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#043 Joel Greene - The Immunity Code: Reboot Your Gut, Fix Your Metabolism & Halt Ageing
Episode 437th December 2025 • vP life • vitalityPRO
00:00:00 01:02:50

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Joel Greene is a nutrition researcher, biohacker, and the founder and CEO of VEEP Nutrition System, launched in 2009 as the world’s first commercially available nutrition program built around gut-microbiome optimisation.

Over the course of more than five decades in the health and fitness world — beginning with early strength training, experimentation with MCTs and keto diets in the 1980s and 90s, intermittent fasting, and eventually gut-microbiome research — he developed a distinct “immune-centric” model of nutrition and longevity.  Greene is the author of The Immunity Code — a book proposing that long-term health, fat loss, metabolic flexibility, and anti-ageing stem not from arbitrary calorie-counting or rigid diets, but from nourishing and balancing the gut biome, supporting immune function, and using dietary diversity and timing as tools.

His work involves consulting with nutrition companies, programming for corporate wellness, speaking and publishing extensively, and advocating for a paradigm in which gut health, immunity, and metabolism are deeply interconnected.

 > During our discussion, you’ll discover:


(00:12:37) What problems was he trying to solve with his book

(00:17:33) How does the immune system govern the body's inflammatory responses

(00:21:30) Probiotics vs prebiotics

(00:26:18) The validity and accuracy of gut health tests

(00:29:24) How Joel Greene thinks through health challenges 

(00:34:49) Will removing a certain macronutrient group improve your health

(00:42:38) Why is excess iron in the body an issue

(00:47:06) Different sources of lactoferrin

(00:52:22) Using copper to increase iron levels

(00:56:04) The sugar diet

(01:00:46) Any interesting new longevity molecules on the market


The vP life Podcast is brought to you by vitalityPRO, a supplement company based in the UK that provides you with the latest in health, anti-ageing and longevity supplementation. What makes vitalityPRO unique is that it third-party tests every product batch for quality, purity, heavy metals and other contaminants. vitalityPRO’s mission is simple: provide you with confidence in the quality and effectiveness of your longevity supplements that focus on restoring your cellular health.

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Transcripts

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Welcome to the VP Life Podcast, the show

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where we bring you actionable health

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advice from leading minds.

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I'm your host, Rob.

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My guest today is Joel Green, author of

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The Immunity Code and the Way, and a

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pioneer of immune-centric nutrition whose

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work has completely reframed how many of

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us think about metabolism,

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aging, and the gut immune access.

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Expect to learn why excess iron and the

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Fenton reaction may be the hidden driver

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of oxidative stress,

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ferroptosis, and accelerated aging.

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How lactoferrin, food-first strategies,

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and the smart use of tools like IP6 and

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phlebotomy can help control iron while

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supporting gut and immune health.

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And Joel's latest thinking on metabolism,

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muscle gain, sugar diets, and how his

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deep range fits into the bigger picture

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of long-term health and performance.

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Now, on to the

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conversation with Joel Green.

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Good morning, John.

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Thank you for being here

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and joining us on the podcast.

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I know it's early there, so yeah, thank

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you for being flexible.

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Like I mentioned, or fair, this is a

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conversation I've been pretty sacked out

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for a while now, so yeah, like I said,

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bit fanboyish, but what can I say?

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So I suppose I first heard

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about you, learned about you,

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when a lot of people did back when you

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first appeared on Ben Green's Perfels

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podcast, or was that kind of circuit

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2020, 2021, somewhere around there.

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In any case, yeah, like I said, you

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pretty much framed, reframed everything I

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sort of understood about sort of biology,

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and especially as it

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pertains to nutrition.

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And again, sort of, I spent five years in

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textbooks, and then sort of took a long,

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deep sort of soul searching, looked at

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everything and thought, why?

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Anyway, that's me, of course.

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And I know that while there are many on

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our audience who are likely familiar with

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you and your story, there

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are probably those who aren't.

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So yeah, just your backstory, we have

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plenty of time for the details.

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Over to you.

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Yeah, well, first of all,

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thank you for having me.

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It's a pleasure, and

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looking forward to the condo.

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Just kind of briefly, my backstory,

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I just, my mother was, my mother was just

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a failed competitive athlete, I think, in

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the sense that she never really competed,

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but she was hyper competitive.

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And so she always encouraged us or me.

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And so just from the time I was five, you

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know, fitness was part of my life.

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Growing up watching Jacqueline, and then

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I was kind of my family's personal

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trainer, like, you know, trying to get

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him to do calisthenics at age seven, and

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then get them to run around the block.

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And I got into weightlifting about fourth

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grade, where I just took apart a hammock.

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And I just started kind of because my

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brother used to beat me up all the time.

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So I thought maybe if I could do this,

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you know, I could, so I started just

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doing curls, whatever I

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could figure out with these bars.

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And I actually started gaining a little

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bit of muscle oddly, you

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know, like in the fourth grade.

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So and then I wanted to

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be fast in the fifth grade.

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And so I started going to the blacktop

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during the summers and sprinting, because

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I really wasn't very fast.

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And the running craze kind of blew.

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So this is way back.

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This is like way back during the 70s.

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So the running craze kind of bloomed, and

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I got into running, and I could see that

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my quads were coming out as a kid.

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I didn't really

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understand like what that was.

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I just thought it was cool.

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So I was always into it.

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I was always tracking bodybuilding really

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kind of just, I would just say you're

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prototypical consumer, like if you could

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just stamp like, you know, like sycophant

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consumer, that was me.

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And so I was lucky enough to go to high

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school in San Jose, California, where at

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that time during the, I guess it was the

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mid 70s, late 70s, early 80s.

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But a treasure trove of Olympic athletes

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trained at this local junior college, you

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had the gold medalist in the discus, Mack

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Wilkins, you had Bruce Jenner, you had

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you know, all these

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Olympic athletes training there.

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And there was a spillover to my high

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school because my high school coach was

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himself an Olympic level pole halter, who

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was pretty renowned in the

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area as the best vault coach.

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And so all the Olympic athletes would

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come over to train there.

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So we had quite the quite the advanced

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weight training program.

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I mean, it was it wasn't bodybuilding.

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It was it was Soviet style power, Soviet

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style training, like like cleaning jerks,

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and you know, stuff like that.

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So and my big thing was, yeah,

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yeah, exactly.

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Yeah.

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My big thing was I had a growth spurt

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right about one of us right about age 12.

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And I shot up to six

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to by the time I was 12.

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And I was 160 pounds.

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So I was so skinny.

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I was I was I was I was embarrassed to go

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to school, like because I was so skinny.

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So I always wear long sleeve shirts,

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because I didn't want

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anybody see how skinny I was.

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And so I just started going to the gym

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every night and just doing

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what the power lifters were doing.

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So I was just doing cleaning jerks, you

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know, like, like nonstop.

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And it just became part of my life.

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So I became your

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prototypical bodybuilding.

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Sick of fan.

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Yeah.

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And I was just I would devour everything

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and anything in the magazines.

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And, you know, starting in the early 80s,

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when Tom Platts exploded, and, you know,

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just I just tracked everything.

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And back then, the interesting thing was,

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the way that information was

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disseminated, you didn't have

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influencers, which you

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had was the magazines.

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And then the magazines kind of promoted

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who they wanted to be stars.

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And so you had this

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controlled information source.

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And so you had this this thing of like,

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you know, well, how do

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I get to look like you?

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What do I have to do?

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I'll do whatever you do.

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And of course, it was

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all a giant deception.

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It was, you know, the huge scam, because

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all these guys were on steroids.

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And they just lied their butts off about

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it, like literally everybody.

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And so the thing was like, you could

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never actually look like that.

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Okay, you might get close, you might look

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pretty good if you're genetically gifted,

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but you're never gonna be like that,

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because they're there, they've got a

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secret you don't have.

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So I went down that track as a consumer.

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And because I was so voracious as a

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reader, whatever came

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out, I would jump on.

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So like, I remember, I think it was 86,

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there was a supplement that

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came out called hot stuff.

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And the marketing was

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very different back then.

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Like back then, the marketing was they'd

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write an entire page, and

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you would read the whole page.

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You would go long from copy.

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Yeah.

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And just get sucked into it, you know,

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and so out came this supplement with

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boron and, you know, wild game and you

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know, all of these things that a lot of

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them actually worked like yo and vine.

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And stuff.

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And I just started whatever came out, I

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would just use so that led into that led

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into MCTs kind of in the late 80s, when I

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was in college at UCI.

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And then in the early 90s, the big big

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thing for me was the

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meal replacement craze.

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So metrics came out.

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And I didn't,

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I wasn't that was the the original sort

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of meal replacement in the same space,

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wasn't it just about

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well, it was it was the first

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that really thought about it.

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So that so prior to that, what it did was

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it changed the category.

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So prior to metrics, they were called

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metabolic optimizers.

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And the leader was champion nutrition,

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and other guys that were

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sticking MCTs in theirs.

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And then Dr.

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Scott Conley came out.

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And he really thought his thing through

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and he really knew

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what he was talking about.

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So his big thing was he stuck in

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glutamine and lactoferrin in metrics.

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And that was light years and I had a few

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conversations with him actually, because

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he owned a gym right where I lived.

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And so and he would work the front desk,

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like an MD working

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the front desk at a gym.

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So I just I would go in and after

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training, just kind of ask

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him like, Hey, does this work?

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And he would just he would go down the

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bio babble role, and I would just kind of

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sit there kind of glazed over like maybe

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picking up every hundredth

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word he was talking about.

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But so that led me down this road of a

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lifetime of doing that stuff.

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Which is ironic, because today where I

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sit is I you know, I go to the gym once

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or twice a week, I do that

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stuff once or twice a week.

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But it's not the main thing I do.

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And it's certainly not the thing that I

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think keeps you young.

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I think it does the reverse, I think it

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destroys the body over time.

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But the irony of that was that now that's

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where all the doctors are.

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So they've all adopted meat headology.

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They've all adopted the the

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the pattern of of, you know,

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they call they don't call it 70s

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bodybuilding, they

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call it strength training.

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Oh, no, you got to do strength training.

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Yeah, it's a Gabriel lines of the world

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that sort of approach.

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Yeah, when you break down what they're

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talking about what to do, well, what is

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it I should be doing?

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Well, strength

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training, what's that look like?

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Oh, well, see, here's a lat row.

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Oh, the thing we were doing in the 70s.

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Yeah.

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Okay, here's a behind the neck press.

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Yeah, yeah, that one too.

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What else?

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What else you got a T bar row?

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Yeah, yeah, that was in the 70s too.

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So bodybuilding.

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So the answer is bodybuilding.

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No, no, it's not because I

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tell you, I've been there.

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It's not.

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So about 2006, I kind of culminated for

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me, I was, I was running a company, we

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had our revenue had just shot up to like

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25 million in just

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two years from nothing.

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And it's not bad.

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Yeah.

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And, and like a lot of entrepreneurs, I

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was working crazy hours of crazy stress.

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And for me, the kind of hands on

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discovery was that that stuff only works

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when you're in the fitness bubble.

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Yeah, if you get out of that bubble, and

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it doesn't work that great.

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And I just I got really well, the

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interesting thing is, um, I was training.

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So I was huge.

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I mean, I was, I was just big, I was

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about 260 pounds, I was fat.

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So I was both hugely

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muscular and fat at the same time.

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Super strong muscles, like but fat.

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And so I kind of came out of that,

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rethinking things and that led to where

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I'm at today, basically.

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Thank you for that.

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That was, that was an amazing story and

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one I've heard before.

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And yeah, just speaks volumes to what

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you've been able to sort of develop over

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the years consequently, because I know

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you've fundamentally just worked all of

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this out, sort of on the back end of

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different life

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experiences that you've had.

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And I know you've obviously talked about

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this a lot on various podcasts, including

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Mark Bell's one, I believe, when you

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originally, I think was a Daisy Carter

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protocol that you originally did, and

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then you sort of got down to what was it,

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single digital body fat, and he was

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completely sort of just in disbelief of

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this fact at the time.

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Is that more or less correct?

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Yeah.

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So basically it was, it was 2007.

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I had been, I had been at it for about a

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year, just whittling down all the fat I'd

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gained during that period, working.

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And I was about 229 and pretty, pretty

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muscular, you know, but,

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but still kind of not peeled.

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And then I did the, I

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did the Daisy Carter.

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And that was probably for me, the single

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most shocking body fat thing in my entire

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life ever still to this day, because I

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went from 229 to 212 in seven days.

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And then I went into a local place that

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measures your body fat in water.

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And it was, it was either between six and

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seven, it was pretty low.

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And that was, that was after, that was

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after pigging out, like for several days

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coming off the day because the Daisy

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Carter will make you insane.

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So coming off that I was just eating

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pizza or whatever I get.

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So I'm sure I was probably lower.

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And then there was just a, I was in a

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tech stream with Mark Bell and quest

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owner Ron Pena and Carl Carlin or and

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Mark, I was telling about that and Mark's

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like, I don't believe you prove it.

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So I just, I just sent him the, the PDF,

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I called the place up and said, Hey, I,

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you know, can you give me the PDF?

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And they sent it to me

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and I just sent it to Mark.

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And so fair.

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Anyway, perfect.

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Okay.

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So what I really want to do

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today is to dig into iron.

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I know that people are always

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interested in the sugar diet.

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And to be honest, that excites me about

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as much as watching paint dry.

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We'll keep the, we'll, we'll

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aim to keep the people happy.

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And maybe we can chat

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about that a little later on.

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To start with, I think it would be, maybe

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it would be best if we just step back a

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little to discuss the

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immune system as a whole.

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I know that's fundamentally the lens

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through which you sort of view metabolism

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and health in general, and just to

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provide some context, maybe

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the rest of the conversation.

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Now, obviously, I started off with with

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the immunity code, your first book, which

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for anyone who's not read

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it is, is absolute gold.

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So yeah, get a copy.

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Now, of course, I know from here, we

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could go into 30 different directions,

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all of which are fundamentally going to

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be come back to the fact that by

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regulating the immune system of the gut,

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you can make a dent in a lot of health

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conditions and challenges.

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So yeah, I'll ask the lazy question,

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which is, what problems were you trying

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to solve with the immunity code, and

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subsequently, your follow up the way?

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The primary problem is really the problem

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everybody runs into, which is, there's a

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force pushing against you over time.

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Loosely, we could describe that as aging.

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But the big picture of that is that it

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has multiple pathways for dysregulation.

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So, you know, one is that body fat is

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going up, senescent cells are going up,

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inflammation is going up,

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mitochondrial density is going down,

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muscle is going down, body fat

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characteristics are shifting into a

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pro-inflammatory pattern, all kinds of

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all kinds of things are

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happening all at once.

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And everybody faces these problems

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collectively, they haven't really been

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well defined as a group to say, okay,

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well, let's make a list and let's start

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with number one and go down the list.

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Let's do that.

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And even if they were made into a list,

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the problem you're still going

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to have is the issue of time.

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The average person, so the big secret in

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the fitness bubble is

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just two hours a day.

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I mean, no one's ever

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going to tell you that.

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But that is the C, if you were to follow

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anybody around, you're going to see

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they're putting into it.

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That's like two hours a day.

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That's like, who has that?

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Who has two hours a day?

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Yeah.

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So that's the problem.

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The problem is you've got

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this problem of decline.

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And then the only solution that you've

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been given to solve it is, oh, that's no

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problem, just increase time.

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Just increase time, that'll solve it.

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That doesn't work for most people.

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So for me, the issue really was just

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coming down to economy and looking at,

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well, if we only had a couple of minutes

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a day, what would be the most important

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things that we could hit

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in a couple of minutes?

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What would be the 80-20?

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It wouldn't be doing barbell curls.

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That wouldn't really be the thing.

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What would it be?

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And when you begin to go down that road,

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where you're going to wind up at is the

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intersection between the immune system

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and several different organ sets and

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systems in the body.

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One way or another,

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you're going to run into that.

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So fundamentally,

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let's start with oxygen.

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Just getting oxygen into the body.

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What's happening with most people with

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age is that the

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airway begins to collapse.

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The tissue at the back of the throat

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begins to push into

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the back of the throat.

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So you're getting apnea

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events during sleeping.

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You're getting desats during sleeping.

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You're getting stabilized

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hypoxia as a result of that.

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And that alone will sink the whole ship.

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That alone will kill you.

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Just that.

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Hypronorpha levels, right?

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Yeah.

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That alone will sink the entire ship.

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We don't even need to look any farther

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than that if you were going to just start

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with, well, what's number one?

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That's number one,

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really, if you think about it.

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And that converges on a key mechanism

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that essentially is a switch, helping the

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body flip its metabolic state between

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oxidative respiration

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and then glycolysis.

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When you look at that, and

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that master switch is HIF-1,

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hypoxia-inducible factor one, it

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regulates not just the general switching

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between metabolic states, but

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tissue-specific and cell-specific.

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And when you get cell-specific, it gets

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very, very interesting and compelling.

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So when you begin to look at the effect

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of that on immune cells, it can be

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massively beneficial or

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catastrophically disastrous.

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It just depends on the tissue and what.

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But in terms of our coming back out of

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the deep dive into what's our simple fix,

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it's let's fix that first.

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Why don't we fix that?

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And that converges on the immune system.

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And so that whole line of thinking, that

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way of thinking led me down this road.

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Okay.

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Fair enough.

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And then just specifically, what about it

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is, I suppose, just to maybe elaborate

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that a bit more for the audience, how

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does the immune system then regulate and

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govern the subsequent inflammatory

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responses in the body that then drive so

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much of this dysfunction at a level?

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So it's a big question.

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One of the key functions of the immune

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system is to sort of allocate when to use

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what we would call weapons.

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Okay.

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One of the weapons the immune system has

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is to induce an inflammatory state.

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Now that can be massively beneficial in

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the case of an infection, because you

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want to kill the infection.

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So the immune system can ramp up and it

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can produce free radicals and shoot

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superoxide through immune cells and

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pathogens and invaders.

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And that's a good thing.

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That's not such a good thing when you

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have billions of cells that have

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stabilized into a senescent state and are

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essentially trafficking out signals to

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recruit the immune system.

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That's not such a good thing at all.

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Because then what happens is the immune

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system sort of acts like an echo chamber.

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And it propagates these signals across

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the entire body and recruits more and

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more and more resources into dealing with

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this problem that it thinks is an injury,

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but it really it's just getting old.

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So what it is, would that be a case where

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maybe somewhere like excess fasting could

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actually be an issue,

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an actual detriment?

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Yes.

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Yes, because this gets to the

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body needs to balance itself.

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It needs a balance between growth

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pathways and degradation pathways or

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however you want to put it, you know, the

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body's autophagic pathways.

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There needs to be a

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balance between the two.

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And when you see an excess of either one,

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you're going to see some kind of

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pathology either way.

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So if you see too much growth, you're

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probably going to see cancer.

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If you see too much, too

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much autophagy, too much

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action with respect to protein

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degradation, then

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you're going to see issues.

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So

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that's just homeostasis.

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So that's an interesting thing.

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I don't want to spend

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too much time on this.

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But homeostasis is such a simple concept.

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It's so simple to get this.

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It's just simply

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balance.

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Like the thing needs to be balanced.

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You can't be too much on either side.

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Okay.

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That's so simple.

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And you wouldn't know it, listening to

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the world of influencers nowadays,

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because it's all polarized thinking.

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It's all, "Oh yeah, fasting's only good.

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Meat is only good.

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Saturated fats is only good.

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Carbs are only bad."

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You know, there's this polarity of

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thought that to me reflects a bigger

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problem, a problem of thought.

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But the fact that such a simple concept

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is missing from the picture and it's

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essential just blows my mind.

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Yeah, I know it is interesting that you

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mentioned that actually.

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I mean, there are sort of, and I'll just

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use it in the literal sense, sort of very

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left and far and right leaning

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individuals just sort of on

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the vegan and the carnival side.

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And it's interesting just watching your

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poor saladinas and such over the world

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with these sort of extreme views.

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And what I've just found over the years

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is that a lot of these people with these

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extreme views on nutrition generally tend

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to fall back to the middle, whether it's

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reintroducing honey or carbohydrates, or

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what have you, or reintroducing meat.

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So many, yeah, just to sort of maybe sort

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of build on your point.

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Balance is key and it's just interesting

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to note that people with sort of extreme

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views ultimately do come back to sort of

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this fairly centered state.

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And Joel, I'd like to sort of maybe take

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a little bit more into that, into the gut

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side of it quickly before we carry on.

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Now, I know obviously sort of the gut

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being sort of the hub of the immune

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system to an extent anyway.

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A lot of your work sort of that you've

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put out there revolves heavily around

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sort of rebuilding the gut and that you

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aren't generally speaking a fan of

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prebiotics and that you would,

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probiotics, excuse me, that you generally

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sort of prefer prebiotics as a whole.

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Obviously, again, within the industry and

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there's always been a

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push for probiotics.

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And I'm in two months about that.

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I deeply admire the work of Dr.

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Mark Ruschow, who you might know of, and

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he is a very sort of probiotic

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forward-facing and he's very adamant that

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they are effective at helping

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to modulate the immune system.

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I know at least having listened to other

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podcasts you've done that you share,

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maybe someone to have a

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different take on that.

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Could you sort of just guard us through

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your thoughts on probiotics versus

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prebiotics in general as it pertains to

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the gut and maybe the

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immune system more broadly?

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Well, the merger point

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in the road is bacteria.

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That's all we're talking about is taxa

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and representation of species.

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That's what we're talking about.

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The question is, how do we get there?

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That's the only thing

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we're talking about.

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So to say that probiotics work is to say

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that certain taxa can

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exert beneficial effects.

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Duh.

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I mean, we all know that.

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Everybody knows that, right?

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So it's just how do we get there?

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What's the optimal way to get there?

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Keeping in mind not the

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short term, but the long term.

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And that's a problem.

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That's a big problem though, because

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we're in an industry

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that equates results to...

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We're in an industry that has no regard

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for the impact of the most important

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variable, which is time.

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It doesn't exist.

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Time does not exist.

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You listen to the most high level

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influencers and they'll talk as if the

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outcome we get now is going to be the

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outcome we're always going

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to get because we got it now.

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And again, that's going back to this

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paucity or poverty of

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thinking that is just...

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It's similar to homeostasis.

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When you begin to inventory, why aren't

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you taking this into account?

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There's no good reason.

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There's no good reason.

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Only stupidity.

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So the issue becomes,

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okay, so there seems to be sort of a

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youthful profile that more or less seems

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to be consistent among young people.

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And you see a lot of Bifidobacteria,

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healthy representations

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kind of in this respect.

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And it's quantifiable to some degree.

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So the question is, how

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can we proximate that?

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How can we get there?

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I'm not against probiotics at all.

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I think that they can

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be incredibly helpful.

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I'm just against their indiscriminate

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use, particularly among consumers,

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because as soon as you tell consumers,

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hey, our clinical results showed an

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improvement of blah, blah, blah, blah,

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blah, taking our probiotic.

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First, they're probiotic.

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Yeah.

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Well, then they become chiclets.

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They become like M&Ms

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or just gummies.

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They become like just candy.

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And the net result of that, once we

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insert the variable of time, is that

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you're probably going to do more harm

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than good long-term.

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A lot of SIBO problems now are the result

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of a lot of probiotic usage going back.

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And so the question becomes, what's the

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optimal way to get what we want?

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And the really

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surprising thing is how powerful food is,

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to completely, completely retune the gut

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in very short periods.

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And this is empirical in its nature.

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Going back to 2009, there are studies

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that show that you can rapidly recolonize

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the gut in just a few days with food.

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So with that in mind,

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as a generality, if food is so powerful,

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where do we need probiotics?

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And that becomes a

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medical issue then, I think.

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And I do believe the rightful home of

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probiotic strain usage is probably with

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practitioners who can look at something,

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look at a GI map and say, "It seems like

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maybe if we added this

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strain for a few weeks."

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Now that, to me, is really intelligent.

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That's really smart.

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And I think that's kind

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of the right way to do it.

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It's just really a question of what's

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going to do more harm than good.

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And it's probably the

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indiscriminate use of probiotics.

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Fair enough.

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Just speaking of those tests quickly,

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there are a bunch of them

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out there, various labs.

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Well, as you

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mentioned, there's the GI map.

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There are a bunch of them.

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What do you think about their validity

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and their specificity?

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Again, now that we're just on this track,

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I'd just love to get

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your thoughts on this.

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You often hear practitioners on podcasts

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talk about the fact that they sent off

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two samples of the same piece of stool to

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the same company, and they would have got

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back completely different results on

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their GI map or their whatever.

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I mean, the gut is your

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game, let's be honest.

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Do you have any thoughts

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on GI testing in general?

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Do you think it's there yet?

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Or is it still a bit of a north star

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we're trying to get to?

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I think it could be useful.

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I think it could be useful.

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I think the mistake is to see it as

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the gospel.

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I think it's a mistake to

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calcify it into like, "Oh, ha!

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Well, this is me.

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That's it.

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Nothing more to know."

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What I never hear are seldom, very

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seldom, what you'll hear is a breakdown

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of mechanistically,

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"How'd you get that answer?"

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When you begin to ask,

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you'll get crickets because

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I've found a lot of

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practitioners don't know.

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They actually don't know

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how they wrote that answer.

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When you begin to break that down, what

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you find is that many of

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those tests rely on a single gene.

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They're looking for one gene, the 16RS

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ribosomal RNA, and they have a database

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that they're matching

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that gene up against.

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The outcome you're getting is only as

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good as your database.

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Then there are several

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problems within that.

Speaker:

We could list what those problems are,

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but just suffice to say that a good

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example is acromancia.

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I think in the last couple years, there

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have been several new

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strains discovered of acromancia.

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One of the most common things that I hear

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is, "Oh, I did a GI map

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test and I have no acromancia."

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My response to that

Speaker:

usually is, "Yeah, you do.

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They just can't test for it."

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"No, how do you know that?"

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"Because you'd be dead,

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probably, if you didn't."

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Yeah, it's more than just

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meanest failure in existence.

Speaker:

The truth is there's probably dozens of

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strains we haven't yet found.

Speaker:

To get a GI map test back, and it says,

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"Oh my gosh, I have no acromancia.

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I better go start taking

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pendulum or some tool like that."

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Well, again, it's like,

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"Mm, yeah, you probably do."

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It's just the tests

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don't have that in there.

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They don't have these undiscovered

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strains in the database.

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That's the answer.

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Fair enough.

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I often think that this is a sort of

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wildlife-ure approach.

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It reduces it to the bare basics and then

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just sort of builds upon that instead of

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trying to sort of isolate variables that

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we don't have access to.

Speaker:

I really like the way you frame and

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conceptualize things.

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To be honest, I'm not very bright.

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I doubt that.

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I seriously doubt that.

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I tend to just look towards using

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frameworks to try and understand complex

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topics and data sets.

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Then, yeah, maybe it's just a result of

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looking at information from that point of

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view, but I always end up trying to find

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flaws in a given model, a

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stress test the best I can.

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Well, to me, I can then form an opinion.

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I can then try and find

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limitations based on that

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opinion relative to that model.

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I can then sort of make cross-reference

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things and try and come to some sort of

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logical conclusion,

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whether it's correct or not.

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I know that's a fairly convoluted, but

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it's kind of served me well.

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Of course, it doesn't mean I'm right.

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It's just the way I think through things.

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I'd love to sort of explore the way you

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think through things and whether you

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think there are any sort of limitations

Speaker:

to the model that you've put forward when

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it comes to helping people work through

Speaker:

various health challenges.

Speaker:

I'm sorry, that was probably 10 questions

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in one and very convoluted, but I'm sure

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you follow the logic.

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Yeah, no, I like it.

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I like it.

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I kind of approach things

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from a macro perspective in that

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there's a bit of a dichotomy with respect

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to how do we get the answer?

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People always want to

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know, what's the answer?

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What's the answer?

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We're led to think that the

Speaker:

individualized factors just are the

Speaker:

answer, that they're so overpowering that

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the only way that I can know me is I got

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to go do all these tests that tell me me.

Speaker:

Just in my experience, what I have found

Speaker:

is it's the generalities

Speaker:

where all the horsepower is.

Speaker:

If you take five massive generalities,

Speaker:

like let's take vitamin D levels, let's

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take hypoxia, let's take the microbiome,

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and you see where I'm going with this.

Speaker:

You can just kind of go down this road of

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things that are just generalities.

Speaker:

Then you take someone who their metabolic

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state is and optimal

Speaker:

isn't what they want it to be.

Speaker:

We just apply the

Speaker:

generalities to them consistently.

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What you will see are these massive

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game-changing improvements

Speaker:

that are life-changing.

Speaker:

That's not getting to the level of like,

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"Well, I see you're

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missing a genetic snip for it."

Speaker:

It's not getting to that level.

Speaker:

It's just taking the generalities.

Speaker:

So I generally tend to approach things

Speaker:

like, "Let's fix the low-hanging fruit.

Speaker:

Let's go after that and

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then see where we're at."

Speaker:

Then usually with what's

Speaker:

left, that's called medicine.

Speaker:

Usually with what's left, now we're

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talking about things that don't fit the

Speaker:

generalities, things that require very

Speaker:

types of specific tests.

Speaker:

That's really for doctors to do.

Speaker:

I think that's great.

Speaker:

I think that's where it should be.

Speaker:

But all that to say, it's that what we're

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missing here is that in the simple

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things, the big things, the generalities,

Speaker:

there's so much horsepower, so much power

Speaker:

for change that you should really,

Speaker:

collectively, it makes sense to take a

Speaker:

look at those things first

Speaker:

and then see where we're at.

Speaker:

That's just how I approach things.

Speaker:

The other piece of the

Speaker:

equation for me is math.

Speaker:

I've just found historically that

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everything boils down to math.

Speaker:

Everything boils down to

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the law of large numbers.

Speaker:

Everything boils down to

Speaker:

percentages and probabilities.

Speaker:

That lends me to think in a couple

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different directions.

Speaker:

One is that it's very difficult to know

Speaker:

anything with certainty.

Speaker:

It's just very difficult to know it, but

Speaker:

the mind loves certainty.

Speaker:

The mind loves,

Speaker:

"Ah, yes, this is it."

Speaker:

You really see that in the social media

Speaker:

sphere where you have influencers that

Speaker:

speak with salesman-like certainty on

Speaker:

topics they don't actually understand.

Speaker:

Then a few years down the road,

Speaker:

completely revise their stance.

Speaker:

That's called a learning curve.

Speaker:

What would serve them and everybody else

Speaker:

better is to just begin to introduce some

Speaker:

maybes in there and some mightbees and

Speaker:

possibilities rather than

Speaker:

speaking with abject certainty.

Speaker:

We're always up against degrees of

Speaker:

probabilities, probabilistic space.

Speaker:

We can begin to say things like, "Well,

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we're creating very strong probabilities

Speaker:

that we might get the

Speaker:

outcome that we want."

Speaker:

I'm just really just cloaking math talk

Speaker:

by talking like that, but

Speaker:

that's how I approach things.

Speaker:

Okay, perfect.

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Thank you very much.

Speaker:

I just had to ask.

Speaker:

I love the way you build on

Speaker:

the data that you've always gotten.

Speaker:

It's just so elegant the way you are able

Speaker:

to frame and construct relationships.

Speaker:

A bit of a selfish question, but anyway.

Speaker:

I recently had the chance to chat to Dr.

Speaker:

Thomas Seafreet.

Speaker:

I'm sure you're familiar with, and for

Speaker:

those in the audience who aren't or maybe

Speaker:

haven't listened to that podcast, he's

Speaker:

currently championing the idea that

Speaker:

cancer is fundamentally a metabolic and

Speaker:

mitochondrial disease.

Speaker:

That's by regulating glucose metabolism

Speaker:

in some way, shape, or form, you can

Speaker:

essentially starve cancer cells

Speaker:

selectively and reduce the need to some

Speaker:

extent for additional or

Speaker:

adunctive cancer therapies.

Speaker:

Obviously, his work is based in the

Speaker:

backbone of what Otto Warburg did, I

Speaker:

think probably around a century ago now.

Speaker:

In any case, he's obviously a big

Speaker:

proponent of

Speaker:

carbohydrate reduction in general.

Speaker:

Unfortunately, we ran out of time.

Speaker:

I wasn't really able to ask him about his

Speaker:

thoughts on how different types of fatty

Speaker:

acids, polyunsaturated fatty acids,

Speaker:

saturated fats, et

Speaker:

cetera, might affect his model.

Speaker:

I'm not a cancer biologist.

Speaker:

I'm strictly the imagination, but when

Speaker:

you look at his glucose ketone index,

Speaker:

which I know he's now making more

Speaker:

publicly available for people to

Speaker:

understand their own metabolic health,

Speaker:

it's very much

Speaker:

focused on the macro level.

Speaker:

It doesn't seem to really

Speaker:

focus on the fatty acids.

Speaker:

I know this goes into the order of

Speaker:

operations side of it as well.

Speaker:

But what do you generally think about

Speaker:

when you start talking about fatty acids

Speaker:

in particular and the

Speaker:

immune system in the gut?

Speaker:

What do you think about

Speaker:

this approach in general about

Speaker:

removing one macronutrient, be it

Speaker:

carbohydrates, to

Speaker:

improve the health of a system?

Speaker:

And then, yeah, if you've got any

Speaker:

thoughts on maybe how we overly rely on,

Speaker:

I suppose that's the C to all debate.

Speaker:

Let's leave that if you, yeah, the first

Speaker:

part would be great.

Speaker:

Again,

Speaker:

the variable that's missing

Speaker:

in my opinion would be time.

Speaker:

So you could inject that question in

Speaker:

under the eugis of the variable of time

Speaker:

and say, "Hey, what about for a little

Speaker:

bit of time if we

Speaker:

restrict this macronutrient?"

Speaker:

We might see some very significant

Speaker:

improvements depending on

Speaker:

what we're talking about.

Speaker:

However, when you begin to look at the

Speaker:

long term, which is what

Speaker:

we always have to look at,

Speaker:

there are a couple of magnetars that are

Speaker:

always pulling at us.

Speaker:

Okay, one of them is insulin.

Speaker:

And it's very difficult to obtain real

Speaker:

and lasting health without insulin

Speaker:

functioning optimally.

Speaker:

Really, you're not going to.

Speaker:

That's just the answer,

Speaker:

unless insulin's functioning.

Speaker:

Because it's so pleiotropic in its

Speaker:

nature, it affects so many things.

Speaker:

So the problem you get into with that is

Speaker:

that in order to properly stimulate

Speaker:

insulin, there's an inventory or a suite

Speaker:

of hormones that need regular stimulation

Speaker:

through foods, through macronutrients.

Speaker:

And they oppose each other.

Speaker:

So I've spoken quite a bit about the

Speaker:

example of glucagon

Speaker:

because it's kind of in our face.

Speaker:

But it's a fun one to pick on because

Speaker:

glucagon has been the

Speaker:

hero of a low carb movement.

Speaker:

And if you go down that road far enough,

Speaker:

what you'll see is that actually by

Speaker:

overstimulating that, and by not

Speaker:

stimulating other hormones, particularly

Speaker:

insulin now to connect in through key

Speaker:

types of carbohydrates, you

Speaker:

actually get insulin resistance.

Speaker:

And then the result of

Speaker:

that is hyperinsulinemia.

Speaker:

So sort of briefly in the muscles, one

Speaker:

might argue though, that the macular

Speaker:

glucose bearing effect,

Speaker:

what would you say to that, that long

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term ketosis drives this peripheral

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insulin resistance, but it's typically

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just within the muscle.

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Yeah, I would say that probably doesn't

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hold up to scrutiny for

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some very good reasons.

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One is that

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in order...

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So I did a debate with

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Sean Baker that never aired.

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And I really...

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I was going to ask about that.

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Yeah.

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I really crushed this particular aspect

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of it, which was to look at like, is

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long-term ketosis really even something

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we'd want to consider?

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And I don't know how deep you want to go

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down this road because it's quite

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complex, but I would offer no for lots of

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reasons that nobody's talking about, but

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just to kind of sum it up.

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So long-term ketosis, we're going to need

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a fuel source for that,

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which is oxaloacetate.

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So you're going to need

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that for a subtle CoA.

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Normally your source for oxaloacetate is

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glycolysis, but what's going to happen is

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that when you're doing oxaloacetate for

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extended periods, you got to switch to

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the liver to produce it for you.

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Okay.

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Well, the issue that you get into there

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then is you get a mismatch between the

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TCA cycle and fatty acid oxidation.

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So you begin to get kind of an incomplete

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oxidation that happens.

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And then that incomplete oxidation will

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lead to a spillover of very specific

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types of acyl carnitines into the serum.

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And some of these moieties or very

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distinctive types of acyl carnitines are

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going to drive

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systemic insulin resistance.

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And it's all a result of basically you're

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creating this backlog within the

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mitochondrial membrane of transporter

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mechanisms that aren't, and then that

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spills over into the serum.

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Yeah.

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And so, and it really gets to

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is the liver equipped to supply a

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glycolysis to the entire body on an

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extended basis, you know,

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to every cell in the body.

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And I think we can make a pretty good

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case that it's not that, that, you know,

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you begin to see over time, these

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disparities between fuel sources and

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things that are

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required to sustain this state.

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And then you begin to

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see a buildup of things.

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So again, the missing variables time, if

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we will just insert time as the master

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framework and then begin to accept the

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notion that this is a dynamic

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system, not a static system.

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And that is the massive logic error in a

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lot of these arguments is that the

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assumption is we're

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dealing with a static system.

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It isn't.

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What it is, is it's a system that seeks a

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dynamic equilibrium.

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That's what we're talking about here.

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And so in a system that

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seeks a dynamic equilibrium,

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you can get in my book, the way I talk

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about this, I call it the forces of time.

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It's accumulation.

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You can get an accumulation of something.

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You can get a degradation of something.

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You can get a compensation of something.

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You can get attenuation of something.

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So all of these forces

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of time begin to play out.

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And in the case of oxaloacetate,

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acylcarnitines, and, you know, all of

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these sort of intermediates required to

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sustain ketosis over time, you begin to

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see a buildup of certain things that you

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can make a very good case will drive

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systemic insulin resistance.

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And in some cases,

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perhaps it's not recoverable.

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Okay, I'm going to relisten to that,

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especially that last part.

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Thank you for that.

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That's definitely a sort of solidified a

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few thoughts in my head.

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Joe, I'd love to talk

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about metabolism all day.

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I really would.

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And maybe I can convince you to join me

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for another episode at some point.

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A bit deeper into that.

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But I think just of the sake of brevity

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and time, I'd love to

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sort of jump into iron.

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Young Gut Ultra, I know that's a new

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product you've launched.

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It's exciting.

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And it looks to solve the problem of sort

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of excess iron brought up in the body.

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Now I know there's a

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lot to dig into here.

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And maybe we can start with why excess

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iron is an issue, maybe from the

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perspective of the Fenton reaction, maybe

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it's a sort of a decent

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sort of lens to view it from.

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But yeah, why did you sort of choose to

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focus on iron as an issue with developing

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that product, I suppose?

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Yeah, it wasn't really so much out of a

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need to deal with iron.

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It's more out of a need to deal with very

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specific problems that are intractable

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for everyone over time.

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One of those problems has to do with the

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impairment and degradation of the

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peroxisome membrane within the

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intracellular space.

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So if you're in the audience and you're

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not familiar, peroxisomes are an energy

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organelle within the cell.

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And they're kind of

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co-partners with the mitochondria.

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There's this notion that the mitochondria

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kind of exist at the top of the hill, you

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know, by themselves.

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And it doesn't really

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hold up to scrutiny.

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It's more like a co-emperor sort of

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situation at the top of the hill where

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the peroxisomes of the mitochondria form

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a single system and they very much peddle

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the bicycle together.

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So the issue you get into with age is

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that there are these transporter proteins

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in the mitochondrial

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membrane called PEX proteins.

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And they begin to malfunction.

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And so part of the function of the of the

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peroxisomes apart from energy production

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is to basically dismutate hydrogen

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peroxide down into water.

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The hydrogen peroxide by itself can be an

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extremely important signal molecule as a

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free radical within the cell.

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It's very much

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involved in insulin signaling.

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The problem is that if you get too much

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of it, it really kind of becomes maybe

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just by again by virtue of math, by

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virtue of sheer weight and sheer numbers,

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possibly the most detrimental free

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radical in the body.

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Now on an individual basis, it's not

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nearly as damaging as something like the

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hydroxyl radical or superoxide when

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superoxide goes wonky.

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But because there's so much

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of it, it's really a problem.

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And so what happens with age is that you

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get a buildup of hydrogen peroxide in the

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cell and at the same time we tend to

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build up iron with age.

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That's bad.

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That's very bad because hydrogen peroxide

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can mediate through iron a reaction

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called the Fenton reaction that produces

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a very damaging free radical

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called the hydroxyl radical.

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And you get a lot of you get a lot of

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cell damage from this.

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You could make the whole argument that

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that's where your

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gray hair is coming from.

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Is that it tends to torch the

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polyunsaturated fats

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in the cell membrane?

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Is that right?

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Yes.

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In addition to, well, in particular,

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the mitochondrial membrane

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takes a lot of damage from that.

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So that's a huge problem that needs,

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we're all going to face.

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And like, let me just make it simple.

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Everybody wants to

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fix for their gray hair.

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What's the fix?

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We got to fix this problem because it

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isn't just your gray

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hair that it's affecting.

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Your gray hair is just a marker for how

Speaker:

fast the damage is progressing.

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So that's a big problem.

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And that was the motivation behind it.

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The other thing was that when I first

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really laid into this focus of how can we

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modulate a few switches in the immune

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system to get massive results?

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One of the key variables in that is

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lactoferrin because lactoferrin, I guess

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the best way to describe it is that it's

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kind of like the glue

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of the immune system.

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It sort of holds the whole thing together

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and it acts as an intelligent

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intermediary with the immune system.

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So it sort of acts as the

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glue that drives homeostasis.

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And in my first iteration of this back in

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the 20 teens, there

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wasn't really a way to do it.

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We didn't really have

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human lactoferrin back then.

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And so it's going to be my next question.

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Yeah.

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Yeah.

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So the focus was, go ahead.

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No, I was just going to say the

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difference there being the difference

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between human lactoferrin and then

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obviously bovine and

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other forms of lactoferrin.

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Why is lactoferrin coming from bovine

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sources or other sources?

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Maybe such an immunological issue.

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Why is it sort of less preferential than

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finding the, I think it's Iphira, is that

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the brand of human lactoferrin?

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But yeah.

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Yeah.

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So bovine and human

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lactoferrin are very similar.

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It depends on who you're reading.

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They're somewhere

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between 68 to 77% identical.

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So that's not bad.

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That's pretty good.

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The difference is binding sites.

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So bovine and

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lactoferrin has five binding sites.

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Human has three.

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But the issue you get into really becomes

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one that it's a foreign protein.

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So lactoferrin is a glycoprotein.

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And you run a bit of a risk for an immune

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reaction like the body would

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have to any foreign protein.

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So where lactoferrin, generally speaking,

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human lactoferrin is meant to be the

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master regulator of the immune system,

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bovine lactoferrin can

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actually trigger the immune system.

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Now, I want to be fair, that's not true.

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Probably in a majority of cases.

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Yeah.

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Like bovine lactoferrin

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can be highly beneficial.

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So I don't want to sit here and just go,

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"Eh, mine's the only stuff that works."

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But no, bovine lactoferrin can

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be highly, highly beneficial.

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In fact, it's one of the reasons why

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dairy is really so beneficial in the long

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term for so many reasons.

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That just triggered off

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a firestorm right there.

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But we'll let that go.

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I can hear all the anti-dairy

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crowd just going, "Ah, click."

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But all that to say that

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there's a thing called glycosylation.

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So I'm trying to tailor

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this to the audience here.

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I don't want to...

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Yeah, we've been pretty deep here.

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So let's just go there.

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So much of the information and

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communication in the body happens based

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on what are called PTMs or

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post-translational modifications, which

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are things that happen after

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transcription, after making proteins.

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They're modifications to the proteins.

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One of those modifications is adding

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sugars to those

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proteins to form glycoproteins.

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And then those sugars, depending on their

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structure, essentially act as a second

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messenger system or a

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communication system.

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So the specific structure of those sugars

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carries information.

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And so lactoferrin...

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Go ahead.

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Sorry, would that include ATEs as well?

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Just out of interest?

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Yeah, all glycosylation related

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activities are information carriers.

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So in my first book, this was actually

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going to be a chapter and I gave up

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because there was no way to do it.

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It was a book talking about PTMs.

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It's just way too much.

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Suffice to say that apart from DNA,

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there's a whole information-bearing

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system in the body based on the structure

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of sugar proteins, glycoproteins.

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So anyways, all that to say that

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bovine lactoferrin and human lactoferrin

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share a lot with respect to

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glycosylation, but

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there's also some differences.

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And those differences translate into very

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practical things like

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how absorbable is this.

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And the human lactoferrin just is always

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going to be more absorbable

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than the bovine lactoferrin.

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You're going to need more of the bovine

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to get the same results.

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In fact, so in milk,

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the best estimate so far is that there is

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1.5 to 2 milligrams per gram of bovine

Speaker:

lactoferrin in milk.

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So at a kilogram level, roughly 150 to

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200 milligrams of bovine lactoferrin, but

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then the absorption is not the same.

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So in other words, like in my young gut

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ultra product, there's 200

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milligrams of human lactoferrin.

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To get that same dose in bovine

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lactoferrin, you'd need

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a kilogram and a half.

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That's a lot.

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Yeah.

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So that's a lot.

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Yeah.

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And then I'm sorry, I jumped some

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completely sidetracked here, but then how

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is lactoferrin, I suppose, sort of

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solving broadly

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speaking, the ion problem?

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So lactoferrin, the interesting thing

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about lactoferrin is that

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it drives iron homeostasis.

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So if you have too little iron or too

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much iron, it tends to push the pendulum

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back towards the middle.

Speaker:

So lactoferrin, it's a member of the

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transferrin family, which

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are iron binding proteins.

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The thing about lactoferrin is its iron

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binding capacity is so astoundingly high.

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It's hundreds of times

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higher than your ferritin.

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And so lactoferrin,

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it's like a sponge.

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It has this amazing

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ability to soak up iron.

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Kind of a simple way to put it.

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Fair enough.

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That's perfect.

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And then, yeah, I suppose there are other

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few competing molecules out there on the

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market, things like IP6 phosphate, or I

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suppose the main mechanism is probably

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phyto-gasol to some extent

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binding up iron in the gut.

Speaker:

And then obviously, you can go down the

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copper route to which I know Morley

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Robbins has done a pretty deep dive on.

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I mean, I think he's based the latter

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part of his career around that.

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And the idea that by regulating coppin,

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ceruloplasma, you can sort of convert

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excess ferrous iron, let me get this

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right, I think, to ferric iron.

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And then that can then be transported,

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combined to transferrin and then get

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yanked out of the bloodstream.

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What do you think about that as an often

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not a competing product or competing

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theory, but as an odd competing mechanism

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to sort of regulate iron, the idea of

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just sort of increasing copper intake?

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Well,

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first of all, I don't want to do a

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disservice to his work.

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Just anecdotally, what I've heard is that

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he's had some very good outcomes.

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And I'm not 100% expert in his work, so I

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don't want to misspeak.

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As I understand it, which I will say up

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front has room for error.

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So please correct me if I'm wrong.

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So a significant portion of the actual

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protocol involves dietary modifications.

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And when I look at those dietary

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modifications, what the net, which I

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haven't heard anybody talk about, that

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they're going to do is you're going to

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produce a shift in the gut taxa that

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favors bacteria with

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iron binding cytoform.

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So what you're going to get is this

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variable that doesn't get

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talked about a lot, which is that,

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and this gets to the phytic acid thing.

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As you increase certain taxa in the gut,

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like the phyto bacteria,

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they bind iron in the gut.

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And then in terms of your IP6 problem,

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that actually prevents that

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from binding iron in the gut.

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So shifting the gut taxa can have this

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tremendous impact with respect to a

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number of variables that we could kind of

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anecdotally attribute to

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quote unquote the protocol.

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But it's really possibly to some extent

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has to do with just

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simply shifting the gut taxa.

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That's kind of the theory I'd offer on

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that with respect to copper.

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The thing is,

Speaker:

lactoferrin can also bind copper.

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And I would just offer that the master

Speaker:

regulator of iron naturally

Speaker:

in the body is lactoferrin.

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So if I were to approach the problem, I

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would kind of start with what exists

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naturally, which is not to say that maybe

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he's not having fantastic results too.

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So I don't claim to have the market

Speaker:

cornered on solving the lactoferrin iron

Speaker:

problem or the iron problem.

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So that's what I would say.

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Yeah, that's perfect.

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And of course, no disrespect to Molly,

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though, I'm actually getting more on the

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podcast in a few weeks.

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So I'm just always interested in speaking

Speaker:

to individuals obviously with opposing

Speaker:

but similar sort of understandings of the

Speaker:

problem, just looking from a different

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lens and just trying to

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get a broader picture of it.

Speaker:

I mean, ultimately, all rosary trim.

Speaker:

And I suppose one could also just stick a

Speaker:

needle in the ROM and just do some sort

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of venus section as well.

Speaker:

I'm sure that is

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effective as well as anything.

Speaker:

But yeah,

Speaker:

Joel, you'd be amazing.

Speaker:

And I just want to be

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respectful of your time.

Speaker:

But I've got a few rapid-ish fire

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questions that I'd love to

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go through if that's okay.

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Perfect.

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Okay.

Speaker:

To keep the sugar diet crowd happy.

Speaker:

I know you've covered this

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on your Instagram recently.

Speaker:

And seemingly, it has more to do with I

Speaker:

suppose, one of my other protein

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restriction, although as we chatted about

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earlier, if you sort of remove a

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macronutrient entirely, you're going to

Speaker:

get a massive sort of swing in

Speaker:

metabolism generally speaking.

Speaker:

And I know that there's obviously an

Speaker:

issue there with high fat diets sort of

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triggering an increase in FGF21

Speaker:

hepatically, which is why maybe that's

Speaker:

not the best way to

Speaker:

sort of protein respect.

Speaker:

But just overall, I suppose, what's your

Speaker:

take on the sugar diet?

Speaker:

And do you think it's efficacious?

Speaker:

I know time will be available, but yeah.

Speaker:

So first question,

Speaker:

can quote unquote the sugar diet work to

Speaker:

help you lose body fat?

Speaker:

Answers, yes, absolutely.

Speaker:

Yeah.

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Is there anything new there?

Speaker:

No, nothing.

Speaker:

That's been known for decades that just

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take any macronutrient to

Speaker:

zero and you can see fat loss.

Speaker:

Mechanistically,

Speaker:

personally, I don't think any of the

Speaker:

reasons apart from protein restriction

Speaker:

are what's going on.

Speaker:

The two big reasons

Speaker:

nobody's really talked about.

Speaker:

Number one is glycolysis.

Speaker:

So again, this gets to kind of my

Speaker:

worldview, which is math

Speaker:

always drives the equation.

Speaker:

In a carbohydrate restricted state, you

Speaker:

have less substrate

Speaker:

available for glycolysis.

Speaker:

And so you're going to have less

Speaker:

glycolysis in general.

Speaker:

When you reintroduce substrate into the

Speaker:

equation, remember, we're talking about

Speaker:

trillions of cells here.

Speaker:

Every one of them can run glycolysis.

Speaker:

So when you have more substrate

Speaker:

available, you're going

Speaker:

to increase glycolysis.

Speaker:

Glycolysis will shred you up.

Speaker:

That's why sprinting works.

Speaker:

That's why high altitude training or high

Speaker:

altitude kind of

Speaker:

hypoxia works to lean you up.

Speaker:

It's been proven.

Speaker:

So cancer patients know

Speaker:

this glycolysis leans you up.

Speaker:

So when you increase glycolysis through

Speaker:

increasing substrate,

Speaker:

you're going to get lean.

Speaker:

The other variable that no one's talking

Speaker:

about is just simply that you're

Speaker:

recolonizing the gut.

Speaker:

And I think it's something that a lot of

Speaker:

low carb influencers have stumbled onto

Speaker:

and they don't even know it.

Speaker:

And it's just simply

Speaker:

that I've experienced this.

Speaker:

When you recolonize the gut rapidly,

Speaker:

there are very specific proteins that are

Speaker:

related to fasting and fat loss.

Speaker:

One of them is ANGLP4, PT4, or FAFE,

Speaker:

fasting induced adipose factor.

Speaker:

That is a protein that is secreted during

Speaker:

fasting that actually

Speaker:

drives fatty acid liberation.

Speaker:

And what you will find is that that same

Speaker:

protein can be

Speaker:

stimulated by the microbiome.

Speaker:

So when you increase taxa during a fed

Speaker:

state that produce this protein,

Speaker:

you drive fat loss.

Speaker:

It actually helps prevent fatty acid

Speaker:

storage and drive fatty acid release.

Speaker:

So you can actually drive fat loss

Speaker:

through the microbiome through mimicking

Speaker:

fasting through that.

Speaker:

So you have glycolysis and you have the

Speaker:

recolonization of the microbiome along

Speaker:

with protein restriction.

Speaker:

So those are three variables that all

Speaker:

work together all at once.

Speaker:

And so that explains things, I think

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pretty well, would be my answer.

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Okay, that's perfect.

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And do you think maybe a bit more that I

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spoke not really, it's not like we

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haven't talked about anything technical

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to stay listy honest.

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And when somebody is going through some

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sort of disease statement, maybe when

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there's some impaired match or conjugal

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function, there's an elevated sort of

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cell dangerous responses at work.

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There's obviously in those states is

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going to be impaired oxfoss down

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regulated use of fatty acids.

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Do you envisage that being maybe a

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potentially effective strategy for people

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who do have some sort of matcha conjugal

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impairment to sort of bypass that block

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in energy production, it'd be in the

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short term while you're dealing with

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maybe the underlying issues.

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Yeah, I certainly think so.

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I think it could be.

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I would just say it's

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certainly something to try.

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Fair enough.

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Perfect.

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Okay.

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Last one, and then I'll let you go.

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Any new molecules you're particularly

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excited about, just generally speaking,

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not giving away any

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trade secrets or IPF course.

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Yeah, there's...

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So we're in the burgeoning era of

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precision fermentation.

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Basically, we can get bacteria to make

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very specific immunoglobulins or proteins

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or different things we want it to make.

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And where this gets really interesting is

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in the replication of milk proteins.

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So lactoferrin is kind of the most

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conspicuous example, but there are other

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ones that are blowing up.

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They're not blowing up.

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You're going to see...

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What you're going to see is the

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introduction of additional co-factors of

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unique things that are present in

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mother's milk that are additive with

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respect to the equation of

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optimizing the metabolism.

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And it gets back to

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mother's milk is growth serum and it

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triggers all the right things in all the

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right way when you're young.

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And it makes sense that there could be

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some significant benefits to

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replicating aspects of that.

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And through precision fermentation now,

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we're seeing kind of a release of that.

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Okay.

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Perfect answer.

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Thank you.

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Cheryl, like I said, you've been a star.

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This is a conversation I've been wanting

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to have for a while.

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So thank you.

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I appreciate your time and hopefully

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we'll be able to do this again soon.

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Just to finish off,

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where can people find you?

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Should they wish to connect, learn more

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about what it is you do, your work, your

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company, Veep, et cetera?

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Yeah, probably the best

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place is my Instagram.

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So that's real Joel Green.

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And then my link tree has

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all those goodies in it.

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And then I'm trying to

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grow my ex, my Twitter.

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I just don't post often enough, but if

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you want to follow me,

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same thing, real Joel Green.

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And then our URL is a veepnutrition.com.

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Perfect.

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Joel, thank you so much for your time.

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Thank you, Rob.

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I really enjoyed the convo.

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Really great.

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