't only "transport"; it reshapes where the enemy can exert pressure and how quickly they can shift forces from one axis to another. The Yuliao section measured 45 kilometers and included eight strongholds: Yushe, Yanbi, Wangjing, Guantou, Pushang, Xiaolingdi, Shixia, and Liaoxian. These were guarded by the 13th Battalion of the Japanese 4th Independent Mixed Brigade. A line of strongholds along a highway is the occupier's version of a corridor defense: it enables them to keep movement inside a protected chain. If that chain is cut, movement becomes vulnerable and the "deep penetration route" turns into a dangerous liability. On September 22, 1940, the 129th Division issued basic orders: launch a surprise attack to eliminate the enemy from Yushe to Xiaolingdi, recapture strongholds, destroy the highway, and then press forward toward Liaoxian to recapture it when the opportunity arose. This is a textbook example of how the offensive combined surprise, seizure, and destruction. Surprise prevents the defenders from organizing a coordinated response. Seizure eliminates their nodes. Highway destruction prevents them from restoring their corridor quickly, forcing time and labor—exactly what the second phase wanted. The assault began on the night of September 23. On September 24, the left wing captured Yanbi and Wangjing, while the right wing captured Pushang and Xiaolingdi. By September 25, Yushe and Jucheng had also fallen, leaving only the enemy at Guantou on the Xiaolingdi–Yushe line still resisting. Concurrently, detachments attacked on related axes: the Pingliao Detachment captured Hanwang Town north of Liaoxian; the Qinbei Detachment sabotaged roads and attacked frequently, pinning Japanese forces on the Wuxiang and Baijin routes. On September 26, the 129th Division ordered part of the right wing to continue besieging the enemy at Guantou, while the main force and the left wing moved east to recapture Liaoxian and eliminate reinforcements. At dawn on September 27, the right wing attacked Shixia west of Liaoxian and captured it that night. On September 28, the left wing reached near Majiu in preparation for an attack on Liaoxian that night. Then battlefield logic reasserted itself: the Japanese did not sit idle once their corridor was threatened. Troops from Heshun and Wuxiang reinforced Liaoxian and Guantou respectively. The Eighth Route Army headquarters ordered the Liaoxian attack halted. Some forces were to contain the enemy advancing south from Heshun, while the main force moved to the Hongyatou and Guandinao areas to prepare to annihilate enemy reinforcements arriving from Wuxiang. This decision reveals a deeper stake: even if an army can seize targets, it must avoid exhaustion and must avoid allowing the enemy to convert a partial tactical loss into a larger opportunity. Headquarters essentially chose the operation's "survival path": shift from capturing more nodes to annihilating the reinforcements that would otherwise restore the corridor. Following these orders, the 129th Division attacked Guantou and took it at 24:00 on September 29. In the narrative description that follows, the enemy reinforcements moving through ambush terrain clashed with Communist formations in an engagement where aircraft coverage and terrain allowed the enemy to seize high ground and resist stubbornly. The battle lasted two days and one night, with heavy casualties on both sides. That is an important background lesson: the offensive could still destroy corridor nodes, but the enemy's ability to bring aircraft support and seize terrain meant that the "destroy and move on" approach wasn't always enough. Sometimes, momentum had to be re-channeled into another kind of contest—one closer to a blocking ambush and a battle of endurance. By the evening of October 1, more than 500 Japanese troops from Liaoxian broke through the right wing's blockade and approached near the left wing's command post. The left wing was ordered to withdraw from the battle. Headquarters then assessed that Japanese troops from Liaoxian and Wuxiang had joined and that more than 1,000 Japanese troops from Yangquan had reached Hanwang Town north of Liaoxian. Combined with the 129th Division's exhaustion and heavy casualties, headquarters decided to end the Yulin–Liaoxian Campaign—not because the offensive had no value, but because the risk of allowing the enemy to "sweep" the Taibei area could outweigh further gains. This termination decision illustrates a stake that is often overlooked: in insurgency-style campaigns, operational survival is part of success. The second phase did not merely chase targets; it sought to transform conditions so that the enemy would have to spend strength defending a failing network. If continuing a battle risks letting the enemy regroup into a larger counter-offensive that clears base zones, then ending becomes strategic. While the 129th Division wrestled with corridor defense around Liaoxian and Guantou, the 120th Division pursued a transport-centered strategy against the Tong-Pu Railway—because rail disruption was not a supporting detail; it was a main axis of pressure. On September 12, 1940, the 120th Division issued an action plan for the northern section of the Tongpu Railway, deciding to attack the Ningwu and Xinxian sections (with emphasis on the section between Ningwu and Daniudian) starting September 20. This timing shows planning designed to synchronize with broader operational pressure. Rail sabotage required engineering preparation and coordination across units, and the campaign sought to create disruption when the enemy would be most vulnerable to delayed reinforcement. On September 14, the 358th Brigade left its base west of Loufan and crossed the Jingle–Lanxian Highway to the north. It assembled at Majiagou on the 16th, then launched an attack on Toumaying using its 3rd Detachment (comprising the 7th and 8th Regiments and the special service battalion). At 24:00 on September 18, that detachment attacked Touma Camp, while the 7th and 8th Regiments attacked reinforcements. Fighting continued until the following morning when more than 40 Japanese soldiers from Ninghuabao reinforced Touma Camp. Once reinforcements reached Shanzhai Village, they were surrounded and annihilated. On September 20, around 200 Japanese soldiers from Yangquanling went to Liyan Village to counterattack. The 716th Regiment attacked at 14:00, and by dawn the next day, the enemy fled back to Yangquanling. These battles are more than local clashes. They serve the background logic of sabotage campaigns: before destroying rail infrastructure, you need to reduce the enemy's ability to respond instantly. Fighting reinforcements and counterattacks clears windows of time. Those windows can then be used to sabotage tracks, bridges, and related installations. If sabotage occurs under active reinforcement pressure, the enemy can repair quickly or trap the sabotage teams. If sabotage occurs after the enemy's response capacity is disrupted, repair becomes slower and the operational effects last longer. Parallel operations reinforced this logic. On the night of September 16, the Independent 1st Brigade crossed the Fen River east. On September 18, it was learned that more than 400 Japanese troops had attacked the Yanbei Detachment at Yangquanling but returned to Shangzhuang after failing to find them. The brigade then chose to encircle and annihilate the enemy rather than chase endlessly. The attack began at 13:00 on September 18 and lasted until early morning on September 19. The main force withdrew to sabotage the railway, while the remaining enemy retreated to Yangquanling. The engagement inflicted 105 casualties on the Independent 1st Brigade, while killing or wounding about 200 Japanese. Once the blocking threat was removed, units quickly moved into sabotage actions on the Tongpu Railway. Then sabotage itself proceeded systematically. On the night of September 22, the 4th Regiment of the 358th Brigade—attached to the division's engineering company—and the division's special service regiment advanced to the area between Duanjialing and Xuangang to sabotage several sections of the Tongpu Railway. At the same time, the 2nd Regiment attacked Qicun, and the 715th Regiment attacked Xinkou and Loubanzhai. On the night of September 23, the 2nd Regiment sabotaged the railway south of Xinkou while the 715th Regiment sabotaged it north of Xinkou. On the night of September 25, the 715th Regiment sabotaged between Daniudian and Xuangang. The Independent 2nd Brigade also sabotaged several railway sections between Shuoxian and Ningwu. After six days of sabotage operations, the 120th Division again caused the Tongpu Railway to be interrupted. The background stakes here are straightforward but huge: a rail interruption forces the occupier into repair work, escorts, and re-routing. During the second phase—when the Japanese were already under pressure across multiple theaters—the need to continuously handle repair reduces the capacity for offensive operations and for rapid reinforcement to any single contested point. It also slows their ability to respond to new threats as quickly as they would like. By connecting all these threads—Laiyuan and Lingqiu strongholds, Renhe Dasu containment and roadbreaking, the Yuliao highway corridor fight, and repeated Tongpu railway sabotage—you can see the deeper logic of the second phase. The campaign aimed to create a battlefield environment where Japanese forces could not enjoy stable mobility and where strongpoints could not function as a reliable cage. Transportation disruption isolated strongholds. Stronghold destruction and capture shrank the enemy's local control points. Highway and rail sabotage forced the Japanese to defend not only troops and walls, but also the infrastructure that enabled their coordination. That's why the second phase emphasizes disrupting transportation and destroying some strongholds penetrated deep into base areas. It wasn't simply "hit more places." It was a deliberate attempt to force the Japanese to abandon their preferred operational pattern: a networked system of strongpoints supported by transportation reliability. If that reliability breaks down, the occupier's "cage" becomes porous and unstable, and Communist base areas gain room to expand and persist. By early October, the second phase was winding down, while a third phase was developing: reinforced Japanese columns sought to engage and destroy 8RA units. Over the next two months, several fierce counterattacks occurred, and after that the Hundred Regiments campaign was considered to be finished. I would like to take this time to remind you all that this podcast is only made possible through the efforts of Kings and Generals over at Youtube. Please go subscribe to Kings and Generals over at Youtube and to continue helping us produce this content please check out www.patreon.com/kingsandgenerals. If you are still hungry after that, give my personal channel a look over at The Pacific War Channel at Youtube, it would mean a lot to me. After earlier setbacks in the 1930s, the CCP sought national leadership in resistance while maintaining political room to maneuver within an uneasy arrangement with the KMT. By early 1940–1941, the strategy shifted toward "strongpoint" and transportation warfare: guerrilla actions were used to fracture Japanese defensive networks and sabotage logistics. Japanese attempts to consolidate territory, through local administration and security practices—often provoked the CCP's dual struggle, militarily and politically. As Japanese sweeps temporarily gave the CCP advantages, the situation forced rapid adaptation.

Send comments and feedbackNearly one-third of people with autism also have epilepsy. Researchers aren't sure why. For people on the spectrum, epilepsy can prompt unique challenges. Seizure symptoms can be misinterpreted as common autistic behaviors. Treatment may also be difficult due to the stress of a clinical setting, or the impact of anti-seizure medications on autism symptoms. Currently, some experts argue that there is a lack of research in assessing these care pathways.  To learn more about diagnosis and treatment for people with autism and epilepsy, Joy Mazur spoke to Dr. Colin Reilly and Dr. Stéphane Auvin.Related studies/links:Epilepsy in patients with autism: links, risks and treatment challenges Besag FMC, et al., 2017Neurobehavioral Comorbidities in Children with Active Epilepsy: A Population-Based Study Reilly C, et al., 2014Traditional and non-traditional treatments for autism spectrum disorder with seizures: an on-line survey Frye RE, et al., 2011Epilepsy and autism - National Autistic Society Sharp Waves episodes are meant for informational purposes only, and not as clinical or medical advice.Let us know how we're doing:  info@ilae.orgThe International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, Instagram, and LinkedIn.

Presented by Agri Financial: https://linkly.link/2iQk2Thanks for coming! Produced by Atlas AG Media Solutions:https://www.atlasmediagroup.usFollow Clayton:https://www.instagram.com/clayton.atlas/Find Neil on Instagram:https://www.instagram.com/neil_denton_farms/Subscribe to @Atlas-Agriculture

On this month's Film Seizure: Now Playing, Geoff and Jason have a full slate of movies to talk about from Mother Mary to Erupcja, Alpha to Dolly, and an excellent crime drama coming soon to a theater near you - Carolina Caroline. Plus, they catch up on some of what they watched at the 23rd Indy Film Fest! Episodes release on Wednesday at www.filmseizure.com "Beyond My Years" by Matt LaBarber LaBarber The Album Available at https://mattlabarber.bandcamp.com/album/labarber-the-album Copyright 2020 Like what we do? Buy us a coffee! www.ko-fi.com/filmseizure Follow us on Facebook: www.facebook.com/filmseizure/ Follow us on BlueSky: https://bsky.app/profile/filmseizure.bsky.social Follow us on Mastodon: https://universeodon.com/@filmseizure Follow us on Instagram: www.instagram.com/filmseizure/ You can now find us on YouTube as well! The Film Seizure Channel can be found here: https://www.youtube.com/c/FilmSeizure

Coast Guard Seizure Turns Into a Crime Scene | What Really Happened?  Good afternoon, everyone. Bill Cannon here from Police Off the Cuff. We're discussing a complex true crime story that has become a baffling mystery. This incident is a real crime that will be analyzed as a true crime show, focusing on the missing person mystery and the ongoing investigation to bring justice. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

Mexican authorities have arrested José Antonio Cortes Huerta, a leader of a cell linked to the Northeast Cartel, along with an associate, recovering significant quantities of narcotics, cash, firearms, vehicles, and seven live tigers. The operation highlights the ongoing activities of the Northeast Cartel, a violent organization operating near the U.S. border and designated as a foreign terrorist group. This episode examines the details of the seizure, the broader context of cartel operations, and the implications for regional security and law enforcement efforts.

Coast Guard Seizure: The Pattern Nobody Noticed On Monday, May 11th, Bill Cannon from Police Off the Cuff discusses the disappearance of Lynette Hooker, a compelling true crime stories. A significant development in this mystery involves the Coast Guard seizing the sailboat belonging to Brian and Lynette Hooker, as Brian's account of events is met with skepticism in the true crime community. This analysis delves into the unfolding crime case and the ongoing investigation Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

Amy MacIver is joined by violence monitor, Mary De Haas to discuss policing issues in South Africa. Presenter John Maytham is an actor and author-turned-talk radio veteran and seasoned journalist. His show serves a round-up of local and international news coupled with the latest in business, sport, traffic and weather. The host’s eclectic interests mean the program often surprises the audience with intriguing book reviews and inspiring interviews profiling artists. A daily highlight is Rapid Fire, just after 5:30pm. CapeTalk fans call in, to stump the presenter with their general knowledge questions. Another firm favourite is the humorous Thursday crossing with award-winning journalist Rebecca Davis, called “Plan B”. Thank you for listening to a podcast from Afternoon Drive with John Maytham Listen live on Primedia+ weekdays from 15:00 and 18:00 (SA Time) to Afternoon Drive with John Maytham broadcast on CapeTalk https://buff.ly/NnFM3Nk For more from the show go to https://buff.ly/BSFy4Cn or find all the catch-up podcasts here https://buff.ly/n8nWt4x Subscribe to the CapeTalk Daily and Weekly Newsletters https://buff.ly/sbvVZD5 Follow us on social media: CapeTalk on Facebook: https://www.facebook.com/CapeTalk CapeTalk on TikTok: https://www.tiktok.com/@capetalk CapeTalk on Instagram: https://www.instagram.com/ CapeTalk on X: https://x.com/CapeTalk CapeTalk on YouTube: https://www.youtube.com/@CapeTalk567 See omnystudio.com/listener for privacy information.

In this Episode, Drs, Hassinger, George and Stibley, discuss hot car fatalities, seizure safety, sun protection, and summer activities. Times: Hot Car Fatalaties: 2:17 Seizure Safety: 3:28 Summer Health and Safety: 5:22 Sun Protection: 7:34 Summer Activities: 10:11 Trivia: 14:51 Episode time: 17:18 This episode was recorded on July 16th, 2025

A drug enforcement team raids a Westland home and seizes fentanyl, crystal meth, a gun and cash. WWJ's Jackie Paige has your Friday morning news. (Photo Credit: Michigan State Police)

Patrick Bet-David and the panel react to a Seattle AI founder fleeing Washington's new millionaire and proposed wealth tax, warning that “tax the rich” really means tax everyone, predicting blue‑state exit taxes, and breaking down why today's intangible assets make capital flight unstoppable.

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A federal judge has ordered the Justice Department to explain why it seized election records from Fulton County, Georgia, the same jurisdiction that indicted Donald Trump in 2023. Subscribe to our newsletter to stay informed with the latest news from a leading Black-owned & controlled media company: https://aurn.com/newsletter Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

This week on Film Seizure: Now Playing, Geoff and Chuck discuss Ready or Not 2: Here I Come while Chuck tells us what Normal is, and Geoff tries to sort out The Drama about Lee Cronin's The Mummy while he and Adam Scott check into a mysterious Irish hotel in Hokum. Episodes release on Wednesday at www.filmseizure.com "Beyond My Years" by Matt LaBarber LaBarber The Album Available at https://mattlabarber.bandcamp.com/album/labarber-the-album Copyright 2020 Like what we do? Buy us a coffee! www.ko-fi.com/filmseizure Follow us on Facebook: www.facebook.com/filmseizure/ Follow us on BlueSky: https://bsky.app/profile/filmseizure.bsky.social Follow us on Mastodon: https://universeodon.com/@filmseizure Follow us on Instagram: www.instagram.com/filmseizure/ You can now find us on YouTube as well! The Film Seizure Channel can be found here: https://www.youtube.com/c/FilmSeizure

VLOG April 27 DDC beat: Awaiting US v Cole Allen, progress to unseal 3 seizure cases https://innercitypress.com/ddc122dunsealfaruquiszicp042526.html DC Hilton experience https://substack.com/home/post/p-195616244 Harvey Weinstein, Mann day. Tornado Cash Oct 26, UNSG race needs more candidates, Qs: https://innercitypress.com/unsg1candidatesquestionnaireicpfunca031726.html

In this episode of History 102, 'WhatIfAltHist' creator Rudyard Lynch and co-host Austin Padgett examine Prussia's evolution from a frontier marshland into a hyper-militarized powerhouse. Hosts analyze how capable Hohenzollern leadership and Bismarckian diplomacy unified Germany through structural discipline and strategic warfare. -- FOLLOW ON X: @whatifalthist (Rudyard) @LudwigNverMises (Austin) @TurpentineMedia -- TIMESTAMPS: (00:00:16) Intro (00:03:12) Leadership, Authoritarianism, and the Hohenzollern Dynasty (00:06:20) Bismarck's Aristocratic Monarchism and Social Concessions (00:10:14) 19th Century Ideologies: Hyper-Modernism vs. Postmodernism (00:18:16) Industrialization, Social Trust, and Comparisons to Japan (00:25:26) The Prussian School System and Training Interchangeable Cogs (00:30:12) German Colonization of Eastern Europe in the Middle Ages (00:33:43) The Settlement of Brandenburg and Ethnic Geopolitics (00:46:20) Declaring an Independent Kingdom at the Start of the 18th Century (00:51:45) The Teutonic Knights and the Formation of the Junkers (00:57:35) The 30 Years War and the Psychic Scar on Brandenburg (01:00:36) Frederick William I and the Foundation of Prussian Militarism (01:03:38) Frederick the Great, the Seizure of Silesia, and European Great Power Status (01:06:44) Tactical Innovations: Vertical Attacks, Light Artillery, and Iron Drill (01:21:46) The Seven Years War: A Campaign of Defensive Survival (01:30:46) The Relationship Between Frederick the Great and Voltaire (01:41:31) The Revolutionary Phase and Dismemberment of Poland-Lithuania (01:46:20) Napoleon, the Battle of Jena, and Total Social/Military Revolution (01:57:32) The Divergence of East and West Germany and the Congress of Vienna (02:12:11) Kaiser Wilhelm II's Diplomatic Errors and the Path to World War I (02:18:37) The Socialization of Prussian Norms and Mandatory Conscription (02:23:06) Learn more about your ad choices. Visit megaphone.fm/adchoices

Iran seizes two ships and fires on vessels in the Strait of Hormuz, the EU approves a €90 billion loan for Ukraine, Trump blocks dollar shipments to Iraq to curb Iran-backed militias, RFK Jr faces questions in the US Senate, Meta reportedly plans to track employees' keystrokes to train AI, Indonesia passes a law protecting domestic workers, the Southern Poverty Law Center is indicted on federal fraud charges in Alabama, Florida probes OpenAI over a shooting at Florida State University, Uber is found liable in a driver assault case in North Carolina, and a study finds that cocaine entering waterways affects the behavior of salmon. Sources: Verity.News

U.S. seizes Iran tanker before scheduled Rd. 2 of peace talks. Will Iran cancel the Pakistan meeting? Will the war resume Wednesday? Iranian analyst Kamran, and Israeli Analyst Margot join Tony.

Will the weekend showdown in the Strait of Hormuz collapse the US-Iran ceasefire?After Iran opened and then closed the Strait, attacked an Indian tanker and turned around ships, Donald Trump ordered the seizure of a sanctioned Iranian vessel that was attempting to pass through the US blockade. What followed was a new first for the war: shots fired at the Iranian container ship's engine and the whole vessel taken into custody. Retired Royal Navy commodore Steve Prest looks at how such seizures normally happen, the tricky question of what will happen to the vessel now and the long-term prospects of the Strait of Hormuz being reopened for global trade. Plus, with the deadline for ceasefire talks in Pakistan fast approaching, Venetia Rainey looks at the signs today that talks may go ahead on Tuesday despite Iranian denials. She also explains the latest updates from Lebanon, where Hezbollah killed two Israeli soldiers over the weekend. CONTRIBUTORS:Venetia Rainey, co-host @venetiaraineySteve Prest, ex-Royal Navy commodore @fightingsailorCONTENT REFERENCED:Akhtar Makoii: Hormuz chaos shows Iran is too fractured to speak with one voice‘Vacate your engine room': US Navy warns Iran ship before firingYou're firing, let me turn back: Panicked sailor pleads with Iranian attackersIsraeli soldier smashes Jesus statue in face with sledgehammerTimes of Israel: 26 years later, IDF restores its south Lebanon security zone — with key changesProducer: Peter ShevlinExecutive Producer: Louisa Wells► Sign up to our most popular newsletter, From the Editor. Look forward to receiving free-thinking comment and the day's biggest stories, every morning. telegraph.co.uk/fromtheeditor► EMAIL US: Contact the team on battlelines@telegraph.co.uk ► GET THE LATEST HEADLINES: Find all our latest Iran coverage here: https://www.telegraph.co.uk/iran-war/ Hosted on Acast. See acast.com/privacy for more information.

Iran talks collapse after U.S. ship seizure, Israel escalates in Lebanon, and U.S. gun violence exposes a system prioritizing force over life.Subscribe to our Newsletter:https://politicsdoneright.com/newsletterPurchase our Books: As I See It: https://amzn.to/3XpvW5o How To Make AmericaUtopia: https://amzn.to/3VKVFnG It's Worth It: https://amzn.to/3VFByXP Lose Weight And BeFit Now: https://amzn.to/3xiQK3K Tribulations of anAfro-Latino Caribbean man: https://amzn.to/4c09rbE

The U.S. seizes an Iranian ship in the Strait of Hormuz, a Louisiana mass shooting claims 8 children, Brazil's Lula and Spain's Sánchez lead a bilateral summit in Barcelona, the U.K.'s Peter Mandelson is reported to have failed the vetting process for his U.S. ambassador role, U.S. Congress approves a 10-day term extension of a surveillance law, the U.S. Commission of Fine Arts approves Trump's 250-foot Triumphal Arch, a fugitive Philippine lawmaker is arrested in Prague, Acting ICE Director Todd Lyons resigns, finance leaders warn of Anthropic's Mythos as U.K. banks prepare to use the AI tool, and a review concludes that anti-amyloid Alzheimer's drugs offer "trivial" benefits. Sources: Verity.News

This week on Film Seizure: Now Playing, Geoff flies solo, just like Ryan Gosling in Project Hail Mary or Evy caring for her mother alone in Undertone. Plus, he'll catch up on some other early-year movies he saw like Send Help, How to Make a Killing, and The Bride! Episodes release on Wednesday at www.filmseizure.com "Beyond My Years" by Matt LaBarber LaBarber The Album Available at https://mattlabarber.bandcamp.com/album/labarber-the-album Copyright 2020 Like what we do? Buy us a coffee! www.ko-fi.com/filmseizure Follow us on Facebook: www.facebook.com/filmseizure/ Follow us on BlueSky: https://bsky.app/profile/filmseizure.bsky.social Follow us on Mastodon: https://universeodon.com/@filmseizure Follow us on Instagram: www.instagram.com/filmseizure/ You can now find us on YouTube as well! The Film Seizure Channel can be found here: https://www.youtube.com/c/FilmSeizure

4. Guest Author: Eric J. Dolin. After their eventual rescue, Barnard regretfully leaves his dog, Scent, with a Britishcaptain for a better life. Returning to New York bankrupt, Barnard and the ship's owners successfully appeal the seizure of the *Nanina*. Barnard later published his memoirs in 1829, documenting his incredible ordeal. (4)1914 FALKLANDS

On the April 10th edition: A joint operation between the U.S.Marshals Service and Clayton County led to the seizure of illegal drugs and firearms, and more than 75 arrests; Current gas prices in Georgia are below the national average; And a new bill awaiting the Governor's signature will make it more difficult for homeowners' associations to foreclose on members' homes over financial disputes.

On the April 10th edition: A joint operation between the U.S.Marshals Service and Clayton County led to the seizure of illegal drugs and firearms, and more than 75 arrests; Current gas prices in Georgia are below the national average; And a new bill awaiting the Governor's signature will make it more difficult for homeowners' associations to foreclose on members' homes over financial disputes.

King Reveals Starseed Origins, Galactic Federation Missions & What's Really Happening Behind the VeilWatch Now:• What REALLY happens during a “spiritual upgrade” (it's not what you think)• The truth about astral travel—and why you may already be doing it• How to discover your Starseed origins and cosmic lineage• The hidden role of the Galactic Federation in humanity's awakening** More with Debbi King Cash and Debbi will be speaking at the New Living Expo in April. To get your tickets, join us and your spiritual, ET community, go to: https://newlivingexpo.com/ King Cash is here—and in this conversation, you're going to discover how astral travel really works, what happens during a spiritual “upgrade,” and why humanity is on the brink of a multidimensional awakening you can feel in your body right now. Stay with us—because before this episode ends, you'll understand how to recognize your own spiritual upgrades… and whether you're already in one. To learn more: ⁠https://planoly.store/kingcassius ⁠My gift to you, purchase any of the 17 media or shamanic-galactic programs for 20% off (now through May 1st): ⁠https://debbi-s-school.thinkific.com⁠/ Use Code: cruise (for 20% off all programs)

A CalMatters column says California’s governor race looks less like a sprint and more like a game of chicken. With a crowded field and no clear Democratic front‑runner pulling away, candidates are hesitating to go all‑in as the primary rapidly approaches. California media outlets are suing to unseal secret warrants used to seize more than 600,000 ballots in Riverside County. The case pits election transparency advocates against Sheriff Chad Bianco and raises new questions about law enforcement’s role in election disputes. Please Like, Comment and Follow 'Philip Teresi on KMJ' on all platforms: --- Philip Teresi on KMJ is available on the KMJNOW app, Apple Podcasts, Spotify, YouTube or wherever else you listen to podcasts. -- Philip Teresi on KMJ Weekdays 2-6 PM Pacific on News/Talk 580 AM & 105.9 FM KMJ | Website | Facebook | Instagram | X | Podcast | Amazon | - Everything KMJ KMJNOW App | Podcasts | Facebook | X | Instagram See omnystudio.com/listener for privacy information.

Silicon Bites Ep309 | 2026-03-30 | The alarm sounds from inside the community of regime loyalists – Russia's own z-patriots warn of a new 1917 revolution. This episode is based on Maxim Kalashnikov's Telegram warnings, February–March 2026. In February 1917, the Russian Empire collapsed from within — under the weight of a war that had gone on too long, demanded too much sacrifice, and offered no benefits in return – an economy that had cracked under the strain, and soldiers at the front who had simply stopped believing in the men who had sent them there. Women lined up for bread in Petrograd. Factory workers walked off their jobs. Soldiers — sent to fire on the crowds — refused. And in a matter of days, three centuries of Romanov rule was over.One hundred and nine years later, a man who has spent his career cheer-leading for Vladimir Putin, for the war in Ukraine, for Russian nationalism and imperial ambition, is invoking that exact moment. And he's not invoking it as a threat to the West. He's invoking it as a warning to Moscow and specifically, to Valdimir Putin. His name is Maxim Kalashnikov. And what he's saying from inside Russia's pro-war Z-blogger ecosystem should be required reading — and required listening — for everyone who wants to understand where this war is going.----------SUPPORT THE CHANNEL:https://www.buymeacoffee.com/siliconcurtainhttps://www.patreon.com/siliconcurtainhttps://www.gofundme.com/f/scaling-up-campaign-to-fight-authoritarian-disinformation----------SOURCES:@visionergeo / X (Twitter) — "If a Storm Lies Ahead..." — Kalashnikov Telegram post translated and published (2026)@visionergeo / X (Twitter) — Shakhty mine soldiers: "if Ukraine is not defeated by December, a wave will come from the front" — July 2025 Telegram postCharter'97 — "Z-Propagandist: US And Ukraine Have Trapped The Kremlin In A Trap" — February 22, 2026Charter'97 — "The Kremlin Is Preparing For A Social Explosion" — March 6, 2026Window on Eurasia — "Russia's Fate Being 'Decided by the Economy and Not with the Seizure of Some Village in Ukraine,' Kalashnikov Says" — February 2026@NatalkaKyiv / X (Twitter) — Kalashnikov February 17, 2026 post: "if the economy collapses, no shutdown of Telegram or communications will help. Both the 'elite' and the security structures will begin to fall apart."----------SILICON CURTAIN LIVE EVENTS - FUNDRAISER CAMPAIGN Events in 2025 - Advocacy for a Ukrainian victory with Silicon Curtainhttps://buymeacoffee.com/siliconcurtain/extrasOur events of the first half of the year in Lviv, Kyiv and Odesa were a huge success. Now we need to maintain this momentum, and change the tide towards a Ukrainian victory. The Silicon Curtain Roadshow is an ambitious campaign to run a minimum of 12 events in 2025, and potentially many more. Any support you can provide for the fundraising campaign would be gratefully appreciated. https://buymeacoffee.com/siliconcurtain/extrasWe need to scale up our support for Ukraine, and these events are designed to have a major impact. Your support in making it happen is greatly appreciated. All events will be recorded professionally and published for free on the Silicon Curtain channel. Where possible, we will also live-stream events.https://buymeacoffee.com/siliconcurtain/extras----------

Broadcast from KSQD, Santa Cruz on 3-26-2026: li> Dr. Dawn announces a UCSF study recruiting participants for psilocybin therapy to help patients cope with chronic low back pain, requiring ages 25-70 with failed prior treatments. A caller preparing for bladder stone surgery asks about avoiding a repeat of severe post-anesthesia disorientation. Dr. Dawn recommends pharmacogenomic testing through 3x4 Genetics to identify slow acetylator status and other detoxification enzyme variants that can guide anesthesiologists toward better drug choices. A clinical trial found that 24 minutes of music with binaural beats—where slightly offset audio in each ear generates synchronized brainwaves—significantly reduced anxiety in medicated patients. Dr. Dawn encourages trying this accessible, low-risk intervention. Chronic noise exposure triggers oxidative stress, inflammation, and endothelial dysfunction, increasing cardiovascular disease risk. Data centers and server farms are emerging noise pollution sources, and Dr. Dawn recommends affordable noise-canceling headphones as a health investment. A Crohn's patient in Switzerland reports alarming neurological symptoms including speech arrest with preserved awareness and transient visual disturbances. He is having trouble finding any Functional Medicine trained physician and Dr. Dawn recommends emailing to info@ifm.org. Furthermore, Dr. Dawn suspects possible seizure activity from brain inflammation and recommends pursuing a sleep-deprived EEG and MRI through a neurology referral. MIT researchers discovered Interlectin-2, a protein that both strengthens the mucus barrier by cross-linking mucins and directly traps and kills pathogens like Salmonella and Shigella. Imbalanced levels may contribute to inflammatory bowel disease. Synthetic versions may be an effective treatment for inflammatory bowel disease. A 33-year-old man survived 48 hours without lungs after flu-triggered bacterial pneumonia caused ARDS and multiple organ failure. Surgeons removed both lungs treat septic shock while ECMO (extracorporeal oxygenation)sustained him until a successful double lung transplant. A meta-analysis of 43 studies involving millions of births found no evidence that acetaminophen use during pregnancy increases autism, ADHD, or intellectual disability risk, contradicting recent political claims. Green tea contains about 30% more L-theanine than black tea, with studies showing 200mg daily improves verbal fluency, sleep quality, and reduces anxiety. Decaffeinated green tea retains full theanine content. Pop star Robbie Williams developed scurvy while on GLP-1 weight loss drugs, highlighting that only 2 of 40+ major GLP-1 trials assessed vitamin intake. Dr. Dawn urges anyone on these medications to take a comprehensive multivitamin.

Episode 5171: Judge Order On Fulton Ballot Seizure; AI Revolution In The Department Of War

Episode 5161: Georgia Meltdown Continues Over Seizure Of Fulton County Ballots

Last week, F.B.I. agents searched an election center in Fulton County, Ga., seizing truckloads of ballots from 2020. The move escalated the investigation into President Trump's claims of voter fraud in the state after his 2020 defeat in the state.It has since been learned that Tulsi Gabbard, the director of national intelligence, was present during the search.Devlin Barrett, a Times reporter who covers the F.B.I., discusses the presence of the nation's top intelligence official and the stunning phone call that shows how personally involved Mr. Trump has become in the investigation.Guest: Devlin Barrett, a New York Times reporter covering the Justice Department and the F.B.I.Background reading: Mr. Trump had an unusual call with F.B.I. agents after the election center search.The move to seize ballots has thrust the F.B.I. into Mr. Trump's election conspiracy claim.Photo: Nicole Craine for The New York TimesFor more information on today's episode, visit nytimes.com/thedaily. Transcripts of each episode will be made available by the next workday.  Subscribe today at nytimes.com/podcasts or on Apple Podcasts and Spotify. You can also subscribe via your favorite podcast app here https://www.nytimes.com/activate-access/audio?source=podcatcher. For more podcasts and narrated articles, download The New York Times app at nytimes.com/app. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

FBI Search of Fulton County, Georgia Election Office The FBI executed a court-authorized search warrant at the Fulton County Election Hub related to the 2020 presidential election. The action is evidence that past claims of election fraud—particularly those advanced by Donald Trump—are finally being taken seriously. Judicial approval of the warrant is proof of legitimacy. Seizure of ballots, computers, phones, and election records. Allegations that early votes were improperly certified without required signatures. The dismissal of the prior state-level prosecution against Trump in Georgia as vindication. Assertion of Broader Election Manipulation Concerns Foreign interference, specifically claiming that Mexican consulates worked to influence U.S. elections via immigration and cultural influence. These claims are tied to a book (The Invisible Coup) and used to argue that U.S. elections are structurally compromised. Trump’s Georgia Election Claims Trump’s assertion that he “won Georgia” is reinforced. The FBI investigation is a potential confirmation that the 2020 Georgia results were altered or fraudulent. Media skepticism of these claims is dishonest or politically motivated. Second Story: Death of Alex Pretty in Minnesota The media portrays Alex Pretti as an innocent victim of ICE violence. Newly surfaced video shows Pretti: Assaulting federal agents, Damaging government vehicles, Carrying a firearm during protests. Law Enforcement Justification Narrative Federal agents involved in the shooting were placed on administrative leave (presented as standard procedure). Pretti posed an ongoing threat and that agents acted in self-defense. Family and attorney statements with video evidence to accuse the media of intentional misinformation. Broader Media Critique Mainstream media is misleading the public, The political left is covering up violent behavior, Institutions are suppressing truth about election integrity and immigration enforcement. Please Hit Subscribe to this podcast Right Now. Also Please Subscribe to the The Ben Ferguson Show Podcast and Verdict with Ted Cruz Wherever You get You're Podcasts. And don't forget to follow the show on Social Media so you never miss a moment! Thanks for Listening X: https://x.com/benfergusonshowYouTube: https://www.youtube.com/@VerdictwithTedCruzSee omnystudio.com/listener for privacy information.