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#949 What if you could build digital real estate that pays you every month? In this special episode, we're sharing a fan-favorite interview from Nick Loper's The Side Hustle Show, featuring rank-and-rent expert Luke Van Der Veer. Luke breaks down how he builds simple local service websites, ranks them in Google, and rents them to business owners for recurring monthly income. He shares his process for choosing profitable niches, finding low-competition opportunities, generating leads, and scaling a portfolio that eventually grew into a six-figure-per-month business. Plus, stick around for an updated conversation where Luke reveals how his business has evolved, how AI is changing local SEO, and why he believes lead generation remains one of the most powerful online business models today! What Nick discusses with Luke: + Rank and rent business model + Local SEO fundamentals + Finding profitable niches + Blue-collar service opportunities + Keyword research strategies + Google Business Profile optimization + Lead generation websites + Finding contractor partners + Pricing monthly site rentals + Scaling digital real estate + Revenue-share partnerships + AI and local SEO trends Thank you, Nick and Luke! Check out The Side Hustle Show. Check out Luke Van Der Veer. To get access to our FREE Business Training course go to MillionaireUniversity.com/training. To get exclusive offers mentioned in this episode and to support the show, visit millionaireuniversity.com/sponsors. Learn more about your ad choices. Visit megaphone.fm/adchoices
This Morning's Headlines1. Lee in Italy2. NCG meeting3. Ballot probe4. Coupang fined5. Peace talks
This Morning's Headlines1. Korea-Belgium summit2. Korea-EU summit3. Ballot shortage4. Helping Korean firms5. New phase
Dr. Deb Muth 00:00:09 Hi there, how are you? Bob Miller 00:00:10 Excellent! Pedaling as fast as humanly possible, but doing okay. Dr. Deb Muth 00:00:14 Good, good. Well, I’m looking forward to our conversation today. This should be amazing. Bob Miller 00:00:20 Yeah, it should be a lot of fun. Dr. Deb Muth 00:00:22 Yeah, anything that’s off-limits for you in, our conversation? Bob Miller 00:00:28 No. Dr. Deb Muth 00:00:29 Okay, anything you want me to make sure we cover for you? Bob Miller 00:00:33 Well, I mean, is it okay if we put a little plug-in for our software? Dr. Deb Muth 00:00:35 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:38 Hey, can we… can we do a screen share? Yes, we can. Yeah, because I want to show you some maps, and… Dr. Deb Muth 00:00:43 Okay. Things like that, yeah, so… Perfect. So just let me know when you want to do screen share. Bob Miller 00:00:48 Okay. Dr. Deb Muth 00:00:49 And yeah, feel free to plug your software wherever you want to. Bob Miller 00:00:53 Okay, well, good. Let me pull up a, a slide for that, and give me one second, I just want to shut the door to my office to get the noise down. Dr. Deb Muth 00:01:01 No worries. Bob Miller 00:01:16 And, how should I refer to you? Dr. Debb? Dr. Muth, what do you like? Dr. Deb Muth 00:01:18 Dr. Deb is great, or Deb, either way, I’m pretty informal, so… Bob Miller 00:01:22 Yeah, and… Bob is fine for me. Okay. Yeah. Yeah, there you go. Why people feel like they need this, son. Special name, it’s like, seriously. Dr. Deb Muth 00:01:33 Right? I agree. Bob Miller 00:01:35 When I work with my clients, it’s like, Dr. Millison, just, just bop, just, just bop. Dr. Deb Muth 00:01:41 Yep, that’s how I am, too. Just call me Deb, it’s good. Dr. Deb Muth 00:01:44 They feel a little awkward with that, you know? They’re not used to that, but… Bob Miller 00:01:48 Alright. And you’re a naturopath, medical doctor. Dr. Deb Muth 00:01:52 A nastropathic doctor and a nurse practitioner. Oh, nice. Yeah, so I got the best of both worlds, right? Bob Miller 00:01:58 Yeah, damn. Okay. Alright, so here we go… There we go. Alright, so I got that ready, and then I will do a, I will do a screen share. I think you’re gonna really, appreciate what we’ve come up with. We’ve come up with the concept of, Cellular CPR. Dr. Deb Muth 00:02:23 Oh, nice! Bob Miller 00:02:24 And that is, construct the cell membrane, Protect the cell membrane. And restore it if it’s damaged. Dr. Deb Muth 00:02:32 Love that. Bob Miller 00:02:34 I love that. Yeah, so that’s what we’re focusing on, and then how, You know, we want to get to the point that, you know, most people think of genetics, they think of, like, 23andMe or Ancestry. Dr. Deb Muth 00:02:44 Yeah. Bob Miller 00:02:45 And then you have the professional geneticists who are looking at, you know, odd things that could create a disease. We’re looking at functional genomics. Dr. Deb Muth 00:02:54 Which is so much better. Bob Miller 00:02:56 Yeah. Are you familiar with what we do here, or… Dr. Deb Muth 00:02:58 A little bit, a little bit. So, it’ll be new to me, too, so I’m excited. Bob Miller 00:03:03 And how much time do we have? Dr. Deb Muth 00:03:04 We have an hour, give or take a little bit on either side. Do you have a hard stop anywhere? Bob Miller 00:03:10 No, no, I put a, I moved my clients around, and I don’t have anybody till, 3.30, so we’re good. Okay. Dr. Deb Muth 00:03:16 Perfect. Alright. Bob Miller 00:03:18 It’s like we’re getting started early as well, so… Dr. Deb Muth 00:03:19 Yeah, we’re getting started a little bit early, so that’s good. Bob Miller 00:03:22 Yeah, I just got my office cleaned up, so… Dr. Deb Muth 00:03:23 Okay, good. All right, are you all set to get started? Bob Miller 00:03:28 I’m good to go, my friend. Dr. Deb Muth 00:03:29 I’m gonna just record a little intro and a little bit of a, hook for people, and then we’ll get started. I’ll ask you to kind of tell us a little bit about yourself, and then we’ll just take this conversation wherever it’s supposed to go. Bob Miller 00:03:39 Okay, you got it. Dr. Deb Muth 00:03:40 Alright, sounds good. So what if the reason you’re not healing isn’t your diet, your supplements, or your labs, but it’s actually your genes? Dr. Bob Miller is uncovering how genetic variants, when combined with modern toxins, explain why some of us stay sick no matter what we try. Today, we’re talking genetic pathways, detox blocks, and the new science every wellness warrior needs to know. Welcome back to Let’s Talk Wellness Now, the show where we uncover the root causes of chronic illness, exploring cutting-edge regenerative medicine, and empower you to heal from the inside out. I’m Dr. Deb, your medical detective, and today, our guest, Dr. Bob Miller, is a true pioneer in functional genomics. He’s a board-certified traditional naturopath and the founder of Neutrogenetic Research Institute. And he’s the leading groundbreaking research on how genetic variants influence chronic illness, inflammation, and detoxification. His work has been recognized on international stages, uncovering links between genetic expression and conditions like Lyme disease, mast cell activation, or MCAS, and mitochondrial dysfunction. I’m so excited to talk to Dr. Bob today. He is gonna reveal some things that even I don’t know about, so I’m excited to learn alongside of you guys. So… Dr. Bob, let’s get started. Tell us a little bit about yourself, and kind of how you got on this journey. Bob Miller 00:05:04 Well, that’s, that’s interesting. I was sort of like a mid-career coming to the natural health field, because in my early 30s, I found myself with a severe case of ulcerative colitis. Bob Miller 00:05:15 And I was in the hospital for 21 days. probably within hours of death, pleading to death. And they told me I’ve got one option, and that is cut out the colon and wear a bag. Didn’t sound like a lot of fun. Dr. Deb Muth 00:05:27 Not an option I would want. Bob Miller 00:05:29 So, you know, the medical folks wasn’t real happy with me, but I said, yeah, I’d like to explore some alternative things.Never thinking that I’d get into this field, and then I just, you know, worked with some herbalists and things that I found absolutely fascinating. So, that’s how I got into this around 30 years ago. And, haven’t looked back since, and just having a… having a blast as we now move into how our genetics impacts things. So, that’s what we’re gonna… that’s what we’re gonna talk about today. Dr. Deb Muth 00:05:58 I’m excited to talk about this genetic thing. When you started over 30 years ago, what kind of patience and problems first inspired you to dig deeper into that root cause healing and kind of get into the genetic piece of it? Bob Miller 00:06:10 Sure. Well, you know, as a… now, I’m in a part of the country called Lancaster County, Pennsylvania, where there’s a lot of Amish and Mennonite, and they gravitate towards these things.So, this is their first thing to do, and that doesn’t work, then they’ll go other routes. So, you know, back then, we just saw typical, you know, a little tired, constipation. You know, a little bit of fatigue, arthritis, those kind of things. But things have changed dramatically over the years, as people are now getting more chronically sick. You know, it’s worse than it’s ever been. And what we’re finding is the, the culprits Primarily is mold exposure and Lyme disease. When people get those two together, they’re just… it’s an inflammatory cascade that nobody can seem to unravel. So that’s where we spend a lot of our time. And we’re also spending a lot of time looking at mental health, like ADD, ADHD. And, we give… this year I’ll be speaking at three autism conferences. And we can dig into that a little bit as to why we think we’re seeing such a dramatic increase. And aside from autism, that used to be 1 out of 1,000, now it’s 1 out of 33, or 23. You know, we’re also seeing dramatic increases in ADD, ADHD. People are stressed out. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. Dr. Deb Muth 00:07:37 This should be a fun visit. We can cover lots of topics. I am so excited. So, you founded Nutri Genetic Research Institute in 2015. What did you hope to accomplish, and what kind of surprised you in your findings so far about that? Bob Miller 00:07:51 Well, you know, let’s back up at what, you know, genetics is used for. Everybody’s familiar with 23andMe and Ancestry that, you know, tells you where your ancestors came from. Then you have your professional geneticists. I mean, these are people with a degree in genetics. And they’ll look for, you know, very odd sort of things that are prone to relate to a disease. So there are disease-related genetics. Well, in functional, we don’t look at either of those. We look at For example, how you’re breaking down your fats and utilizing them. How you’re recycling your glutathione. How you might be handling your iron. And none of those are disease-causing on their own.And none of those are disease-causing on their own. But when they pile up on you, and then combine that with environmental factors, that’s when things start to go south on us. So, that’s what we’re doing, we’re looking at patterns. And our first foray into this was, we did studies on Lyme disease. And our first foray into this was, we did studies on Lyme disease. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. Others have a little more struggle, and then others are struggling terribly for years. So there’s an old adage of genetics loads the gun, environment pulls the trigger. Dr. Deb Muth 00:09:14 Yeah, that is so true, and I think when we’re talking about Lyme and mold and things like that, we forget sometimes that our genetics can predispose us to be more sensitive to those things, and if we have genetic pathways where we don’t clear things properly, it’s harder for us to get them out of the body. And then you add on that whole rain barrel effect that we’ve always used as a functional medicine term, right? If the barrel’s half full, you’re okay. If it’s full, and now it’s spilling over, it’s a bigger problem. Have you guys found, too, that some of these environmental things actually are changing the genetics of people, or how they’re processing their own genetics? Bob Miller 00:09:53 Well, let’s go back to, Genetics 101. But we’ll go back a little bit further. So, what an interesting mechanism, what a miracle the body is. Bob Miller 00:10:03 Fats, carbohydrates, proteins, drink water, breathe air, expose the sunlight, and somehow everything gets made. I mean, when you just step back and think about that, it’s like, It’s pretty darn amazing. Dr. Deb Muth 00:10:15 I always tell women, you know, the fact that we get pregnant and we have healthy pregnancies and births is a miracle, because if we had to try to control that, that wouldn’t work so well. Bob Miller 00:10:25 Right. Well, that’s another miracle. These microscopic sperm and egg, human being, 9 months later, it’s like. But even inside of us. We are making our hair, our skin, our nails, our blood vessels, our ATP, our energy, it’s all being created. Well, that gets created by enzymes. So, enzymes take one substance, combine it with something else, and make something new. Then another enzyme comes along and does the same thing. Your DNA is the instructions on how to make the enzymes. So, when we are conceived. If it’s a, if it’s a female, of course, it’s the XX, the two chromosomes. You know, we’ve… everybody’s seen those… the genetics that… Listed pair. So, if it’s a female, the father donated the X enzyme. And the mother has no choice but to give the eggs, so that’s female. If the father donates the Y, you have a male that’s in chromosome number 1. Then 2 through 23 is the rest of the instructions on how to make enzymes. So, what can happen? We can get what are called SNPs, single nucleotide polymorphisms. And SNPs just mean that the instructions to make the enzyme’s not quite as good. So, if one parent gives a SNP on the making of an enzyme, The enzyme’s fine. It works. But, general rule of thumb, It may only work at 70-80% of efficiency. Now, a good analogy is think of an 8-cylinder and a 6-cylinder car. If parents give you good information, that’s like having an 8-cylinder car. If one parent gives you that snip, it’s like having a 6-cylinder car. Now, is a 6-cylinder car a fine car? Sure. It’ll get you from point A to point B, but it’s just going to have the power of an 8-cylinder. Then if both parents give you a SNP on the same enzyme, it may be 30-40%, and that’s like having a 4-cylinder car. Sits in the driveway, looks the same, puts gas in it, everything. But if you’ve got a 4-cylinder car. Probably not a good idea to go cross-country pulling a trailer behind you up and down mountains. Dr. Deb Muth 00:12:29 This is true. Bob Miller 00:12:32 So… We can get an 8-cylinder, 6-cylinder, or 4-cylinder enzyme. Now, if it’s not under a lot of stress, if that 4-cylinder car is just taking you to the bank and the grocery store. It’s just as good as an 8-cylinder car. But if you gotta pull that trailer, and there’s a lot of stress on it, being mountains, it’s gonna struggle. Now, there’s one other little caveat to this, and that is some genetic mutations are gain-of-function. They actually work faster. Now, we have enzymes that do all kinds of things. We have enzymes that make and recycle our antioxidants, but we also have enzymes that make inflammation. No, that’s a good thing, because if we get a virus or bacteria, if you didn’t make inflammation to kill it, well, we’d all die of infection. So, you know, we tend to think of free radicals as bad, antioxidants as good. They both play an important role. But interestingly, some of the major enzymes that make inflammation, they can be overactive. They can be turbocharged. And when they’re stimulated by environmental toxins, they overreact. Bob Miller 00:13:40 And therein lies the problem. When they overreact, we have a problem. Bob Miller 00:13:46 So, if we have genes that overreact when stimulated. And then the enzymes that take care of inflammation are underactive. Then you’re gonna be more inflamed. You know, the majority of people that, you know, come for functional medicine Or naturopathic help, or… Inflammation that they can’t seem to get under control. Dr. Deb Muth 00:14:06 Right. Bob Miller 00:14:07 And we will be, you know, during this hour, we’re going to look at some of the pathways that make that happen. So, what we can do then, we can’t change our genetics. When you’re conceived, that’s the hand you’re dealt. When your life would be over, if someone would take some tissue and measure, it’d be exactly the same as conception. Does it change. Bob Miller 00:14:28 The enzyme’s ability to do its job may be compromised. Because remember I said there’s a, the enzyme takes a cofactor. So an enzyme takes substance A, cofactor, make substance B. Well, if that cofactor’s not there, the enzyme’s not going to work either. So, you could have an 8-cylinder car, and if there’s no gas in it, it’s not going anywhere. So… It’s the strength of the enzyme, it’s the cofactor to do the A to B conversion. And that’s what we’re going to get into. So, many people say, well, where did these SNPs come from? Nobody knows for sure. Sometimes they’re what’s just called de novo, when the sperm and egg go together, the instructions get mixed up a little bit. We do believe a lot of it came from a long time ago, when we were almost wiped out by sexually transmitted diseases. And those STDs were altering the genes when the conception, in other words, when the sperm went into the egg, the STDs were interfering. And causing the problem, so… I often joke, if you want to blame somebody. Blame your great-great-great-great-great-great-great-grandparents for, being a bit promiscuous, so… Dr. Deb Muth 00:15:31 Yeah, for being… having a little too much fun, right? Bob Miller 00:15:35 So, we don’t know for sure, but, you know, there are some that, But most of the SNPs that we get inherit from our parents. So, if you look at a child. And you look at the SNPs. 99.9% of the time, it came from one of the parents. Dr. Deb Muth 00:15:50 In identical twins, do they have the exact same identical makeup? Bob Miller 00:15:54 Yep, Dr. Deb Muth 00:15:56 But not in fraternal twins, correct? Bob Miller 00:15:59 No, no, those could be different, Jeff. Dr. Deb Muth 00:16:00 It could be different because they have different sacs, they’re not sharing that same genetic makeup. Bob Miller 00:16:04 Yeah, so keep in mind, both your mother and your father have, you know, the two And so you get one from one parent, one from another. Dr. Deb Muth 00:16:13 So… Bob Miller 00:16:14 Interesting situation. I had, 3, 3 boys. And, we were looking at an enzyme related to breaking down oxalates. Now, the mother and father each had one SNP, and that’s called heterozygous. Three boys, and they all come together, they’re Amish boys, they’re a lot of fun. And I looked at their genomes, and the one boy didn’t have any SNPs at all. And one had won. And the other one had two. Dr. Deb Muth 00:16:41 Interesting. Bob Miller 00:16:42 So, we don’t quite know how these things get handed off, but with the parents each having one, you could have a child with none, one, or two. So, the one, his ability to break down oxalates, which is fine. The other one was slightly impaired, and the other one was dramatically impaired. So, you can have 3 children, and it all depends what the parents have. Now, if a parent has a homozygous, or 2 copies. And the other parent has nothing. Every child will have one. Okay. If both parents are homozygous, that they both have two, Every child will have two. Dr. Deb Muth 00:17:19 too. Bob Miller 00:17:20 Yes, so that’s the way it works, but, you know, but it’s somewhat rare that both parents are homozygous on an enzyme, but it can happen. Dr. Deb Muth 00:17:27 Do we think that infections today, like Lyme disease or mold exposure, things like that, if the parent, the woman, primarily, I’m thinking, is pregnant, and she actively has these infections. Can those infections affect the genetics, kind of like a past sexual transmission did where we thought back in the day? Bob Miller 00:17:47 Yeah, I… I mean, I’m not that much of a geneticist to answer that for sure, but my thought would be no, that at conception, the pattern’s made. Dr. Deb Muth 00:17:55 Okay. And then that’s… that’s the hand you’re dealt. Bob Miller 00:17:58 Yeah. So, I tell people we have good news and bad news. The good news is we can compensate for the weakness. The bad news is we can compensate for the weakness. Dr. Deb Muth 00:18:09 That is so very true. Bob Miller 00:18:11 Yeah, we can’t, because I often get asked, so we’ll do some things now, and we’ll check my genes again, and they’ll be better. It’s like, nope. Dr. Deb Muth 00:18:18 Oh, – – Bob Miller 00:18:19 You gotta play the hands you’re dealt, so… Dr. Deb Muth 00:18:21 That’s right. Bob Miller 00:18:22 You can test your genetics… if you’re looking at the same enzyme, you can test it every year. It’s not gonna change. It’s like the blueprint. Dr. Deb Muth 00:18:30 It’s good and bad, right? It’s the one test you only have to do once in your lifetime. Bob Miller 00:18:34 No, unless, you know, like, our. Dr. Deb Muth 00:18:36 All the time. Bob Miller 00:18:37 Yeah, now our test looks at, called the Functional Genomic Analysis Test of your genomic Resource. We look at 220,000 steps. Dr. Deb Muth 00:18:46 Wow, that’s a lot. Bob Miller 00:18:47 That’s not all of them. Dr. Deb Muth 00:18:49 Right. Bob Miller 00:18:50 So, maybe in the next year, we’re gonna come out with our third version of the chip. And then, if someone wants to get those new things that weren’t on it, they’d have to repeat. But whatever we measured is gonna stay the same. Dr. Deb Muth 00:19:03 That’s a lot of SNPs to look at. Bob Miller 00:19:05 Keeps us busy. Dr. Deb Muth 00:19:06 But there’s still, but there’s still SNPs that we. Bob Miller 00:19:09 That we’d like to have that we don’t have, so… Bob Miller 00:19:11 We started out with version 1 on our genetic test, then we worked with version 2, and we’re already compiling a list of what version 3 would look like. So if somebody has our version 2, And we’re saying, you know what, it’d be nice if we could see these, well, then you’d repeat, but it won’t change what you already know, so… Dr. Deb Muth 00:19:29 Got it, got it. So, when you started out, and you started looking at the research of Lyme disease and chronic infections, which detox pathways are most important for people who struggle with those conditions? Bob Miller 00:19:43 Okay. You know what might make sense as we do a screen share, and I’ll actually show you the pathway. Does that make sense? Bob Miller 00:19:48 Alright, so… let’s see if I… let me just press the share… Dr. Deb Muth 00:19:52 Yep, you should just be able to press share. Bob Miller 00:19:54 And… number 2. Okay. Are we seeing the screen there? Bob Miller 00:20:01 Okay. Dr. Deb Muth 00:20:02 So, this is a map that we made. Bob Miller 00:20:05 And by the way, this is not… All-inclusive of all the things we look at, but we believe this is a core issue. So, where we’re going to start here, there’s something called the microglia. And the microglia are glial cells. They’re in the brain and the central nervous system. And they’re very interesting little creatures, because most of the time, and this is just a drawing of what they sort of look like. Most of the time, they’re in what’s called the M2 anti-inflammatory mood. What that means, these little guys pick up dirt, debris, Recycle them. Turns on an enzyme called interleukin-10 that’s anti-inflammatory. And just kind of does general housekeeping. And just kind of does general housekeeping. However, when a trigger comes along. However, when a trigger comes along. They… it’s the same glial cell, but it moves over to a very pro-inflammatory enzyme. A pro-inflammatory glial cell. And it triggers these 3 enzymes, Actually, these four. That are pro-inflammatory. Tumor necrosis vector alpha, Interleukin-6. NF Kappa B, Inos. Now, these create inflammation. So you might think, well, why is that good? Well, if you have some foreign invader, virus, bacteria coming in, parasite. If you didn’t have these guys coming to the rescue, you would just die of infection. So, these guys are your friend unless they’re your worst enemy. Because TNFA, and we’ll show you when we actually do a demo account, TNFA can be overactive. So, in other words, it over-responds. Interleukin-6 can be overactive. And if Kappa-B can be overactive. The INOS, and I’ll explain each of these as we go through a demo, can be overactive. Now, what that means is, you’re very good at killing virus and bacteria. But this is where autoimmune disease comes in, and just inflammatory conditions. Now, this is just speculation, but we think what happened is, as you know. Thousands of years ago, we didn’t have refrigeration, we didn’t have sewer, we didn’t have pure water, and we didn’t have antibiotics. So, if you made it to 40, you were an old-timer, because everybody was dying of infection. So, what we believe happened is, by what’s called natural selection, Having these overactive. A thousand years ago was to your advantage. Dr. Deb Muth 00:22:31 Hmm. Bob Miller 00:22:32 But now… We have pure water, we have refrigeration, we have sewers, we have antibiotics. But now we have environmental factors that are stimulating them. Now it’s to our disadvantage. And we’ll talk about that a little bit as it relates to the hemochromatosis genes and maybe the G6PD. Dr. Deb Muth 00:22:48 Yep. Bob Miller 00:22:49 Now, why are we becoming so inflamed? Let’s look at the triggers. Now, one of my, favorite expressions is. I was born all the way back in 1954. Dr. Deb Muth 00:23:01 And it was a different world back then. Bob Miller 00:23:05 These are some of the triggers. And we’ll get into these, but right now, high fructose corn syrup, And the high-fat diet. High fructose corn syrup only came about in 1968. So now we’re being exposed to high fructose corn syrup. Then… we didn’t have these, these viruses like COVID. Dr. Deb Muth 00:23:26 Yeah. Bob Miller 00:23:27 Now, there’s now pretty strong evidence that COVID Was actually, you know, made as a gain of function. It’s debated, and I’m not taking an opinion on it, but there’s some people who believe Lyme disease was also a part of experimentation. Dr. Deb Muth 00:23:40 Go. Bob Miller 00:23:41 Then we have molds, and it appears as though mold is getting stronger. you know, 20 years ago, when I was seeing folks, mold wasn’t on the radar. I would say 7 out of the 10 folks we speak to today have mold problems. Yeah, 20 years ago, we talked more about mold allergy being an issue versus mold toxicity being an issue. Right. So… I know some folks are, you know, speculating what’s happening, but one of the theories out there is that EMF is strengthening mold. I don’t know if you ever heard that theory, and I don’t… Dr. Deb Muth 00:24:13 I have. Bob Miller 00:24:14 I’m not claiming it’s true, but it’s an interesting theory. Then even, you know, your black mold from water-damaged buildings. Then our air pollution is getting worse. We’re getting more toxic metals. Dr. Deb Muth 00:24:26 You know, if we have a… Bob Miller 00:24:27 You know, we’re gonna look back someday and say, what were we thinking, smearing aluminum into our armpits? The, what were we doing putting mercury in our teeth? Then, you know, glyphosate. When I was a kid, there was no glyphosate. So, all of these herbicides and pesticides. Polychlorinated biphenols, And then EMF. So, we love our cell phones, you know, and I think unless you, or in the middle of the desert, or down in a cave, you’re being exposed to EMF somewhere. So, you know, we have our cell phones with us, we have, We have Wi-Fi, the towers are everywhere. And we don’t know long-term, but we may find that this can… this creates some inflammation. And I don’t know if you get any folks, but do you have any folks that have… are they EMF sensitive? Dr. Deb Muth 00:25:16 Oh yeah, we have a whole bunch of them. Bob Miller 00:25:18 Yeah, and then if you have any TBIs, So, plenty of things here. that will stimulate into the microglia, M1. Now, you could say, well. We’re all pretty much exposed to the same thing. Why do some people get hit harder than others? So here’s where we’re gonna start. There’s an enzyme called Nrf2 and RF2. And Nrf2 is the enzyme that senses when there’s inflammation. And turns on hundreds of anti-inflammatory enzymes. We’ll show when we do the demo, you can have genetic weakness on NERF2. And NERF2 inhibits and slows down microglia M1. supports M2. Now, if it’s not complicated enough, there’s an enzyme called KEEP1. And KEEP1 inhibits NRF2. And you can actually have gain of function on keep 1, that makes Keap 1 stronger. So… A lot of the people who land on my doorstep So… A lot of the people who land on my doorstep Both parents gave a mutation on KEEP1, making it overactive. Both parents gave a mutation on KEEP1, making it overactive. Dr. Deb Muth 00:26:31 Hmm. Dr. Deb Muth 00:26:31 Hmm. Bob Miller 00:26:32 Suppressing Nrf2, nerve 2 might be weak. So, nobody’s putting the brakes on, M1. And by the same token, Nerve 2 supports M2. Then there’s a process called mTOR and autophagy. mTOR stands for mammalian tard of rapamycin, the growth of new cells. And then autophagy, taking our dead cells and recycling them. We need a balance between the two of them. If we didn’t have mTOR, the sperm and the egg would never become the baby, the baby would never become the adult, we wouldn’t make new cells. But our cells are constantly, you know, the old cells dying off. Autophagy is where we take that debris from the cell and recycle it, just like a farmer Plows the crop under at the end of the year. The dead plant then becomes the fuel for the spring, your dead cell becomes the fuel for the spring, and that’s autophagy. So we’re gonna look back someday and say, what were we thinking? We give our animals growth hormones so they get fatter faster. Oh my. So, we consume those animals, and inventory runs faster. Now, for anybody who’s, You know, maybe above 40, 45 years old. Think back when you were 12, and what did girls look like? They were primarily flat-chested little girls. Now they look like 16-year-olds. Because environmentally, we’re jacking up mTOR. So, mTOR stimulates microglia M1, suppresses microglia M2. Probably 80% of the folks we visit with. This is the part of the problem. NRF2 is weak. mTOR is strong. Environmental factors come along. And this guy gets carried away. He doesn’t do that burst and move back. Stays here. We’re calling that How environmental factors create a locked-in, pro-inflammatory. and neurotoxic phenotype. In other words, once it starts, it just keeps… Feeding upon itself. Alright, so what happens now when microglia is overactive. it triggers these 3 enzymes, TNFA, N of kappa B, And interleukin-6. Each one of these can have genetics that make them run stronger. Then it stimulates an enzyme called NLRP3, Which makes what are called inflammasomes. Now, guess what inflammasomes can be? Your best friend or your worst enemy? Because they will, if you’ve got, again, a virus or bacteria, or possibly even some bad cells in the body. They will zap them. Well, that’s good. Unless it’s overactive. Unless it’s overactive. And then what it does, through interleukin-1 beta, makes excess glutamate. And then what it does, through interleukin-1 beta, makes excess glutamate. Anxiety, gut inflammation, OCD, ADD, autism. And, you know, glutamate, we’ll talk about that a little bit, but glutamate makes you intelligent, highly motivated go-getter. but can also be excitatory. And then, look what it does. Let’s see, do I have the drawing tool here? Yes, I do. Okay. So, it comes down through here, Makes the glutamate. Comes back up through here. through the ADORA 2A enzyme, Then we’ve got a feedback loop that feeds upon itself. Then, through interleukin-18, we make histamine. and mast cells. And then through histamine receptor site number 1, we come back and spin it. And now you’ve just got this spinning feedback loop. So, the glutamate will make you anxious, the histamine will give you allergies and make you anxious. And you’re allergic to everything, and you’re feeling horrible. Now, it doesn’t end there, Dr. Dad. It then goes on to make something called gast dermins that creates pyroptosis, where it actually starts punching a hole in the cell membrane. And you’re only going to be as healthy as your cells are. Just a little background. You know, we’re made up of trillions of cells, and each one of them has what’s called a lipid bilayer, made from lipids, which comes from fats. And you’re only going to be as healthy as those membranes are. So that’s why we coined an interesting phrase. Cellular CPR. Construct the cell. Protect the cell. And restore the cell membrane. And we believe that’s going to be revolutionary in the functional medicine world. So… It’s not hard to figure out that if you start punching holes in the cell membrane, that’s not a good thing, okay? Bob Miller 00:31:22 Now… There’s an interesting molecule called NAD. Thicotide adenoside dinucleotide. And anybody who’s in the, you know, listening to the health podcasts and things, they’re… They’re, they’re learning about NAD. And I’m going to show you a chart later, all the good things that NAD does, but For the most part, it helps what’s called sirtuins. And sirtuins are quite interesting. If anybody’s looking at longevity. The sirtuins is where they’re looking at.Because sirtuins turn on good things. Turn off bad things. And I’ll show some charts on that later. So for right here, this sirtuin uses NAD, to slow down NF-kappa-B. CERT 2 uses NAD to slow down an ORP3. So, if we’ve got genetic weakness on these, or we don’t have enough NAD, We don’t hold this pathway back. Make sense? Dr. Deb Muth 00:32:24 Yeah, makes perfect sense. Bob Miller 00:32:25 Now, I’ll show this a little bit later. So, people are like, oh, well, I’m gonna start taking some NAD. Dr. Deb Muth 00:32:31 Right. Bob Miller 00:32:32 And there’s functional doctors who give NAD intravenous. It was just this morning, I was talking to a woman who said, Oh my gosh. I went and got intravenous NAD, and it took me a month to recover from that. Dr. Deb Muth 00:32:45 Hmm. Bob Miller 00:32:46 what happens is, and I’ll show this in a little more detail, there’s an enzyme called CD38, that’s stimulated by NF-kappa-B. And it takes NAD, To make intracellular calcium. that stimulates NLRP3 and actually makes things worse. So, if we have this guy upregulated, and I’ll show a chart what does that. taking NAD will make you worse. Again, when I go into the software, I’ll show you that whole pathway, so… I would encourage people, you know, just don’t go out and start taking massive amounts of NAD, you know, stick your toe in the water, see how you do. Because everything you’ve heard about, how good it is, is true, unless this guy says, oh, thank you very much, let me make more inflammation. Now, this might be part of our innate immune system, that if we have some pathogen that’s gonna kill us. By golly, we want that to happen. But if this is happening by environmental factors, Then it’s detrimental. So the immune system that protected us a thousand years ago now might be turning on us because of the environmental factors that we showed earlier. All right. Then there’s an enzyme called PARP that’s NAD-dependent, and that actually repairs strain breaks in your DNA. Now, the next thing that happens… is there’s an enzyme called NADPH oxidase that gets stimulated. and something called INOS. Now, I’m sure most people know about nitric oxide. It’s a gas that dilates your blood vessels. That’s why sometimes they’ll even give people drugs, nitroglycerin, to boost their nitric oxide. That’s why people are doing beetroots and other things to boost their nitric oxide. But there’s an OS3 enzyme that makes the nitric oxide that’s good for blood flow. But there’s an INOS That makes nitric oxide to kill pathogens. probably might be the third or fourth time I’ve said this. That’s a good thing, unless it isn’t. So, if it’s killing some pathogen, great. It was just misfiring. it combines… With superoxide that’s made by this enzyme, and makes something called peroxynitrite, which is one nasty free radical that chews you up and spits you out. So, the NOx enzyme, NADPH oxidase, uses NADPH, To make this free radical called superoxide. If we have time, we’ll get into it. NADPH is what your body needs to recycle your antioxidants.So, I coined the phrase, the NADPH steel. Where the NOX enzyme takes this very important NADPH, And rather than being useful, makes superoxide. Now, again, is that fine if you’ve got some bacteria to kill? Of course. But if it’s just chronically running, it’s just making all this chronic inflammation. Then it makes something called hydrogen peroxide. And we need to clear hydrogen peroxide by 3 enzymes, catalase, thyroid reduction. And glutathione peroxidase. If we have genetic issues on here, or we don’t have the cofactors. There’s something called the Fenton reaction, discovered in 1895 by Dr. Fenton. Where hydrogen peroxide combines with iron to make what are called hydroxyl radicals. And guess what they do? They create lipid peroxides, That damages your cell membranes. Now, again, the body’s pretty darn amazing. We have glutathione, And here’s where your body’s taking glutathione and recycling it. But look who’s needed to recycle it. NADPH. So, if this guy up here is chewing it up, We don’t recycle our glutathione. And then an enzyme called glufon peroxidase 4, Takes this damaged lipid and repairs it. So, here we’ve got this protecting, we want to protect it by not having this happen. But then we also need this guy to do the restoration. So, there’s a lot that can go wrong in here, Dr. Deb. Dr. Deb Muth 00:37:07 There’s a lot that could go wrong. And I can imagine some of my listeners are thinking that lipid peroxidase, is that the same thing as what they’re thinking of when we talk about lipids and cholesterol? Is that the same process that’s happening there? Bob Miller 00:37:22 Well, no, no, the lipids can be used to make cholesterol, but here we’re talking about where they’re going to build the cell membrane. And they’re being… and they’re being, destroyed. If anybody would like to see a visual representation of this, just go on YouTube. And type in, ferrooptosis Animation. cool little video, it’s about 3 minutes long, and it shows the lipids coming over, being oxidized, and now GPX4 fixes them, so… YouTube, Pharaoptosis Animation, cute little video. It’s just that really… Shows vividly what we’re… what we’re talking about here. Now, this is… Dr. Deb Muth 00:37:59 And so this is very common, too. Like, a lot of people do hydrogen peroxide IVs. Dr. Deb Muth 00:38:04 And so, if somebody doesn’t know their genetics, they could have a problem with doing those, just like they could doing the NADHIVs, correct? Bob Miller 00:38:13 Sure, yeah, yeah, yeah. So, I’ve talked to so many, you know, of course, the hydrogen peroxide kills pathogens. I mean, that’s what it does. So… but I’ve spoken to so many people that said. I had one client that said they’ve never been the same after having one hydrogen peroxide infusion. Dr. Deb Muth 00:38:30 Interesting. Bob Miller 00:38:31 Yeah. So… it can be… I see why people use it, because it. Bob Miller 00:38:36 pathogens, But on the other hand. And now’s a good time to speak about… I don’t have it on here, but there’s a, there’s an enzyme called the HFE gene. And that is what causes you to absorb iron. And there’s mutations in it that cause something called hemochromatosis. Were you overabsorb iron? Now, true hemochromatosis is when both parents give you a mutation. But there’s now growing evidence even a heterozygous can cause a little bit more iron absorption, not to the human chromatosis point, but overabsorption. So, if you overabsorb iron, And you have too much hydrogen peroxide that’s not cleared, All kinds of inflammation. Now, what’s happened is sometimes this inflammation Will damage the red blood cells. And some well-meaning doctor says, oh, you need some iron. And they take iron and it makes it worse. So, can’t tell you how many people I’ve said, you’ve got the overabsorption of iron, and they say, well, that can’t be right, because I’m low in iron. Well, that could be because it’s being chewed up here. Dr. Deb Muth 00:39:40 Sure. GPX1 and TXN turn it into, to water. The, catalase turns it into water and oxygen. Dr. Deb Muth 00:39:58 Now, I see a lot of my clients who have mutations or SNPs on that GPX gene, on that glutathione gene. And they really struggle to clear a lot of their toxins. Bob Miller 00:40:12 Sure. Dr. Deb Muth 00:40:14 Yeah, absolutely. Well, GPX4. Bob Miller 00:40:18 is what, repairs, but you can see GPX1 Is what uses glutathione. To turn hydrogen peroxide. So, but it all depends upon having enough glutathione. Dr. Deb Muth 00:40:30 Yeah. Bob Miller 00:40:31 Well, guess who controls making a glutathione? Dr. Deb Muth 00:40:34 Nerf 2. Bob Miller 00:40:37 So, if you have a keep one weakness, or strength to two… I’m sorry, keep one is too strong. Nrf2 is too weak. You don’t make glutathione. So, when a lot of people do that, it’s like, well, I’m gonna take glutathione. Dr. Deb Muth 00:40:51 Right. Bob Miller 00:40:52 And some do great, and some do poorly. You know, because… and I’ll show this on one of the other charts. You can see here that the, The glutathione has to be recycled. And if we don’t recycle it, it actually turns into superoxide free radical. So… NADPH are the cofactors, For taking the oxidi… here’s oxidized glutathione, here’s reduced. So, this is a good glutathione. After it does its job, you can see it becomes oxidized.We need to recycle it. Well, if we have weakness on the enzyme that does that, or a weakness in Nrf2, or not enough NADPH. The oxidized glutathione never gets recycled. So, I’ve talked to a lot of people who said, oh, glutathione made me so sick, and say, well. Dr. Deb Muth 00:41:43 Yeah. Bob Miller 00:41:44 You need it, but you need to recycle it. Dr. Deb Muth 00:41:46 Can you speak for just a brief moment, too, about MTHFR? That is a very popular gene, it’s all over social media as the major gene, but can you speak to a little bit about that, and how that fits into this whole process of things? Because it is just such a small piece. Dr. Deb Muth 00:42:04 understanding genetics. Bob Miller 00:42:06 Yeah, to be honest, it drives me nuts. Dr. Deb Muth 00:42:08 Me too. Bob Miller 00:42:11 Alright, so… You know, there are people on social media I won’t say what I think, I’ll be kind. But… But the, And, you know, they might mean well. But they talk about, if you have MTHFR and COMT and PEMT, that’s… oh my goodness, that’s horrible, and we’ll fix that for you, and you’ll be fine. Bob Miller 00:42:36 it just irritates me to no end. And it really could get anybody who’s doing this legitimately in trouble. I mean, I’m afraid someday, you know, there might be some cracking down on this kind of nonsense. Now, to answer your question about MTHFR. Dr. Deb Muth 00:42:51 I mean, it really is, but I’ll tell you what, why don’t we hold that thought until I go to another map and I can actually… Okay. Bob Miller 00:42:56 But the real… the cliff notes is the MTHFR puts a methyl group on your folate, which is needed, but it has gotten way, way, way too much attention. And people learn they have MTHFR, and they start taking a multivitamin with methylfolate, then they take a B vitamin with methylfolate. Dr. Deb Muth 00:43:13 And they’re pushing it too hard. Bob Miller 00:43:15 Yeah. So I can’t tell you how many people I’ve helped by saying, stop it. Dr. Deb Muth 00:43:20 Yeah, take less of it. Bob Miller 00:43:21 Take less of it, yeah. So, yeah. Yeah, there’s a… If somebody, say, ranked the enzymes at their level of importance, MTHFR might be 40 or 50 on a scale of 100, you know. Keep one Nerf two. big deals. Dr. Deb Muth 00:43:40 deals. Bob Miller 00:43:41 NQO1 that I didn’t even talk about yet, NQO1, takes your, NA… your NAD goes into NADH, To make electrons for the electron transport chain. you need NQ01 to bring that back. If that’s not working, and I’ll show you on the NAD map how disastrous that can be. Now, the next piece is here, and I think You know, if you talk to any school teachers and say, if you’ve taught for more than 10 years, how are the kids today? Every one of them says, more ADD, ADHD, more autism. Just look at human beings, we’ve never been so agitated. You know, everybody, and it might be a social media thing, but people take a position on something, and if anybody doesn’t share that position, they view them as the enemy. Dr. Deb Muth 00:44:29 And it’s kind of scary what’s happening to us. Bob Miller 00:44:33 So, we can’t agree to disagree anymore. We see anybody who has a differing opinion as the enemy. And, you know, there was… there’s people that didn’t have Christmas dinners together, because they had political differences, like… Dr. Deb Muth 00:44:44 Excuse me. Bob Miller 00:44:45 can’t you put your political differences aside to have Christmas together, you know? Dr. Deb Muth 00:44:49 Right? Bob Miller 00:44:50 become that, you know, no matter what your position is, and I’m not saying anyone’s right or wrong, I’m just saying. You know, in the old days, they used to say that the Republicans and Democrats in Congress would argue policy and then go have dinner together. And now everybody’s all up in arms, angry. Dr. Deb Muth 00:45:05 Yeah. Bob Miller 00:45:06 So… There’s likely multiple reasons for that. But let me show you one of them. That, you know, to what degree this is… very important, we don’t know, but I think We’re beginning to believe this is very important. So, there’s something… there’s a neurotransmitter called GABA. And God buys the don’t worry, relax, be happy. Chill. Okay. Dr. Deb Muth 00:45:31 Nobody has enough of that anymore. Bob Miller 00:45:33 Well, yeah, you’ll be surprised what I’m gonna show you. So, let me see if I can find a, Let me see if I can find the right slide here. Let me look for it here. So, there’s something called a GABA receptor site. And here you can see… This is a neuron, and this is where you, The neuron normally is excitatory. However, there’s normally low chloride in the neuron. Dr. Deb Muth 00:46:09 Hmm. Bob Miller 00:46:10 So, GABA itself is neither relaxing. For excitatory, all GABA does, it opens up what’s called a chloride channel. And then chloride, which has a negative charge, will flow into the neuron. Follow me there? Dr. Deb Muth 00:46:26 Yep. Bob Miller 00:46:27 And as it does, it changes this from a positive charge to a negative charge, And it’s relaxing. and inhibitory. Dr. Deb Muth 00:46:34 Hmm. Bob Miller 00:46:36 Now, on the other hand, there’s enzymes called NKCC1, That will push chloride in. and KCC2 that will bring chlor… oops and bring chloride out. And then there’s a sodium channel. And, sodium has a positive charge. And glutamate will push that in. So, as long as this is happening. And GABA says, receptor sites, open, chloride goes in, Chill. However, If NKCC1 Pushes extra chloride in. KCC2 doesn’t pull it out. and GABA hits the receptor site, the GABA comes flowing out, Sodium comes in, And now it’s excitatory. So Gabba didn’t change. GABA just opened the receptor site, that’s all it does. Dr. Deb Muth 00:47:33 Yeah. Bob Miller 00:47:34 But it’s the chloride balance that’s going to determine whether this is relaxing or not. Now, these are the things that go along with when they lose that KCC2 or gain NKCC1. Pain and sensitivity, burning electrical, neuropathic pain. Normal touch hurts. Sound and light sensitivity. Tinnitus can flare. Headaches and migraines. Seizure tendency. Body jolts. Spasticity, cramps, stiffness, startle reflex. Trouble falling asleep, non-restorative sleep. Anxiety, stress, reactivity, that’s what we have now. Hyperarousal, panic-like surges, irritability, racing thoughts. Brain fog, slowed processing, working memory slip-ups. Mental fatigue. Episodes of racing hearts, sweaty palms, guts on edge. Those are all the things that happen when this GABA switch occurs. Now, here’s what happens, and this is what I’m going to be presenting at an autism conference. When you have a newborn, they need that NKCC dominant to develop. By early childhood, it should… or, sorry, early adulthood. we should move over to the KCC dominant, that’s the taking the chloride out. Nice-looking 25-year-old boys, functioning very well. However, when we get microglia M1 upregulated. Because of environmental toxins, processed foods, Tylenol, aluminum. they stay in NKCC1 dominant, and there’s ADD, ADHD, Autism, the whole spectrum. because… They’ve not moved over to the… They’ve not moved over to the KCC2. And again, this is caused by… Environmental factors. Stimulating the microglia. And then, interleukin-1, interleukin-18 weakens KCC2, interleukin-1 beta, Strengthens NKCC1. high chloride. We open up the chloride channel, In Rebell Excitatory. So, I think when, When the pediatricians get ahold of this, they’re going to be very excited to know that This could be why we’re seeing such a rise, and not just autism, but ADD, ADHD, anxiety, the whole shit mess. Dr. Deb Muth 00:49:58 thing. Bob Miller 00:49:59 Yeah, so… and you can see NF-kappa-B stimulates that. These stimulate it, and I think that’s why everyone’s getting so anxious. Now, there’s a little bit more to it, and we’ll get into this when we look at some of the maps, but… The, the glutamate, Which is excitatory. will stimulate the NMDA receptor, make more glutamate, And glutamate will inhibit KCC2. And then we also need an astrocyte To, take both ammonia And glutamate, and… Turn them back into glutamine. And I’m going to talk to you a little bit about arachidenic acid, and if we have too much arachidenic acid. or TNFA is upregulated, that doesn’t happen. Ammonia goes up, and there may be multiple reasons for this, but this is a reason why some of the autistic kids do flapping. Dr. Deb Muth 00:50:49 Hmm. Bob Miller 00:50:50 Because they’re not clearing their ammonia. And you can tell if somebody has high ammonia by… they get that old person smell, you know. Dr. Deb Muth 00:51:00 Yup. Bob Miller 00:51:01 your vehicle cycle’s not taking out the, the ammonia. Now, last pathway here. There’s growing interest in mast cell activation. So, back here, we talked about peroxynitride. And that will stimulate mast cells, and those are white blood cells that are your best friend, unless they’re your worst enemy. Then it’ll make histamine. And there’s enzymes called histidine decarboxylase that’ll make more. Dr. Deb Muth 00:51:28 I’m sure everybody’s heard of DAO, the enzyme that degrades histamine. Yep. Bob Miller 00:51:31 We can have genetic weakness, we don’t make that. There’s an enzyme called histamine and methyltransferase, That, That breaks down the histamine. Then if we don’t do that, it’ll get stuck in the histamine receptor site. And then it’ll make something called, renin. Which will cause angiotensinogen to turn into angiotensin. One, that turns into angiotensin II,And that’s where people make aldosterone, where they’ll get the, The swollen ankles and high blood pressure. But interestingly, there’s an enzyme called ACE2, that takes this guy and turns it into angiotensin 1-7, Which is anti-inflammatory and also inhibits… TNFA. Now, you can have weakness on ACE2, But… and anybody’s saying, that sounds familiar? Dr. Deb Muth 00:52:25 That’s where COVID comes in, using ACE2. Bob Miller 00:52:28 And now we just found there’s literature that if you get COVID long enough, it can actually make ACE2 not be able to work as well. So look what it does. It comes down here, stimulates the NADPH oxidase, More superoxide. More peroxynitrite. And we’re on a cycle here. We’ve actually named this the Home Cycle Hypothesis, the proposed feed-forward loop. That just keeps feeding on itself. All being caused by… Primarily, The environmental factors. But hitting those who have genetic weakness the hardest. That’s why. Dr. Deb Muth 00:53:08 To the people. Bob Miller 00:53:09 Don’t live in a moldy house. One person is sick as can be, and the other person says, well, you must be imagining things, because I don’t feel anything. Dr. Deb Muth Yeah. Same thing with long haul, right? Two people can both get sick, one gets sick and never seems to recover, and somebody else gets sick, and they have absolutely no problems with it at all. Bob Miller 00:53:30 Sure. Well, think about it, if you get COVID, and ACE2 is weak, and some of this other stuff is going on. This thing just starts feeding upon itself. Dr. Deb Muth 00:53:38 Keep creating more inflammation, more complications, nothing’s calming down. Bob Miller 00:53:43 Yeah. Now, you, you ask about, MTHFR. So, this is the, this is the, the software called Functional Genomic Analysis. There’s a demo report we have. So, let’s talk a little bit about, MTHFR. So, we actually have a map called a methylation map. Now, what happens is, when you do your saliva test, you, you know, you spit, you put some saliva. in a collection kit, goes to a lab, takes out the DNA data, sends it to the computer, and now you can actually see it visually. Okay. So, it’s gonna take a second for this, data to load up, it’s, and each of these Circles, each of these ovals, is an enzyme. And the data gets loaded up to see where it is. So, until it gets loaded up here, I didn’t preload this. There it goes. So… The primary thing about methylation is There’s a nasty substance called homocysteine that, if it’s too high, can really be detrimental. The body takes methylfolate, and combines with methyl B12, To bring this back up to methionine. And then through the MAT genes, we make SAMI, S-adml methionine. Which is involved in so many processes. Then after it does its thing, it turns back into homocysteine. And this thing needs to keep spinning around. That’s why, you know, it’s a good idea to keep homocysteine at, do you have a number that you’d like? 7, 8? What do you like for a number? Dr. Deb Muth 00:55:24 Yeah, I like mine below 7. Bob Miller 00:55:26 Yeah. So if the homocysteine goes too high. It, caused all kinds of problems. So, here’s where you ask about the MTHFR. So, here you can see on this individual. I click on MTHFR, and you can see it comes up here, here’s the C677. And you can see here where it says, variants. I’ll… I’ll draw in case somebody’s having a hard time seeing that. So, you can see there’s nothing in there. That means there’s no genetic mutations. If one parent would have given a mutation, there’d be a 1. If both parents did, there’d be a 2. Now, here’s why Yes, methylation is important, I’m not saying it isn’t important, but look at this MTHFRC677. In my software. Only 42.5% of the population does not have a mutation. 44.7% have won. 12.9 have 2. So, this isn’t some rare, oh my god, I’m gonna die… Kind of thing, yeah. Dr. Deb Muth 00:56:27 Right. Bob Miller 00:56:28 So, And then what happens is that, and again, I’m not dismissing methylation, I… we could do a whole show on methylation. Bob Miller 00:56:36 get it. But I think that what people are doing is they’re, they’re learning about MTHFR, they get it measured, they panic. They start taking massive amounts of methylfolate, which many times is to their detriment. Dr. Deb Muth 00:56:50 Well, it’s… and isn’t it true, too, with MTHFR, like, you have to also look at MTR, MTRR, and the more we stack up of those, the more complicated than MTHFR can be. It’s not… it’s not as simple as just saying MTHFR 677 versus 1298. It’s more complex than that, kind of like what you’ve already shown with some of the other things. There’s more to it than just that one little sliver. Bob Miller 00:57:17 Oh, sure, well, let’s take a look. So, remember I said there’s a cofactor? One of the cofactors is called FAD. Just a Bob Miller observation, that’s all. But when people have trouble with their riboflavin and they don’t have enough FAD, They’re doing much worse than people who have just a C677. So, right here, you could have perfect C677th. And if you don’t have the cofactor, it’s not gonna work, okay? Dr. Deb Muth 00:57:48 And as you said, there’s an MTR enzyme. Bob Miller 00:57:51 that takes methylfolate and methyl B12, to spin it around. So, here on this individual. here’s your… here’s your B vitamins, or I’m sorry, your B12s. There’s an enzyme called TCN1 that takes it from the stomach into the blood. Then there’s other enzymes that take it from the blood into the tissue. And if you’re having trouble here. Well, then you’re not going to have this working, so… Even if you don’t have MTHFR, And you have MTR, like this, no, I’m sorry, this person doesn’t. But they have the MTRR, and then they don’t have enough B12, this isn’t gonna work, aside from that. And then there’s a middle pathway. And then there’s enzymes called the MAT1. they take the methionine to the salmon. If that’s not working, we stick… we get stuck in methionine. So, it’s, it’s not just an MTHFR. And then, one of the things that people forget about. is through these CBS enzymes and CTH, We make cysteine, which is needed to make glutathione. The master antioxidant. So, it really is that… I call it the, The 3D chess game played underwater. Dr. Deb Muth 00:59:07 It really is. I mean, I see people who have CVS, COMT, glutathione, MGHFR genes. And some of them function just fine. Like, they have Like, I look at this person and I’m like, oh my gosh, I don’t know how they’re functioning because they’re double mutated on so many pathways, but yet they don’t have a lot of symptoms, they don’t have a lot of complications. Somehow their body has figured out a way to adapt to what it has so it can stay alive and it can function at a high functioning level. Bob Miller 00:59:36 Yeah, and they may be, you know, eating right? Yeah. Staying out of a moldy house. reducing stress. So, it’s diet, it’s stress, it’s genetics, environmental factors. So, yeah, we can’t just say somebody’s gonna be good or somebody’s gonna be bad. You know, some people get scared, oh, I got all these, it’s like, well… Bob Miller 00:59:56 Are you living in a moldy house? You know, and if you live in a moldy house and your glucuronidation pathway doesn’t do well, or if you’re, you know, a smoker, or you’re constantly eating junk food, I mean, all. Bob Miller 01:00:07 things come together. Although, you know, when we focus on genetics, we’re well aware that this is just a piece of it. You know, you could have identical twins, Genetically, and if one… Is exposed to mold and smokes and drinks and stressed out. They’re gonna be a whole lot sicker than their sibling. Bob Miller 01:00:28 Yep. Dr. Deb Muth 01:00:29 Yeah, it’s that concept of taking twins, and one gets raced with one family, and one gets raced with another family, and they don’t have the same… problems that… that each other have, you know? It’s a very unique situation, we don’t think about that enough. Bob Miller 01:00:44 Alright, so again, genetics loads the gun, environment pulls the trigger. So, if you’ve got a loaded gun, but you don’t have the triggers, you’re okay. Dr. Deb Muth 01:00:53 Yeah. Bob Miller 01:00:54 Yeah. So, remember I said I was going to talk about NAD? So, here’s NAD, and what it does, it turns into NADH. And what NADH does, it, Comes down this pathway, what’s called the electron transport chain. And that makes your ATP, that’s your energy. So, if this wasn’t working, we wouldn’t be alive, because we wouldn’t have energy. So it donates an electron, that’s why it’s called electron transport chain. So, we need NAD, To make this, to make the energy. But remember I said that NQ01, this would probably be, like, on my top 10 list of… Bob Miller 01:01:36 Much more important than MTHFR. This one takes NADH back to NAD. If we’re stuck over here, We’re low in this NAD+, But what happens is, NQO1 also provides CoQ10. And CoQ10 Is what’s needed for the electron transport chain to flow. So if we get too many electrons up here. And they don’t turn them into energy. They make a nasty free radical called superoxide. Okay. Now, NAD plus also makes NADPH, And that is needed. Remember I said we need to recycle our antioxidants. So, if we have a problem with FAD from riboflavin. Yeah, we don’t have enough NADPH, Glutathione’s not getting recycled, and you’re gonna be inflamed. And you take glutathione, you’ll feel worse. There’s another enzyme called thimoredoxin. Same thing, needs NADPH and FAD. And same way with your nitric oxide, there’s an enzyme called NOS3, That makes the nitric oxide that dilates your blood vessels. And if we don’t have enough NADPH or fat, You’re gonna make superoxide. Rather than nitric oxide. Now, remember
This Morning's Headlines1. Lee in Brussels2. Submarine project3. Ballot shortage probe4. Reducing troops5. Xi back home
This Morning's Headlines1. Second year plan2. NEC criticized3. Lee to Europe4. Xi in NK5. Halted operations
Send us Fan MailMaster the 5 Phases of Amazon SEO to outrank competitors in the new AI-driven era.Amazon's ranking algorithm has shifted from simple keyword stuffing to "Buyer Intent" and AI-driven questions. In this masterclass, We break down our proven 4-phase SEO framework and introduce the unofficial Phase 5: Intent & AI Prompting. Learn how to optimize your listing for Rufus, Amazon's new AI shopping assistant, and why your A+ content is now your secret weapon for indexing.Get better sales and grow your brand with My Amazon Guy: https://bit.ly/4jMZtxu#AmazonSEO #AmazonSellers #AmazonFBA #AmazonListingOptimization #AmazonRufusWant free resources? Dowload our Free Amazon guides here:Amazon Receiving Delay Guide: https://hubs.ly/Q04cdD4c0Amazon Catalog Spring Cleaning: https://hubs.ly/Q046BVfp0Amazon Proft Margin Defense 2026: https://hubs.ly/Q042trRH0Amazon SEO Toolkit 2026: https://bit.ly/4oC2ClTAmazon Seller Strategy Report 2026: https://bit.ly/3YN1RME2026 Ecommerce Website & SEO Readiness Checklist: https://hubs.ly/Q04btghf0Amazon 2026 PPC guide: https://bit.ly/4lF0OYXTimestamps00:00 - The Problem: Why it's harder to scale organic sales01:32 - The 4-Phase SEO Approach (Overview)03:26 - Phase 5: AI, Rufus, and Question-Based Shopping04:56 - Stop the Stuffing: New Title & Bullet Point Rules11:13 - Using A+ Content & FAQ for AI Indexing19:19 - How to incorporate 100+ keywords without penalties29:00 - Ranking vs. Indexing: What's the difference in 2026?32:44 - The "Strike Zone" Strategy: Moving from Page 2 to Page 1-----------------------------------------------------------------------------------------Follow us:LinkedIn: https://www.linkedin.com/company/28605816/Instagram: https://www.instagram.com/stevenpopemag/Pinterest: https://www.pinterest.com/myamazonguys/Twitter: https://twitter.com/myamazonguySubscribe to the My Amazon Guy podcast: https://podcast.myamazonguy.comApple Podcast: https://podcasts.apple.com/us/podcast/my-amazon-guy/id1501974229Spotify: https://open.spotify.com/show/4A5ASHGGfr6s4wWNQIqyVwSupport the show
This Morning's Headlines1. Lee blasts NEC2. 1 year press conference3. Second PM4. Soaring exchange rate5. Drones shot down
This Morning's Headlines1. Mayoral results2. Submarine talks3. France relations event4. Huang in Korea5. Ceasefire
Milwaukee, WI Mayor Cavalier Johnson won reelection in 2024 with 80 percent of the vote. "Those are Vladimir Putin levels," joked Citizen Co-Founder Larry Platt. "The difference is, Putin's still looking for the other 20 percent!" said host and former Philly Mayor Michael Nutter. Asked why he decided to devote his life to public service, Johnson said, "I fell in love with helping people in my community. I mean, the key word in 'progressive' is progress. And mayors get stuff done. It's truly where the rubber meets the road in cities." From youth workforce development programs ("Ten-year-olds were being recruited to steal cars, here") to rejecting partisanship for the good of the city ("Bringing the RNC to Milwaukee in 2024 was a purely business decision") to his efforts to grow the population of Milwaukee to a million people, Johnson is out earning that 80 percent each day. "We have an awful lot of people who listen to this podcast that we hope will one day run for office," said host and former Atlanta Mayor Kasim Reed. "Right, I think it's important for the people to see their reflection in this office," said Johnson. "It's a powerful thing. It's all about service." Remember to subscribe to the podcast to keep up on all the latest episodes. And watch for new episodes on YouTube and Piksel+ as they become available. As cities go, so goes the nation!
Milwaukee, WI Mayor Cavalier Johnson won reelection in 2024 with 80 percent of the vote. "Those are Vladimir Putin levels," joked Larry Platt. "The difference is, Putin's still looking for the other 20 percent!" said Michael Nutter. Asked why he decided to devote his life to public service, Johnson said, "I fell in love with helping people in my community. I mean, the key word in 'progressive' is progress. And mayors get stuff done. It's truly where the rubber meets the road in cities." From youth workforce development programs ("Ten-year-olds were being recruited to steal cars, here") to rejecting partisanship for the good of the city ("Bringing the RNC to Milwaukee in 2024 was a purely business decision") to his efforts to grow the population of Milwaukee to a million people, Johnson is out earning that 80 percent each day. "We have an awful lot of people who listen to this podcast that we hope will one day run for office," said Kasim Reed. "Right, I think it's important for the people to see their reflection in this office," said Johnson. "It's a powerful thing. It's all about service." As cities go, so goes the nation!
This Morning's Headlines1. DP victory2. Public judgment3. Ballot shortage4. Security meeting5. Tariffs
Agentic e-commerce is already reshaping how consumers discover and buy products online, yet it still accounts for barely 0.2% of total e-commerce traffic. BASE France is the French arm of Base.com, a Polish-born SaaS scale-up that has spent nearly two decades building operational infrastructure for online retailers. Its CEO, Ben Hamilton, brings a practitioner’s perspective to this emerging model: measured, practical, and refreshingly free of the hype that surrounds most conversations on the topic. Agentic E-Commerce: Could AI Become the Shopfront? Imagine an agentic e-commerce world where e-commerce happens on smartphone screens and robots deliver your purchases. We might be on the brink of this future. This image was created using Midjourney. Commerce as conversation: the oldest model in the book Before there were shops, there was conversation. For thousands of years, trade was oral. A buyer expressed a need, a seller responded with what they had, and the two parties negotiated until a deal was struck. The self-service retail store, born roughly a century ago, was a radical departure from this model. It replaced dialogue with browsing. It handed the customer a trolley and pointed them at the shelves. E-commerce then took that self-service model and, as Ben Hamilton puts it, “multiplied it by about 100,000.” The online shopper today faces a near-infinite array of products across dozens of marketplaces, with no guide, no-one to talk to, and no memory of what they looked at three tabs ago. It is efficient in theory. In practice, it is exhausting. Back to future? The agentic model, Hamilton argues, represents something of a return to origins. Instead of browsing, the consumer talks. An agent listens, asks questions, proposes options, and eventually surfaces an answer to a need that the buyer may not even have been able to articulate clearly at the outset. “back to the future,” Hamilton explains, “that’s what I’m getting at. The agentic model takes us back to something closer to how human beings have traded over thousands of years compared to the last ten, twenty or even a hundred.” My own experience bears this out. I recently found a diagnostician for a property I am selling. As a matter of fact, I didn’t find them through a Google search, but through a conversation with an LLM. I clicked through two or three irrelevant links before landing on exactly the right provider. I then completed the transaction on their website. The research was agentic; the checkout was not. That distinction, as it happens, sits at the heart of what Hamilton believes will define the next phase of e-commerce. Ben Hamilton on agentic e-commerce: “I can totally imagine a portion of that market occurring directly on an LLM”. Agentic E-commerce: Where checkout will and won’t happen One of the more grounded contributions Hamilton makes to this debate is his refusal to conflate two distinct phenomena: AI influence over purchasing decisions, and AI completing the transaction itself. Much of the media discourse collapses the two. Hamilton does not. “I don’t think we’re heading to a world where 20, 50 or 80% of online transactions happen on an LLM,” he says. “I would draw the distinction between where the checkout occurs and how much an agent is involved in the buying process.” For the foreseeable future, he believes, most consumers will continue to research via LLMs and transact on familiar websites and marketplaces. The inertia in human purchasing behaviour is simply too great for the checkout itself to migrate rapidly to a chat interface. This view is supported by the data available. According to research by commercetools, 73% of consumers already use AI somewhere in their shopping journey. Yet only 36% are open to AI agents making purchases on their behalf. In the US, the figure for autonomous AI purchasing drops to 14%. The gap between AI as advisor and AI as buyer is vast, and it will narrow slowly. The risks associated with agentic e-commerce are high The risks of handing uncapped authority to an AI agent are no longer hypothetical. In late May 2026, an AI consultant reported to Axios that one of their enterprise clients had accidentally accumulated a $500 million bill on Anthropic’s Claude in a single month, simply by giving employees unrestricted access to the platform with no usage controls in place. Agentic workflows, which loop through tasks repeatedly, consume tokens at a rate orders of magnitude higher than a standard chat query. The bill was not the result of malicious use or a system failure. It was the predictable outcome of deploying autonomous agents without guardrails. The case is far from isolated: Uber reportedly exhausted its entire 2026 AI budget by April, with per-engineer costs running between $500 and $2,000 monthly. “You’ve got to be bold to give them no upper limit on transactions,” Hamilton observed, and the arithmetic proved him right. [Editor's note: I misquoted a similar anecdote about the Davos Summit during the interview. I'd heard or read this story in traditional media but couldn't verify it with facts. I suspect it might have been fabricated. I replaced it with the above, duly sourced information.] The check out must remain on the merchant’s platform OpenAI itself learned this lesson when it launched Instant Checkout in September 2025, which allowed purchases to complete directly inside ChatGPT. By March 2026, the feature had been shut down. Brands rejected the model, citing the loss of traffic, customer data, and loyalty flows. Shopify’s own position makes the point clearly. At the Morgan Stanley Technology, Media and Telecom Conference in March 2026, Finkelstein noted that barely a dozen Shopify merchants were live on agentic commerce at the time. On the Q1 2026 earnings call, he was unambiguous: “LLMs do not bypass Shopify’s checkout.” The checkout, the payment flow, and the post-purchase relationship remain squarely on the merchant’s platform. A natural segmentation Hamilton sees a natural segmentation emerging by category. Low-value, frequently purchased household items lend themselves to fully autonomous agentic purchasing. “I can totally imagine a portion of that market occurring direct on an LLM,” he says. “Hey, I’ve run out of toothpaste, can you order me some?” High-involvement purchases, and anything with significant financial or emotional stakes, will retain human control over the final step for a long time yet. The death of keyword search, greatly exaggerated The brands Hamilton speaks with regularly are, understandably, worried. Most have spent the past two decades learning the rules of a game built around keyword search and performance marketing. That game has not ended, but the goalposts have shifted, and nobody is quite sure where they have moved to. Brands are understandably worried. Most have spent the past two decades learning the rules of a game built around keyword search and performance marketing and the goalposts have shifted, and nobody is quite sure where they have moved to. Gabriel Magalhães didn’t even need this to miss in the 2026 UEFA Cup Final penalty shootout. This image was tweaked with ChatGPT. The scale of the agentic e-commerce shift Key figures: the scale of the shift AI-driven sessions still represent below 0.2% of total e-commerce traffic, though they are the fastest-growing channel (Digital Commerce 360, 2025) GenAI referrals to US retail sites grew 693% year-on-year during the 2025 holiday season (Adobe Analytics) Gartner forecast that traditional search engine volume would drop 25% by 2026 as AI chatbots captured search share (Gartner, 2024) By early 2026, ChatGPT reached approximately 17% of global search queries against Google’s 78% Over 60% of Google searches now end without a click, across multiple industry studies Retailers with AI agent integration grew 32% faster during Cyber Week 2025 than those without (Salesforce) Hamilton’s view on the fate of keyword search is careful rather than apocalyptic. Google will not lose its advertising revenues overnight. But the direction of travel is clear. Search queries will progressively migrate towards conversational interfaces, for the simple reason that we rarely know precisely what we want when we start looking. “We don’t necessarily know what we want 90% of the time,” he observes. “It takes a bit of a conversation to elicit exactly what we’re looking for.” Keyword search was always a crude proxy for intent. LLMs are, at least in principle, better placed to decode it. Agentic e-commerce by the numbers Agentic e-commerce by the numbers. Infographic made with Gemini The question for brands is what to do about this. Hamilton’s prescription is structural rather than cosmetic. Brands need to become machine-readable, which means structured data connected to the right protocols, not just well-written product descriptions. Three open standards now define how AI agents interact with merchants: MCP (Model Context Protocol, originally developed by Anthropic and donated to the Linux Foundation in December 2025), ACP (OpenAI and Stripe, September 2025), and UCP (Google and Shopify, announced at NRF in January 2026). Shopify activated a default MCP endpoint for all its stores in Summer 2025. These are not optional extras. They are the new plumbing. MCP, ACP or UCP and the agentic acronym soup I raised with Hamilton the practical reality for most merchants, who have no idea what MCP, ACP, or UCP even stand for. His response was reassuring on one level, and sobering on another. Platforms like BASE are absorbing this complexity on behalf of their clients. A small or mid-sized retailer does not need to recruit data scientists or build protocol integrations in-house. They can, if they choose; the new generation of coding tools makes that more feasible than ever. But they can equally rely on an operational platform that handles those connections for them. The sobering part comes when Hamilton acknowledges a concern he is genuinely uncertain about. Even if the protocols function perfectly, will LLMs be able to surface smaller independent brands alongside the big players with their vast content libraries and tens of thousands of referring domains? Research from Airops suggests that brands are 6.5 times more likely to be cited in AI answers through third-party sources than through their own domains. According to SE Ranking’s analysis of 129,000 domains, sites with more than 32,000 referring domains are 3.5 times more likely to be cited by ChatGPT than lower-authority counterparts. Scale, in other words, confers an advantage in AI visibility just as it did in paid search. The field may level in some ways; in others, it may simply tilt differently. Operational excellence as the new marketing in this agentic e-commerce world What AI agents actually evaluate Unlike Google’s search algorithm, which can be influenced by ad spend, AI agents query real-time signals: live stock levels, shipping terms, return policies, and customer review aggregates. Structured data across these dimensions is now considered standard for AI visibility by the major platforms. Retailers with AI agent integration achieved roughly 7x better sales growth during Cyber Week 2025 than those without (Salesforce). Perhaps Hamilton’s most interesting claim, and the one most counterintuitive to marketers, is that operational excellence is becoming a direct marketing lever. An AI agent evaluating a recommendation does not care how much a brand has spent on Amazon retail media. It will scrape ten thousand reviews in half a second and draw its own conclusions about delivery reliability, return handling, and product quality. No media budget can substitute for that data trail. “I think we’re heading to a world where operational excellence will count for more in the decision process,” Hamilton says, “and will be less easily brushed behind the curtains with a bit of ad spend.” This is, in theory, good news for consumers and for competent smaller operators who have always delivered well but lacked the budget to outrank wealthier rivals in paid search. Whether it will materialise in practice depends on whether LLMs can actually surface those operators when large brands flood the information environment with well-structured, high-quality content. BASE France sits at exactly this intersection. The platform manages what it describes as the “spinal column” of an e-commerce operation: product catalogue management, order handling, marketplace feeds, stock synchronisation, and shipping. These are also, precisely, the data layers that AI agents query in real time when assembling recommendations. BASE connects to more than 1,700 integrations globally and serves some 30,000 merchants across more than 180 countries. In France, launched in early 2026 and operating from Bordeaux, the platform already counts 150 clients including Kiabi, Back Market, and Spartoo, with connections to around 250 marketplaces and partners. The platform’s value proposition in an agentic world, as Hamilton frames it, is straightforward: merchants who want to be visible to AI agents need to expose the right data through the right protocols. BASE does that for them, whether or not a checkout ever happens inside an LLM. The forecasts, the hype, and the rising tide McKinsey estimates that agentic commerce could redirect between three and five trillion dollars in global retail spend by 2030, with up to one trillion of that in the US alone. Bain puts the US figure at 300 to 500 billion dollars, representing 15% to 25% of total US e-commerce sales. These numbers attract attention and, inevitably, scepticism. Hamilton’s response is precise. He notes that global retail in 2030 will likely be somewhere around 50 trillion dollars. On that basis, the McKinsey and Bain figures imply that agentic commerce will account for somewhere between one and ten percent of total retail within four years. That is plausible, he suggests, if the definition of “agentic” is broad enough to include any transaction where an AI agent played a role somewhere in the funnel, from discovery to decision, not just cases where the checkout itself occurred on an LLM. Physical retail is not exempt either: a consumer standing in a supermarket aisle, consulting Gemini on their phone about which of two products is better, is already part of this story. The honest summary is that we are watching a slow revolution rather than a tidal wave. “Maybe a year or two ago, some people made it sound imminent,” Hamilton reflects. “When it comes to retail, there’s still quite a lot of human behaviour inertia in the system. Things aren’t going to change drastically in the next twelve or twenty-four months. But over ten or fifteen years, it’s pretty difficult to imagine consumer behaviour and the retail experience looking anything like what it looks like today.” Three priorities For merchants wondering what to do right now, Hamilton’s three priorities are: become machine-readable through structured data and protocol connections, maintain high-quality content that reflects genuine expertise, and resist the temptation to flood the market with AI-generated copy. On that last point, he is candid. “Humans are starting to get pretty good at telling what is AI-generated and what isn’t. When you read things now, you almost have a sixth sense for ‘I think a machine wrote that.'” Good news, as I told him, for those of us who write for a living. Three things merchants should do to score high in agentic e-commerce according to BASE.com’s Ben Hamilton. Infographic made with Gemini and Adobe Photoshop The winners: a scenario Hamilton wants to believe I asked Hamilton, as a final question, who he thought would win in this new landscape. Big retailers with scale advantages? Platform giants? Or the long tail of independent merchants who have always competed on product and service rather than budget? His answer was honest about the limits of his own conviction. He described the scenario he wants rather than the one he necessarily expects. In that scenario, agentic commerce levels the playing field by reducing the influence of performance marketing budgets and increasing the weight of genuine operational quality. “I like to believe that those who have superior products and superior service will get more and more traffic,” he said. Whether the reality will be so equitable depends on whether AI recommendation systems can overcome their own structural biases towards scale and data volume. I was reminded, hearing this, of an IBM advertisement from the 1990s that showed an Italian woman selling her homemade spaghetti sauce to the world via the internet. The vision was real. The timeline was not. It took twenty years for that kind of global reach to become genuinely accessible to small producers. The analogy is imperfect but instructive. Agentic commerce will likely democratise access to markets over time. That time will be measured in years, not months. Ben Hamilton and Base.com Ben Hamilton is CEO of BASE France, the French arm of Base.com, a Polish-born e-commerce SaaS scale-up founded in 2006. With nearly two decades of expertise and a presence in more than 20 countries, Base serves approximately 30,000 merchants worldwide and generated €50 million in revenue in 2024. BASE France was officially launched in early 2026, operating from Bordeaux with a team of 20. The platform covers order management, stock synchronisation, shipping, marketplace feeds, and AI-ready product enrichment. Ben Hamilton is a regular speaker on the strategic implications of AI for e-commerce visibility and discovery. The post Agentic E-Commerce, Could AI Become the Shopfront appeared first on Marketing and Innovation.
This Morning's Headlines1. Election day2. 1 year in office3. Security talks4. Submarine project5. Eased tariffs
This Morning's Headlines1. D-12. Expanded cooperation3. Korea-Canada ties4. Chip boom5. Robot investment
Pentecost: Being Baptized in the Holy Spirit means so much more than we settle for... Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
The fullness of the spirit works exactly the opposite way as being drunk with alcohol. It doesn't show you less of reality but shows you more. Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
This Morning's Headlines1. Early voting2. MOU rejected3. Asia Security Summit4. OPCON transfer5. Korea-Africa talks
Send us Fan Mail In this Duda webinar, Darren Shaw and Mike Blumenthal explore the paradigm shift occurring in local search as Google increasingly incorporates generative AI into Google Business Profiles and Google Maps. Through new features like "Know Before You Go" and the conversational "Ask Maps," local discovery is transitioning from a deterministic ranking model to a highly personalized, context-aware ecosystem. Blumenthal demonstrates how to leverage Ask Maps for deep competitive analysis to pinpoint market weaknesses and operational gaps. The speakers emphasize that while traditional SEO remains foundational "table stakes," long-term visibility in the AI era requires businesses to cultivate a deeply revered brand through comprehensive website data, widespread consumer sentiment, community engagement, and niche specialization. Subscribe to our newsletters and other content at https://www.nearmedia.co/subscribe/
This Morning's Headlines1. 400 Trillion Won Market2. Korea-Singapore Top Diplomats3. Rate Freeze Extended4. Live Fire Drills 5. School Trip Liability
This Morning's Headlines1. Iran-linked Missiles2. Global Marine Capital3. Key Geoheritage Areas4. Pay Deal Approved 5. Fund for Shared Growth
This Morning's Headlines1. Nuclear-powered Submarine2. Missile Launch Resumes3. MoU on Ending War4. Public Apology
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This Morning's Headlines1. War in Ukraine
This Morning's Headlines1. Election2. Koreans released3. Global forum4. Samsung deal5. Iran issue
This Morning's Headlines1. Samsung reach deal2. Campaigning starts3. Ship passes4. Activist abuse5. Nuclear submarine
This Morning's Headlines1. Korea-Japan summit2. Implementation talks3. Solar complexes4. Stalled talks5. Final talks
Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
This Morning's Headlines1. Samsung talks2. US diplomacy3. Ship transit4. Unification5. War ending efforts
Send us Fan MailFinding effective targets for Amazon advertising can be challenging for even seasoned sellers. This video demonstrates how to effectively find advertising targets on Amazon, moving beyond basic keyword suggestions and competitor analysis to leverage Amazon's own system for better targeting insights. Learn how to optimize your amazon ppc strategy and improve your amazon sponsored products and amazon sponsored brands campaigns.Need help setting up Amazon ads the right way? Book a coaching call: https://bit.ly/4jMZtxu#AmazonAds #AmazonPPC #AmazonSellers #AmazonAdvertising #MyAmazonGuyWant free resources? Dowload our Free Amazon guides here:Amazon Receiving Delay Guide: https://hubs.ly/Q04cdD4c0Amazon Catalog Spring Cleaning: https://hubs.ly/Q046BVfp0Amazon Proft Margin Defense 2026: https://hubs.ly/Q042trRH0Amazon SEO Toolkit 2026: https://bit.ly/4oC2ClTAmazon Seller Strategy Report 2026: https://bit.ly/3YN1RME2026 Ecommerce Website & SEO Readiness Checklist: https://hubs.ly/Q04btghf0Amazon 2026 PPC guide: https://bit.ly/4lF0OYXTimestamps00:00 - Finding Better Amazon Ad Targets01:03 - Setting Up a Sponsored Product Campaign01:32 - Why One Product Matters01:58 - Automatic Targeting and Bids03:05 - Automated Rules in Amazon Ads03:56 - Creating the Manual Campaign05:22 - Feeding Terms Into Ad Groups06:35 - CTR and Conversion Rate Filters07:08 - ROAS Filter and 30-Day Performance07:32 - Exact, Phrase, and Broad Campaigns08:16 - How the Keyword Funnel Works08:50 - Automating Amazon Keyword Research-----------------------------------------------------------------------------------------Follow us:LinkedIn: https://www.linkedin.com/company/28605816/Instagram: https://www.instagram.com/stevenpopemag/Pinterest: https://www.pinterest.com/myamazonguys/Twitter: https://twitter.com/myamazonguySubscribe to the My Amazon Guy podcast: https://podcast.myamazonguy.comApple Podcast: https://podcasts.apple.com/us/podcast/my-amazon-guy/id1501974229Spotify: https://open.spotify.com/show/4A5ASHGGfr6s4wWNQIqyVwSupport the show
Your SEO traffic is up. Your pipeline is flat. Something broke, and it's not your team — it's the entire model most B2B marketers were trained on. The buyers who used to find you on Google are now getting their shortlists from ChatGPT, and if you're not in that conversation, you're invisible at the exact moment it matters most.In this episode, Josh and Ross sit down with Hadassah Pegado Dalisay, Head of Content Strategy, SEO, and AEO at Outreach — the agentic AI platform for revenue teams — who has spent over a decade watching the search game change and finally break. Hadassah makes a case that will sting a little: the old keyword-volume playbook didn't just stop working, it actively made you worse at the thing that actually matters — being the trusted answer when a buyer asks an AI what to buy. Her fix isn't to abandon SEO. It's to collapse the wall between SEO, content strategy, and revenue intelligence into something that actually earns attention.We also cover:•Why mining your own sales transcripts is the most underrated content research method in B2B — and how Outreach does it at scale every quarter•The difference between signal-driven and keyword-driven content strategy, and why the companies chasing volume right now are building a liability, not an asset•How to make the case inside your org that AI visibility isn't a marketing metric — it's a pipeline metric
Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
Two common Google Search Console questions get answered in this episode: what it means when impressions are rising but average rankings stay flat, and whether keywords still matter for blog posts. The short answer on rankings might surprise you. And the advice around blogging and keywords could save your site from a problem that looks like progress while quietly making things worse.Timestamps [0:00] Introduction [0:24] Listener question: impressions rising but rankings unchanged [0:49] What impressions and average rankings mean in Search Console [1:50] Why rising impressions with flat rankings is actually a good sign [2:20] How new keywords entering the index affect your average ranking [3:15] Why average ranking is a misleading metric to track [3:55] Meredith's question: are keywords still important for blogs [4:22] What bloggers offering "keyword-included" posts are actually doing [5:00] Keyword cannibalization explained [5:45] What the right keyword strategy for blogs actually looks like [6:35] Why keyword stuffing in blogs works against you Try WisprFlowhttps://wisprflow.ai/r?CHRIS37400 --Learn more about the MENTORING PROGRAM:www.meredithshusband.comSubmit questions for future episodeshttps://forms.gle/bqxbwDWBySoiUYxL7
Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
Send us Fan MailWelcome to season 7 of the Nobody Knows Your Story podcast.Mix? What the heck is Johnzelle Anderson's mix story? It won't take too long for you the listener to figure out why Johnzelle chose the title Mixtape for his new book.Johnzelle is a therapist. But he's other things too, a mix of things. His new book is told in tracks rather than chapters. I once made mixtapes and the tracks were usually congruent in other words, in harmony with each other. But, other mixtapes, not so much. As Johnzelle shares his story you'll see why Mixtape is such a great title. The podcast and book will take you on a journey which charts Johnzelle's personal growth, his coming -of-age and how he's learned to help other's steer clear of issues he had to navigate/ deal with.Book:Mixtape
“Every serious follower of Jesus eventually has a moment where they say: Jesus… I trust You, but I don't understand what You're doing.” Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
In our pain and confusion and circumstances, we don't always see Jesus standing right beside us? Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
We are all about ourselves. And no matter how much we strive to say otherwise, we can't help but live for ME. Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
Welcome to Sunday Service Wish you were here! Newsong, Colorado Springs (starts at 10:00am) Subscribe to text updates. Text the words text alert to 94000 Subscribe to emails (bottom of page on newsongcs.com) Listen to podcasts. Keywords newsong foursquare Watch services on Youtube. Keyword newsongcs Follow us on Facebook, Instagram & TikTok keyword newsongcs 3 ways to give to Missions, Disaster Relief, Tithes, or Offerings 1.. newsongcs/com/give 2. Text Giving - text the word EASY to 94000 3. Mail - P.O. Box 75818 • C.S., CO 80970
You know your own body best so why do so many midlife women brush off signs like exhaustion, brain fog, sleep changes, and subtle shifts in mood? When does "it's just stress or hormones" stop being wisdom and start being neglect? This candid conversation names the 10 most common health signals women shouldn't ignore and why tuning in to your body is smart, not overreacting. Keyword: midlife women health. Too often, women in midlife normalize symptoms that can signal real changes mentally, physically, or emotionally. Breaking the pattern of self-dismissal, veteran journalist Natalie Tysdal shares what she's learned covering women's health and living it herself. These are not rare or dramatic symptoms most are everyday signs that get minimized, even as they quietly shape daily life. Beyond offering a simple checklist, this episode guides you through why noticing, asking questions, and naming patterns can be a turning point for your well-being and self-advocacy. What you'll learn: 10 symptoms midlife women should never brush off—including sleep disruption, brain fog, cycle changes, and more How stress, hormones, and lifestyle can interact to shape energy, focus, and resilience Why self-blame and "soldiering on" are so common—and so unhelpful What your gut, mood, and changes in strength or weight may be trying to tell you Clear, compassionate language for bringing these concerns into conversation with your healthcare provider So many women quietly carry a mental list of "it's probably nothing" concerns often putting themselves last in the process. This episode offers validation and pragmatic perspective for every woman who's wondered if she's just overreacting, or if it's time to pay attention. This is a calm, supportive space to trust your instincts and make your own health a priority—no hype, just real context for real life. Links & Resources: https://www.natalietysdal.com https://www.instagram.com/ntysdal https://www.tiktok.com/@ntysdal https://www.facebook.com/NatalieTysdal Listen now and take the next step toward feeling your best. New episodes drop every Monday—subscribe for weekly conversations that support women in midlife. DISCLAIMER: Natalie Tysdal is a health journalist, not a licensed medical professional. The information in this podcast is for informational purposes only and is not a substitute for medical advice, diagnosis, or treatment.
Pastor Matthew Shores...
Discover smart ways to uncover hidden Amazon product and keyword opportunities, track competitor trends, spot seasonal gaps, and find new Amazon business growth angles using Helium 10's Black Box tool.
This time we're diving into something truly under the radar that I've been thinking about for years: the eternal battle of Same SKU versus Other SKU ad sales.A lot of sellers don't even realize one crucial detail. When you look at the revenue column in your ad account, you're not just seeing the sales of the exact product you're advertising. By default, Amazon lumps in the sales of your other products if a buyer clicks on your ad but ultimately chooses a different size, color, or a completely different item from your catalog. In this fresh episode of the PPC Den, we'll break down why this phenomenon can make your ACoS look way worse than it actually is, and how this confusion often pushes advertisers into making bad optimization decisions.We'll see you in The PPC Den!
New AI-powered audio summaries for product detail pages, Helium 10 has a brand-new most-requested feature on Keyword Tracker, and new Kindle advertising placements. We're back with another episode of the Weekly Buzz with Helium 10's Manager of Education and Strategy, Carrie Miller. Every week, we cover the latest breaking news in the Amazon, TikTok Shop, Walmart, and E-commerce space, talk about Helium 10's newest features, and provide a training tip for the week for serious sellers of any level. Amazon's new generative AI-powered audio feature synthesizes product summaries and reviews to make shopping easier https://www.aboutamazon.com/news/retail/amazon-ai-shopping-features-hear-the-highlights Kindle eReader lockscreen ads now available through Amazon DSP https://advertising.amazon.com/en-us/resources/whats-new/kindle-e-reader-lockscreen-ads-now-available-through-adsp/ Seller Café appointments for New Seller Summit are now live https://sellercentral.amazon.com/seller-news/articles/QVRWUERLSUtYMERFUiNHQ0ZXQk5UTE05NVVMRkdM Sign up for the Prime Day Webinar: https://streamyard.com/watch/qUmtMXiMKvKt That wraps up this week's Weekly Buzz. Whether it's AI changing how shoppers discover products, new ad placements opening up new awareness opportunities, or Helium 10 rolling out powerful new automation, the sellers who adapt early are the ones who win. Keep testing, keep optimizing, and keep building momentum. We'll see you next week to find out what's buzzing. In episode 517 of the AM/PM Podcast and Weekly Buzz, Carrie covers: 00:45 - New AI-Powered Audio Feature on Product Pages 03:45 - New Amazon PPC Keyword Tracker Automation 08:27 - Kindle E-Reader Lock Screen Ads Available for DSP 10:45 - Catch Amazon Hijackers Fast with Helium 10 (Strategy of the Week) 13:16 - Seller Cafe Appointments Now Live for Seller Summit 14:23 - Prime Day Strategies Webinar
Join us as we explore the journey of Cathryn Stormont, a seasoned paid media and SEO expert, who shares her insights, mistakes, and lessons learned from over 16 years in the industry. Discover practical tips on campaign structuring, AI integration, and how to turn setbacks into success stories.Key topicsCampaign restructuring mistakes and lessonsImportance of account history and data stabilityUsing AI responsibly in PPC campaignsManaging client expectations and transparencyStrategies for effective campaign monitoring and optimizationQuotes:"Losing campaign history unsettles everything""Turn mistakes into opportunities for growth""Bid on your brand to maximize visibility"Chapters00:00 Introduction to Catherine Stormont03:42 Catherine's Skydiving Adventure06:35 Learning from Early Mistakes in PPC09:22 The Importance of Keyword History12:11 Turning Mistakes into Opportunities15:16 Monitoring Campaign Changes18:02 Applying Common Sense in PPC Strategies18:26 Navigating Account Management Challenges20:01 Learning from Mistakes in Performance Management21:13 Strategies for Recovering from Keyword Performance Issues23:05 The Importance of Honesty in Mistake Management23:28 Common Mistakes in Account Auditing26:27 The Debate on Bidding for Brand Keywords28:26 Leveraging AI Tools Effectively29:47 The Role of Creativity in Digital Marketing31:04 The Value of Discussing Mistakes in the Industry36:55 Outro.mp3ResourcesCathryn Stormont's Website - LinkedIn Profile of Cathryn Stormont PPC Live The Podcast features weekly conversations with paid search experts sharing their experiences, challenges, and triumphs in the ever-changing digital marketing landscape.Join us for PPC Live eventJoin us on SlackSubscribe to our Newsletter
We welcomed St. Louis native and insanely talented Lizzie Weber into the studio, and for a brief, shining moment, things felt like a real, professional music interview… and then we immediately derailed it with debates about Radiohead fans and whether anyone should ever call an album “the most important record of your lifetime” without being legally required to explain themselves.Lizzie's new album Wraiths in the Wake is a deeply personal and atmospheric project centered around the idea of “wraiths”—ghosts, spirits, and the emotional baggage that follows you through life. It's thoughtful, cinematic, and layered… which is exactly why we tried our best not to ruin the conversation. (Keyword: tried.)She talks about working with major collaborators, navigating the music industry as an independent artist, and why pressing vinyl in today's world feels like trying to barter with ancient currency during a nickel shortage. We also get into her musical journey—from dropping out of college and chasing acting in LA, to finding her voice and building her sound from the ground up.Then things take a turn—because of course they do—when Lizzie shares her “musical awakening” moment seeing Radiohead live. This leads to one of the most aggressively unnecessary debates in recent memory, where Riz explains his complicated relationship with Radiohead… specifically their fans. It's the kind of argument that only happens on a funny podcast like this, where passion meets confusion and nobody actually wins.We also go around the room sharing the last concerts that truly “locked us in,” from Nine Inch Nails precision to Tool (yes, again) to Brett Michaels somehow causing a spiritual experience with a harmonica. It's chaotic, it's honest, and it's exactly what you'd expect from a funny podcast that occasionally stumbles into meaningful conversations between jokes.If you're into music, creative journeys, or just listening to a group of adults spiral into debates about bands they both love and resent—this episode of our funny podcast has you covered.Follow The Rizzuto Show → linktr.ee/rizzshow for more from your favorite daily comedy show.Connect with The Rizzuto Show Comedy Podcast online → 1057thepoint.com/RizzShow.Hear The Rizz Show daily on the radio at 105.7 The Point | Hubbard Radio in St. Louis, MO.Woman, 38, Plummets 50 Feet to Her Death at Indianapolis International AirportTourist dies from 'cobra bite' in Egypt after snake charmer let it crawl into his trousersDisney Named in Lawsuit Alleging Bedbug Exposure at Resort HotelNew York woman convicted for throwing dynamite at boyfriend, blowing off his handSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
Pastor Matthew Shores...
#878 Curious about how Pinterest can drive real results for your business — even if you don't have a blog or big following? In this episode hosted by Kirsten Tyrrel, we dive deep into Pinterest marketing with Heather Farris, one of only six global educators officially trained by Pinterest itself. Heather shares her journey from mommy blogger to leading Pinterest strategist, and unpacks how entrepreneurs can use the platform to boost traffic, leads, and sales. Whether you sell physical products, digital offers, or just want more visibility, Heather walks us through everything from SEO and board strategy to pin creation and long-term engagement. If you've overlooked Pinterest or felt overwhelmed by it, this episode will change how you see this powerful “parking lot” for your content! (Original Air Date - 8/25/25) What we discuss with Heather: + Pinterest as a long-term traffic driver + No followers needed for visibility + Differences between search and engagement algorithms + Keyword research using Pinterest tools + Optimizing Shopify listings for Pinterest SEO + Importance of boards and pin clustering + Fresh pin strategies and image variation tips + Using Pinterest for both products and lead generation + Common niches that struggle on Pinterest + Defining success and aligning Pinterest goals Thank you, Heather! Check out Heather Farris at HeatherFarris.com. Follow Heather on Instagram, Pinterest, and YouTube. To get access to our FREE Business Training course go to MillionaireUniversity.com/training. To get exclusive offers mentioned in this episode and to support the show, visit millionaireuniversity.com/sponsors. Learn more about your ad choices. Visit megaphone.fm/adchoices
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