Episode 33

full
Published on:

13th Jul 2025

#033 Gilian Crowther - The Hidden Cause of Chronic Illness: Mitochondria & The Cell Danger Response

GILIAN CROWTHER MA (Oxon), FBANT, mANP, mNNA, CNHC reg., is a fully qualified Nutritional Therapist and Naturopath specialising in complex multisystem disorders. Her key focus is on infectious pathologies and mitochondrial dysfunction. She studied complementary therapy in Germany for many years before completing her training in the UK. She has been a senior member of the Academy of Nutritional Medicine (www.aonm.org) since 2010, and is their Director of Research. She is a committee member of the General Naturopathic Council (GNC) as well as the British Society for Ecological Medicine (BSEM).

 > During our discussion, you’ll discover:


(00:04:52) Understanding mitochondria

(00:09:23) Why mitochondria is important for hormones

(00:14:03) How and why mitochondria become dysfunctional

(00:17:20) The effects of stress throughout the body

(00:20:41) Understanding the Cell Danger Response (CDR)

(00:36:38)  Epigenetic changes

(00:40:12) Mitochondrial tests

(00:44:22) Dietary Approaches and Mitochondrial Health

(00:52:16) The Role of Light and Environment in Mitochondrial Health

(00:58:07) Future of Mitochondrial Medicine


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Transcript
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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 eating minds.

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I'm your host, Rob.

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And my guest today is Gillian Crowther, a

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functional nutritional

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therapist and medical researcher.

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Gillian has a passion for all things

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mitochondria and heads up research at the

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Academy of Nutritional Medicine, UK's

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leading provider of advanced

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mitochondrial and cellular tests.

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Expect to learn how

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mitochondria actually function?

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What the cell danger response actually is

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and whether or not Prignell alone steel

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is based in science or is

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a functional medicine myth.

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Now onto the

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conversation with Gillian Crowther.

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Morning Gillian, it's great to have you

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on the podcast today.

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So this is something that's come up a lot

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of my conversations recently, the cell

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danger response, I mean, which is

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something I know will be just, which is

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something I know we'll be discussing

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during our conversation today.

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Before we get into the nitty gritty of

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that though, would you mind introducing

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yourself to the audience and how you

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ended up in this sort of world of

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functional nutrition,

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one might say, naturopathy?

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I'll get that word

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right one of these days.

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But yeah, just your intro to

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all of this would be amazing.

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Thank you so much.

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Well, thank you for having me here today.

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And I'm delighted to talk about one of

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the topics closest to my heart.

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I suppose, you know, it began with

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studying herbalism when I

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was very young, about 20,

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straight out of the university.

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And then I spent a lot

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of my life in Germany.

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My husband as a doctor was working in a

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very sort of holistic field there.

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And so I came into contact with many,

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many wonderful doctors and began studying

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the mitochondria with a group of

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naturopaths and doctors there in great

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detail, probably about 21 years ago.

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And the Cell Symbiosis Academy, with

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which I was working, was very active.

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It's no longer really in existence.

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Unfortunately, some of the key doctors

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running it have sort of retired now.

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But when I came back to England, I

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continued my studies and certified as a

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nutritional therapist and naturopath and

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found myself working together with the

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Academy of Nutritional Medicine, where I

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still am, about 15 years ago.

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I'm now the director of research and we

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run a lot of fascinating niche tests,

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tests that nobody else is running really,

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like very specific ways to detect stealth

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infections and mitochondrial tests, which

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are really unique worldwide, actually,

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and tests of autoimmune encephalopathy.

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Quite a few different kinds.

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I won't go through them all.

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We also organize events and webinars and

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do a lot of sort of cross pollination.

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We link up a lot of different

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organizations as best we can and hope

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that they'll speak to each other and

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exchange information.

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And that's sort of our mission, really.

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That's quite the story.

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And I suppose having a husband who's

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already in the sort of the alternative

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world, for the want of a better word,

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probably opened your eyes up to a lot of

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maybe where conventional medicine maybe

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doesn't work, perhaps.

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You said you started off in herbalism

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straight out of uni and

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then you went into nutrition.

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Were you at university initially for

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anything medical or

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what was your story there?

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No, I attended Oxford University,

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Bresnose College and

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actually studied German and history.

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So no, it's a slightly different area,

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but I found I moved into sort of

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health-renated topics

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quite quickly after that.

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Okay, fair enough.

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Sorry, I hope you don't mind me asking.

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I'm just sort of fascinated by people's

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backstories and how they

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sort of end up where they are.

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Yeah, no, it's the AONM is something I've

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been sort of looking at on and off for a

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while, especially your mitochondrial

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tests, as you say, they are

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very unique and intriguing.

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However, I'm not going to go down that

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road at all because I've sworn to myself

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to try and keep on today's topic of

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conversation trying

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in the operative word.

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So yeah.

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So the cell danger response, as I

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mentioned earlier, this is something I'm

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fascinated by because, well, for me

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anyway, it's really arguably the lowest

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common denominator when you comes to talk

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about disease in general.

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Obviously, I know that's a bit of a

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blanket statement and it does skew

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towards more diseases that have the sort

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of cellular metabolic

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dysfunction and origin.

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But I do think it opens a lot of doors to

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view disease that we've made the sleep

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that had been previously shut off,

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the idea that we can sort of look at

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disease broadly

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speaking through this CDR lens.

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Before we jump into CDR specifically,

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though, I'd like to backtrack just a

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little bit and maybe discuss

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mitochondria for a little while.

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I know most folks are likely familiar

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with these little organelles, these sort

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of cellular components, in that they are

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that they really help produce energy in

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the form of ATP within the

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cell and within the body.

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However, they do a lot more than that.

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And while we won't have a whole

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discussion about mitochondria, I'd love

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to talk about maybe how they're involved

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in the endocrine system or later on in

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the conversation as well.

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But at a baseline level, can you describe

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what mitochondria are and

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what they do in the body?

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Yeah, maybe asides from

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just creating cellular energy.

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Yes, well, they originated from bacteria.

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And then there was an endosymbiosis event

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where this sort of cyanobacteria and

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archaea joined up and were able to

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produce a lot more energy.

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That way, it's a bit of a complex story,

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but absolutely fascinating.

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And they're responsible for, as you say,

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a lot more than just our energy, though

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they are considered to be the sort of

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power plants of the cell.

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They're responsible for nutrient sensing

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and energy metabolism.

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That's really the sort

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of bioenergetics sphere.

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And then also for biosynthesis, they

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synthesize a lot of molecules.

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For example, heme is synthesized largely

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in the mitochondria.

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And if they're down, then you'll have a

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lot of issues with heme production.

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Cholesterol is cleaved in the inner

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mitochondrial membrane.

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And so without proper operation of the

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mitochondria, you'll find that you don't

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get the steroid hormones downstream that

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you need in the proper order.

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It's also responsible for signaling.

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And the ROS, the reactive oxygen species,

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very much have their

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role to play as well.

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Oxidative shielding is what Dr.

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Navio from the CDR field that we'll be

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talking about soon actually calls it,

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rather than oxidative damage.

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That it's shielding that these reactive

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oxygen species are

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providing as well as signaling.

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A lot of cell to cell communication takes

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place via the mitochondria, too.

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And they're also able to form chains.

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And it's fission as well as fusion.

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They're not just sausage shapes.

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They can actually transfer

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electrons from one to another.

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They migrate to different organs,

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different parts of the body where more

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energy is needed and

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multiply as required.

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So they're very, very

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intelligent little beings.

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I call them sort of our biochips.

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Yeah, I mean, all sorts of jokes aside, I

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mean, if you'd said that a couple of

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years ago, you probably would have gone

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into trouble talking about chips in your

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cells and all of that.

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But, yeah, I think what I'd love to jump

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down with the rabbit hole there that I'd

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maybe like to explore a bit further is

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maybe the hormonal connection.

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So we had Dr.

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Eric Belkowicz from the States on a few

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months back to talk about thyroid.

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And he's very focused on treating the

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thyroid and the endotransystem in general

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and dysfunction there from a

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pharmatic control standpoint.

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And, yeah, that sort of got me down the

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thyroid mitochondrial rabbit hole, which

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maybe we can touch on later as well.

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But it does raise the question of of what

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you really pointed to earlier, this idea

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that mitochondria take and

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let me see if I got this right.

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They take cholesterol and they help turn

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it into pregnenolone.

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That's right.

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And that whole sort of

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steroid cascade there.

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Would you mind breaking this process down

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a little more for us?

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Because I do think it's quite fundamental

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to not only our discussion, but also to a

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sort of a broader discussion on why

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people maybe don't necessarily react as

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well to hormonal replacement therapy as

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they think they would if they've got sort

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of a mitochondrial issue.

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Yes, absolutely.

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It's the cholesterol side cleavage enzyme

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called the P450CC that converts

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cholesterol into pregnenolone and that

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takes place in the inner

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mitochondrial membrane.

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And if your mitochondria are

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dysfunctional, then obviously that will

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not be happening as well as it should.

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Obviously, it's not going to

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break down all over the body.

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But depending on where the dysfunction is

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taking place, you'll find that you don't

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make your steroid

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hormones as well as you should.

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And obviously, that's

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that's a large number.

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So I totally agree with you that if

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you're using bioidentical or even non

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bioidentical hormone therapy, that might

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well be a reason why it's just not

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getting into that cascade and simply not

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functioning if you've got the

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mitochondrial dysfunction underlying it.

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Yeah, it's it's it's definitely something

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that I think a lot of individuals and

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practitioners like miss that that

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hormonal function is always sort of at

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least from a mitochondrial

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standpoint in the way I view it.

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And feel free to correct

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me if you if you see fit.

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It's always sort of the last piece of the

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puzzle to really come into play.

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And I think lots of people will

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oftentimes jump into HRT and then sort of

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still be sort of upset, surprised, sort

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of unhappy about the fact that they still

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got a lot of the symptoms that they they

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currently have because they've been told

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that their issues are just hormonal.

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When in fact, it's it's a mitochondrial

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issue that has

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manifested as a hormonal issue.

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And yeah, I just one more

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question there while we're at it.

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What do you think about this idea of

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pregnant alone, pregnant, no, no, no, no.

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Excuse me, I'll get that word right.

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One of these days, I know it's it's often

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taught in sort of the

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functional integrative space.

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It's something I don't agree with this

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idea that you only have a

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certain amount of pregnant alone.

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And if you use and if you take pregnant

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alone, it's going to be maybe buffered

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towards one or another type of hormone.

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When in reality, the way I view it is

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that each cell, each cell is obviously

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going to contain mitochondria and that's

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going to be specific to each

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organ system or gland system.

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So the way I view it is that pregnant

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alone actually can't be stolen because

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it's always been made.

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It's been made locally within the the

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group of tissues that it's been utilized

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in by those mitochondria.

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Would you agree with that?

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Or do you think that this concept of

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pregnant alone still is real?

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No, I do completely agree with you.

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And it's fascinating actually to see

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sometimes how high cholesterol in the

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serum, which is the only place it's ever

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measured, is often actually due to the

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mitochondrial dysfunction that we're

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talking about and the fact that the

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pregnant alone isn't being converted.

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And therefore, you're getting this

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buildup of cholesterol outside the cells

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in the serum and that's being measured.

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And you're getting alarm signals and

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actually the

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ramifications go far, far deeper.

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Yeah, no, it's something it's it's yeah.

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Like I said, I think a lot of people have

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a lot of opinions about

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it and I'm just a chemist.

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So it's always great to hear this from

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someone who's in clinical practice and

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who sees this in the real world apart

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from me just trying to piece these parts

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of the puzzle together and wondering if

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I'm missing something or not.

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OK, I'd love to sort of start to maybe

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steer the conversation towards CDR and

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where mitochondrial function CDR and

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maybe why we have

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dysfunctional mitochondria.

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But before we get into that, maybe maybe

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if we could explore why mitochondrial

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become dysfunctional to begin with.

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Now, I know there's a lot to unpack there

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again and that mitochondria can be made

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dysfunctional or become dysfunctional for

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a number of reasons.

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Infections, high levels of the toxic

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exposure, et cetera.

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And with regards to the latter, if anyone

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really is interested in toxic exposure, I

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invite them to listen to the podcast,

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excuse me, that we did with Dr.

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Jenny Goodman a few months back.

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It was really was a good listen,

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a good conversation, should I say.

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But from your perspective and clinically

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speaking, I suppose, which is really what

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counts at the end of the day, what are

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you finding to be the biggest triggers

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with regards to why mitochondria are

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becoming dysfunctional to begin with?

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Well, I mean, it falls into several

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categories, biological, as you've just

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mentioned, in the bacteria, the viruses,

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parasites, fungi and then chemical,

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particularly electrophilic chemicals due

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to the energy systems in the cell.

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You know, lyndane and all the different

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sort of chemical additives and metals as

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well, heavy metals, lead and cadmium and

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things like glyphosate

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fall into that category.

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Absolutely as well.

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Yes.

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OK.

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And then, of course,

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psychological slash emotional, which

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converts into physiological stress, too.

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So it stresses all these different kinds.

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And then, of course, metabolic stress, if

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any pathways are not working properly due

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to lack of cofactors.

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And that's a very important stress, too.

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So the stresses along those, I would say,

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four different pathways, biological,

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chemical, metabolic and

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physiological slash emotional.

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Yeah.

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And can I just add one more?

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Which, of course, we've suddenly

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encountered these last five years, which

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is SARS-CoV-2 virus and the spike protein

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is able to fragment the mitochondria.

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And that's very, very serious.

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And it also prevents apoptosis in a much

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more intense way than other viruses that

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we've seen previously.

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And so apoptosis being pre-programmed

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cell death, is that correct?

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Exactly.

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And so the lysosome and phagosome are

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unable to link up as they should and sort

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of get rid of the

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dysfunctional cells and mitochondria.

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And that's really very, very serious

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indeed, making it very

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difficult for people to recover.

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It's being called long covid, whatever

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the condition actually is.

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Yeah, we interviewed Dr.

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Tina Peirce and she's got a she

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definitely looks at the whole long covid

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thing from a mast cell standpoint

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specifically, which I

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do think is interesting.

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I'm not sure it's the entire picture, but

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for a lot of people, I think, yeah, long

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covid definitely seems to drive sort of

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an exacerbated histamine response.

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And I've actually got a

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question on that on that later.

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But I do find it interesting that you

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raised the whole

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psychological side of things well.

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I think what, again, most people miss is

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that stress is stress and everybody's

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always looking for some sort of broadly

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speaking external trigger, I think.

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Somebody's looking for an infection as to

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why they have the ailments they have or

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they are looking at some sort of

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underlying toxic exposure.

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And I think what most people miss,

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unfortunately, is that ultimately the

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body is going to take all that stress at

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some level and it is going to be that

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sympathetic or that final flat response

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in the body, which is then going to drive

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all those transcription factors and

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pro-inflammatory pathways, which then is

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going to drive that mitochondrial

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dysfunction at the level of CDI, as we

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will discuss shortly.

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Absolutely.

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I work quite closely with Dr.

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Dietrich Klinghart, who

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works on five levels of healing.

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And we've seen incredible change in

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patients as a result of even looking at

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sort of ancestral trauma that they may be

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carrying down with them.

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This is something that he learned through

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working with someone called Bernd

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Hellinger, who lived with the Zulus for

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many, many years, working as their priest

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and found how very, very important the

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extended family is and how that sort of

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morphogenetic approach.

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If you begin to sort of look into that

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can also be a missing

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piece of the puzzle.

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Sorry, did you say

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the Zulus as in the S.U.

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Zulus?

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Yes, they sort of have incredible

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practices that do take into account

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missing members of the family, whether

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it's because it was a miscarriage or an

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early death or a murder or whatever, but

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all of that has an impact

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on the larger family, too.

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Yeah, I just mentioned it because I grew

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up in Kuzu-Lunatal in South Africa.

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Did you?

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Yes.

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So originally from the UK, then spent my

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entire sort of, well, most

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of my life in South Africa.

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How fascinating.

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Yeah.

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So it's a lovely country.

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It really is.

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It's going through a sort of, should we

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say, a bit of a struggle at the moment.

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And if you like electricity and I suggest

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you don't live there.

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But beyond that, it

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really is a beautiful country.

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I'm sure I'd love to get in.

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Yeah, no, it's yeah, maybe not somewhere

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to live at the moment.

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But from a just from a cultural

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standpoint, from a geographic sort of

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standpoint, it really

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is an amazing country.

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Anyway, so I'd like to get back on track,

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as I was saying earlier,

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Dr.

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Balcovic, who I interviewed at the

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beginning of the year,

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looks at this through the lens of it

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being adaptive physiology.

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And in his from his vantage point, from

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his viewpoint, he sees all of this

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dysfunction as the body not necessarily

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entering into a state of dysfunction, but

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rather downregulating its physiology sort

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of based on the fact that it's under this

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sort of high elastatic load.

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And that we shouldn't view this

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physiology as broken, per se, but as the

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result of being in the state where it's

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sort of, yeah, it's downregulating these

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vital bodily processes.

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Well, that does sound a little bit

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similar to the CDR in that that's the

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mitochondria sort of ability to detect

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potential harm and damage

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to the cells, organs, body.

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And therefore, they downregulate and

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change a lot of their functions to,

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you know, it's an evolutionary sort of

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conserved protective mechanism.

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Absolutely.

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Yeah.

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And the different steps of it are

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obviously quite complex, but have been

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very, very well mapped out by Dr.

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Navio and his teams.

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Yes, one day I'll get him on to a call.

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I think I sent him an email.

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Oh, that would be fantastic.

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I sent him an email, an

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email at least once a month.

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I get to have a reply,

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but I'll keep on pushing.

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Let's keep trying.

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Yeah.

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Keep on pushing my luck.

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I'm a bit like a dog with

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a bone when it comes to it.

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Honestly, I think that's a perfect time

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to sort of segue into CDR and maybe we

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can discuss that in a

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fair amount of detail.

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I think the way I see it, there's these

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three sort of stages of the cell danger

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response and we sort of

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we get stuck in there.

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However, this is definitely your realm of

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expertise and something I just look at

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with the sort of the from a passionist,

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passionate hobbyist sort of viewpoint.

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So, yeah, I'd love it if you could start

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to how to break down this, to break down

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CDR and help us to understand what

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exactly is going on there.

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Yes.

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Well, according to Dr.

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Navio and his teams, as I say, you know,

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they've even done very large studies

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using NIH grants of millions on this.

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So it's not just sort of a couple of

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articles that he wrote back in 2014.

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It's really been taken up really

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worldwide, though it's not fully

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integrated into, obviously, conventional

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medicine thinking yet.

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It's not reached the

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medical textbooks, I don't think.

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But there's CDR1, which is the sort of

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innate immune response to these various

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different factors

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that I mentioned earlier.

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And if the mitochondria detect a threat

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along any of those lines that I

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mentioned, and I think I forgot to

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emphasize physical as well, I mean,

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obviously, a major car accident or even

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breaking your arm or

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whatever, that's all included.

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Then they will decrease their oxygen

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consumption initially in order to allow

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the oxygen to instead

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suffuse the cytosol.

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And that changes the pH, it changes the

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way that enzymes act.

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And it also,

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it's both oxidant and increases the

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oxygen for antioxidants.

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So, you know, having more oxygen in the

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cytosol has a dual function.

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It's both able to, for example, kill or

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attempt to kill the pathogens that have,

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for example, been found there, but it can

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also power the superoxide dismutase,

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glutathione peroxidase,

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catalase, thioidoptase.

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All these antioxidants need a little

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oxygen to actually power them.

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And if you see higher levels of oxygen

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being used outside the mitochondria in

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the cell, then that's a very good sign

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for this kind of battle that's going on.

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It's often called the power plants

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turning into the battleships, as it were.

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So they're down-regulating in order to

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allow this sort of battle

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to take place in the cytosol.

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And another thing that happens is that

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the cell membranes are stiffened in order

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to prevent egress of, again, you know,

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any pathogens that may be detected.

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For example, spike

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protein to prevent in and out.

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So the composition of

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the cell membranes changes.

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And they also release antimicrobial and

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antibacterial, well, antiviral chemicals.

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Interestingly, they're able to do that.

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Yeah.

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And they increase

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autophagy to the extent they can.

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Obviously, if you've had a major blow

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like the spike protein, as I mentioned,

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preventing that, then they'll do their

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very best to via mitochondrial fission

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and mitophagy, which is the breakdown and

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recycling of the mitochondria themselves.

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And they'll attempt to sort of

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operationalize that.

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And at this point, would cardiolapine be

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damaged within the

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mitochondria within the cell?

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I don't think it

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would be damaged as such.

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It would just be not allowing fats into

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the mitochondria to the

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extent that it normally does.

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That's its key role.

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But I mean, if you're not going to fire

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up the mitochondria like you would

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normally, then you're neither going to

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take in the fats to the extent that you

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would normally know the carbohydrates.

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And it also releases ATP,

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as a sort of, it's called E-ATP,

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extracellular ATP, that acts as a warning

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signal and actually communicates to other

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cells, a bit like the pheromones of sort

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of trees that one hears about in plants,

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sending up warning signals to each other.

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And it also alters post-behavior in that

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the person themselves loses energy,

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becomes a lot less active, you know, may

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just feel they have to

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spend some time in bed.

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But that's all part of

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this healing response.

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The energy simply isn't there any longer

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for those kinds of activities.

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So that would be CDR1.

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And hopefully, if that resolves the

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individual's issue, then soon enough, the

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mitochondria will take up the normal

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activities again and the cell danger

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response will discontinue.

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But it is possible for it

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to get what's called stuck.

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And for, or maybe there's a need for it,

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if it's been very, very major

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inflammation that's taken place, then the

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cell does need to spend a lot of time

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building the new macromolecules that you

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need for new cells to replace those that

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have gone under through inflammation.

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So it's building new lipids and new

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carbohydrates and new proteins.

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And so all of that will

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require the glycolysis.

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And increasingly, if you move to aerobic

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glycolysis of CDR2, which is where there

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is oxygen present, but it's being again

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used for this sort of

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rebuilding of cells outside the cell.

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This is called a sort

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of proliferative phase.

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And obviously, you don't want this to go

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on for too long because proliferation,

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obviously, signals at the

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end of the chain cancer,

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which is just one stage along a

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particular trajectory.

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You know, we shouldn't be frightened of

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that word like we are, but nevertheless,

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this proliferative stage CDR2 of aerobic

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glycolysis will hopefully

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not continue indefinitely.

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But move on to what's called CDR3, which

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is the third stage that Dr.

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Navio and his teams have identified,

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which is where the oxidative

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phosphorylation is

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beginning to start up again.

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But you've still got the cells in many

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parts of the body working and the

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mitochondria as well working

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independently rather than in a sort of

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very coordinated way.

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I have a slide here that includes all the

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different conditions

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under CDR1, 2 and 3 disorders.

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And it's absolutely incredible the number

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of disorders that are even listed under

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CDR3 like autism and chronic fatigue, of

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course, which can persist

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for years and even decades.

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And it's a kind of hibernation of the

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mitochondria that has really

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to a certain extent got stuck.

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What we have is the vagus nerve,

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which is, of course,

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extremely extensive and that has both a

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ventral and a dorsal kind of

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chain to it component exactly.

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And Porges and others have written really

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comprehensive literature on this.

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It would appear that the ventral stage,

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which is the sort of healing component of

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the vagus nerve, is in

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these cases downregulated.

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And instead, you have an upregulation of

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the dorsal, which corresponds to the CDR.

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And that can,

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in some cases, simply become it's a bit

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like cellular memory.

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It can become the sort of

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new normal for the patient.

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It's like a set point

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that has been changed.

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And so a lot of work has been done by

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Porges and others, including,

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interestingly, even Dr.

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Gerald, the Professor Gerald Pollock, you

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know, his work feeds into this massively

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as well to kind of try and regain the

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normal cell functions, including the

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dorsal signaling of the, I'm sorry, not

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the dorsal, the ventral

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signaling of the vagus nerve.

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That's fascinating.

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I wasn't aware Dr.

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Pollock was doing any

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specific research into.

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Well, not directly, but it all links up

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because the EZ water, the exclusion zone

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water, which you'll know about and have

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probably done other sort of podcasts on,

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is so central to getting

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that signaling back again.

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And in fact, the electrons, the neutral

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charge, it's a bit like a battery

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functioning in the cell and getting that

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battery sort of conduction, the

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electrical conduction working again

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properly does appear to a lot be

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connected to this fourth phase of water

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that Professor Pollock talks about.

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So he doesn't directly mention the CDR,

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but it is clearly part of it, as is even,

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you know, deuterium depletion.

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You know, we're beginning to see very,

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very big pictures now, I think, coming

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together, you know, the dots are sort of

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being joined very quickly now.

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Yeah, no, deuterium depletion is

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something I've, it's on my list of things

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to sort of dive into.

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But yeah, I think that's fascinating,

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especially from a sort of an oncological

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standpoint and the research that's been

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done into, yeah, reversing various

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metabolic, again, diseases, again, by

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from a deuterium depletion standpoint.

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Let me just mention, sorry to make that

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connection so that it's a

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bit easier to understand.

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It's because the mitochondria are

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continually producing metabolic water.

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This is the extraordinary thing.

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It's actually water that's been produced

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at cytochrome C oxidase as part of the

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part of the oxidative phosphorylation.

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And this metabolic water, it can be a

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huge amount, it's like

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sort of, I think, 17.

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We'd have to talk to Professor Borish

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about that, but certainly thousands of

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liters a day if it's being

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produced and recycled properly.

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And that's how camels work.

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Exactly.

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Absolutely correct.

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Yes.

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And it's their fat and it's the fats that

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we're eating, actually, that are making

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it possible for us to produce that a lot

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more efficiently than, you know, again,

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if the mitochondria are working.

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So it's gradually encouraging that

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metabolic water in our system to begin

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working again, because without it, the

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mitochondria can't work either.

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And it would appear to be low deuterium

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or deuterium depletion that both the

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Krebs cycle and the electron transport

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chain are creating in our mitochondria.

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And I'm quite sure that Dr.

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Navier, when you speak to him, will agree

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that part of the recovery process will be

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encouraging this metabolic water to be

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created in a much more efficient way.

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That's fascinating.

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I mean, I've taken from that more so than

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anything, is if camels get

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fried, they're probably stuffed.

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Sorry, maybe just a bit more of a

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technical question, if you don't mind.

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Do you think that that that that that

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that EATP that you mentioned earlier, and

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then other metabolites there are so

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things like Saxonate, Adenosine, etc.

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Do you think that they could play a role

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in amplifying also sustaining that that

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CDR response across tissues and cells if

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they're if they're elevated?

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Oh, absolutely, yes.

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But I mean, hopefully they're working in

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an intelligent manner in order to simply

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get the message across.

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Look, there's danger, Ahoy.

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We've got to alter pathways in these

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different manners, but not in a

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completely dysfunctional way.

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But I suppose eventually, I mean, I know

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that it's possible to measure DNA that's

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sort of floating around in the

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bloodstream that

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shouldn't be there as well.

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And to do that.

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Exactly.

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Mitochondrial DNA.

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And that's a bad sign if you see it.

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But again, I very much go with Dr.

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Navier's thinking, which is that we

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shouldn't be considering these things as

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a, you know, from a negative standpoint,

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but just trying to understand what the

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signal is that they're trying to get.

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And I think, yeah.

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Again, just that sort of viewpoint of the

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physiology being

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adapted, not necessarily broken.

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Exactly.

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Yeah.

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What about epigenetic changes?

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And I think maybe the best example is,

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okay, hypothetically speaking, of course,

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say we were exposed to a sort of a

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massive viral pandemic.

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I mean, imagine that.

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And then we were then treated with a

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quickly developed vaccine that may or may

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not have undergone

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any sufficient testing.

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Would it be sort of plausible in your

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view that maybe a vaccine like this could

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sort of create epigenetic changes by sort

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of altering histones and other DNA and

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RNA components that could then drive up

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immune system activation and that and

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that purigenic signaling.

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And then to the extent that the body

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might end up stuck in CDR1, obviously

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through that epigenetic lens, do you

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think that's at all feasible?

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Most definitely.

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I'm very, very unhappy about what we've

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seen over the last four years or so.

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I know it's not a good idea to talk about

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this too much on podcasts that are going

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to go out on YouTube and so on.

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But yes, I mean, the body has such

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incredible intelligence and these tiniest

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little pathways and organelles and so on

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are all working at a rate of knots in

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such a sophisticated way that introducing

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something of the kind that you've just

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mentioned that could

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potentially disrupt that processing is

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I think misplaced on

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many, many different levels.

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Yeah, and it's not for me,

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obviously, really to decide.

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But I think that some of the difficulties

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that therapists and doctors are finding

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worldwide in

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assisting patients to recover,

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finding it much, much harder than they

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used to at the moment, could partly be

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linked to the whole pandemic and set of

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issues related to that we've experienced.

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I think for me, and this is a very slight

Speaker:

tangent, is that maybe the silver lining

Speaker:

of the pandemic and long COVID is that

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it's brought to light this idea of these

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chronic fatigue-like syndromes, myalgic

Speaker:

encephalomyelitis, broadly speaking,

Speaker:

these issues, which I suppose originally

Speaker:

sort of started off as golf wall

Speaker:

syndromes, PTSD and these other issues.

Speaker:

And for me anyway,

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having struggling with

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it myself, to an extent,

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I think it definitely has, yeah, it's

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brought an awareness to the issue at

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large, which obviously, as you know,

Speaker:

dealing with people on a regular basis,

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I'm sure, is a very sort of

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proliferative issue in society.

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So, yeah, I mean, obviously, we never

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would have wanted it to occur, that

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silver lining and all of that.

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I think it's, yeah, it's just brought a

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greater awareness to these mitochondrial

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disorders if you view long COVID

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essentially as a mitochondrial disorder,

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which I think we'd probably agree that it

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fundamentally is when you

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sort of remove all the triggers.

Speaker:

Gillian, I think this would be a great

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time to sort of maybe segue into how you

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start to deal with, well, not deal,

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excuse me, how you start to work with

Speaker:

clients when helping them

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to overcome these issues.

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Actually, you know, first, maybe we could

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discuss mitochondrial tests.

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Sorry, I'm a bit all over the place.

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I know through the AONM, I'll probably

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get that right at one point, there are

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several, you have several options with

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regards to mitochondrial testing, and

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they're all amazing.

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And I'm definitely going to have to

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somehow convince you to

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send me some sample reports.

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Delighted to, yes, we do an ATP profile,

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which shows the total ATP, which is, of

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course, composed of the site of the ATP

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being produced along glycolysis as well

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as within the mitochondria.

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So one must never forget, you know, some

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ATP is obviously being produced outside

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the mitochondria too.

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And then the capacity of the mitochondria

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to produce ATP and of

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the glycolytic pathway.

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And then the alternative sort of reserve,

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as it's called, ATP production as well.

Speaker:

So that's the mitochondria at rest.

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And then there's a second one, which is

Speaker:

called the mitochondrial health index

Speaker:

that shows the

Speaker:

mitochondria under pressure too.

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And that would indicate the, first of

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all, the degree to which oxygen is not

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being used in the mitochondria, as it

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should, you know, a maximum of, you know,

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10% should be used outside for the

Speaker:

processes that we've just talked about,

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but not more than that.

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And if there is more than that, then you

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can usually, you know, what would

Speaker:

determine exactly what

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processes might be causing that issue.

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It is a sign of a cell danger response.

Speaker:

And there are markers, it's an 11-page

Speaker:

report, so it contains a lot of markers

Speaker:

like the proton leak, you know, exactly

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whether, you know, the mitochondrial

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membrane is not quite as sort of patent

Speaker:

as, you know, integral as it should be.

Speaker:

The coupling efficiency, in other words,

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how well the electrons are sort of

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popping from one complex to another.

Speaker:

And the degree of post-exertional

Speaker:

fatigue, you can also work out from

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what's called the reserve.

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When the mitochondria are put under

Speaker:

pressure, they should be able to expand

Speaker:

by about 400% in terms of the energy that

Speaker:

they produce, and often

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it's a lot less than that.

Speaker:

So there's a number of different markers

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that you can sort of put together.

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And there's an algorithm that calculates

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the what's called mitochondrial health

Speaker:

index, which is useful to compare if you

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want to sort of repeat it

Speaker:

after six months or whatever.

Speaker:

And then there are tests to calculate the

Speaker:

mitochondrial DNA

Speaker:

compared to the nuclear DNA.

Speaker:

Obviously, you have one nucleus but many

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mitochondria, so you can work out from

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that how many

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mitochondria there are in the cell.

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And if you have too few, mitobiogenesis,

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which is the generation of new

Speaker:

mitochondria, would be useful.

Speaker:

Whereas if you have too many, then that's

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a sign of the cell having detected a lack

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of energy and attempting to compensate

Speaker:

for it by producing more mitochondria.

Speaker:

But there is also a marker for how

Speaker:

functional they are.

Speaker:

And if a lot of them are dysfunctional,

Speaker:

even if you have many, what's called

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mitophagy, which we discussed earlier,

Speaker:

would be the approach rather than

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generating lots of new ones.

Speaker:

And you can work out the degree to which

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the mitochondria is suffering from

Speaker:

reactive oxygen species actually

Speaker:

beginning to impact the DNA of the

Speaker:

mitochondria, which is serious.

Speaker:

So it's good to pick that up early.

Speaker:

And the lactate pyruvate index actually

Speaker:

shows you the fuels that are getting into

Speaker:

the mitochondria, which is very useful.

Speaker:

Yes,

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you can work out whether the mitochondria are able to process fats or whether

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they're at a stage where they're more

Speaker:

readily able to process carbohydrates, or

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perhaps that the carbohydrates aren't

Speaker:

even getting in and they're being

Speaker:

backpedaled into lactate, which the body

Speaker:

can use, but it's a messier process.

Speaker:

And so if you've got a high lactate

Speaker:

level, then that's a sign that the

Speaker:

mitochondria really have shut down to a

Speaker:

large extent and they're not even

Speaker:

allowing the carbohydrates in.

Speaker:

But they're not allowing the carbohydrates in. So you can tell quite a lot about the

Speaker:

mitochondrial fuels from that.

Speaker:

And there are various others as well.

Speaker:

I'm either going to rob someone, break

Speaker:

the piggy bank or put in for a job

Speaker:

because those all

Speaker:

sound absolutely amazing.

Speaker:

I love the fact that you brought up those

Speaker:

various metabolic shuttles and I think a

Speaker:

poor man's version of that would be to

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measure glucose, ketones, and then

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lactate, which obviously you can do

Speaker:

independently and use those as proxies as

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well, which I think would be interesting

Speaker:

to cross reference those values directly

Speaker:

with some of those tests to identify how

Speaker:

you are, how effective you're utilizing

Speaker:

fatty acids for fuel sources.

Speaker:

I was actually going to ask this later,

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and actually I will.

Speaker:

I was going to ask a question about

Speaker:

ketogenic diets later

Speaker:

and we'll get there.

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Well, we could just throw in now that

Speaker:

that does show quite effectively that in

Speaker:

some cases attempting to utilize a high

Speaker:

fat diet for a patient is simply not

Speaker:

going to be the right thing for them at

Speaker:

that particular time.

Speaker:

You can of course attempt to encourage

Speaker:

ketones by giving beta hydroxybutyrate

Speaker:

precursors and so on.

Speaker:

That's a kind of way of leaping over the

Speaker:

normal pathways into the mitochondria and

Speaker:

hopefully as in the books about how

Speaker:

useful ketones can be for Alzheimer's and

Speaker:

so on, the Newton book and so on.

Speaker:

There's good evidence that you can

Speaker:

encourage that pathway, but actually

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utilizing a high fat diet, which is

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obviously often part of a ketogenic diet,

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is not always the right thing for the patient and they'll probably be able to

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give you a feedback as well.

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Yes, I'm sure they will very quickly.

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I think it's fascinating and again, I

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know people like Dr.

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Mai who are great proponents of the

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ketogenic diet, but as you've just

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alluded to you now, I do think that they

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can be problematic, which can be

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problematic in my view when you start

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dealing with people with these sort of

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apophimating gut tissues as well when

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there are some reactive carbohydrates.

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I think that starts to provide a

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challenge, but I suppose that's where you

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start to look at things like maybe a low

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FODMAP diet to remove potentially those

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triggering FODMAPs to help maybe allow a

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certain amount of carbohydrate ingestion

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while still not creating that

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fermentation that drives

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those dysbiotic conditions.

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Yeah,

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no, it's definitely a rabbit hole.

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Just maybe one more

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question if you don't mind.

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Just regarding the ketones, clinically,

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do you find there's any difference

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between the salts and the esters when

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providing somebody with a ketone

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supplement or do you not

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find it makes that question?

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Well, the esters are very much more

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expensive and so there's often a bit of

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reluctance among patients to use those, but salts have been very effective as well.

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I've had very good reports from patients

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and from doctors who are

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working with them as well.

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One doctor I know who managed to, or at

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least his patient managed to overcome

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this diabetes type 2 by using ketone

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salts along with obviously there's so

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many other things that a patient is using

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that you can't always

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identify that it's the one thing.

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But I do need to mention that I am and

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I'd love you to interview Morley Robbins

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at some point as well.

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He is actually coming over to England on

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the 21st and 22nd of May.

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He'll be holding two events here.

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I've sort of helped to liaise that and I

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have been following his approach with the

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Root Cause Protocol for about three years

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now quite intensively.

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I must say that despite all my, you know,

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a couple of decades of studying the

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mitochondria, I had not realised how

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very, very important bioavailable copper

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is for not just complex 4, you know, the

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cytochrome C oxidase, but also complex 5

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and the PrEP cycle and, you know, the

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production of heme and so on.

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It's absolutely central and also retinal.

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And so the pathway that's been worked out

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over many, many years by the Root Cause

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Protocol group, I first heard him in

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Seattle when I was over

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there actually with Dr.

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Klinghart, who was speaking

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sort of from the same platform.

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And I made a mental note for myself,

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gosh, this is somebody who I've got to

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follow as well and

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finally got round to it.

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And I'm very happy to be here. I've got round to it.

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And I must say this has

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extraordinary knowledge there.

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He's just done a very

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brilliant podcast with Dr.

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Malek that would be worth listening to

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for anybody who wants to sort of, you

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know, understand where he's coming from.

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But it's centrally involved in the

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mitochondria and that's because you were

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asking me what I suggest to patients.

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Very, very often I find that sort of

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sorting that mineral pathway, the

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electrolytes, making sure that they're

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getting sufficient retinol, which is

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problematic if it's a vegetarian or vegan

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patient because you can't really obtain

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retinol from non-meat sources or dairy.

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And then introducing the bioavailable

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copper that can really be miraculous and

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really, really help the mitochondria to

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get sort of back interaction again.

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So that is one of the very

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first pathways that I think about.

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And I sort of think back to cases I've

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had in the past like fatty liver, where I

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now understand the vital importance of

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those pathways in that as well.

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And sort of think, gosh, you know, I

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probably would have gone to that

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immediately in the past

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too if I'd known of it.

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So I think that's extremely useful.

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If you can't make it

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down to London in May,

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well, we're already in May, aren't we?

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For the events, then I'll send you the

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recording if we manage to make one.

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Oh, that'd be lovely.

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And if you could ask Morley Torrance my

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emails, that'd be better.

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Oh, I will do.

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Absolutely.

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I'm sure he gets thousands.

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So I'm not too...

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He publicly displays his

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email address everywhere.

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MorleyRobbins at gmail.com.

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So I'm sure he gets five and a half

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million emails on daily.

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But yeah, I've been trying to...

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As soon as he's over

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here, I'll mention that.

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Maybe he can even find time while he's

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over here, which is about seven days to

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have an interview with you.

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That would be super important.

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Yeah, no, we can make something happen.

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That would be amazing.

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Yeah, I've not dived that deeply into the

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root cause protocol.

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I think as you know, you sort of, you

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have your list of things to get through

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and then inevitably

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something falls by the wayside.

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I know, it took me a long, long time to

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get to it, but I'm so glad that I did.

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And I did want to start to mention that

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because you asked me what

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the different initiatives are.

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Another great

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inspiration I find is actually Dr.

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Jack Cruz.

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I don't know if you know of him,

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the neurosurgeon, but he emphasizes the

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importance of light for the mitochondria.

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Yes, but I mean, if he's different, he

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just doesn't work to...

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Yes, if you were to ask me what sort of

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the key influence for

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the mitochondria is.

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I mean, something that we all find so

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difficult these days

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because of the kinds of jobs and

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residences and where we live.

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It's so hard, but actually getting out

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into the sun and into nature and

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grounding more and so on.

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It all sounds so simple, but

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it's very, very hard to do.

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How much of our day

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do we spend doing that?

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And that's what our mitochondria are

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craving, actually, a lot of the time.

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Yeah, definitely.

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They're photoelectric, photodynamic

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organelles, and they require this input.

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I don't mean this with any disrespect,

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but I think people sort of, they don't

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realize it was sun beings and it's become

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culturally appropriate to analysis in the

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dark room all day, whereas technically we

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photosynthesize to a large extent.

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So by removing that aspect of our

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biology, we are essentially, yeah,

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becoming completely dysfunctional.

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Yeah, Dr.

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Cruz is someone I would also like to talk

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to, although I'll be honest, he scares

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the living day lights out of me.

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And when he goes down the physics rabbit

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hole, I get a bit bamboozled.

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I must admit, I think I did, the last

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time I did physics was maybe second year

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uni, and then that was it.

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Yeah, it's always a long listen, but it's

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just brilliant in there as well.

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No, definitely.

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He is a wealth of

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knowledge, that is for sure.

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So I suppose ultimately dealing with

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these chronic diseases and comes down to

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sort of ultimately

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identifying what causes the trigger.

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And what I'm trying to do is maybe create

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a framework for people who are on

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physicians or

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practitioners to sort of follow.

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And it fundamentally, and feel free to

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interject wherever you see fit.

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But the way I see it is you first got to

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find the root cause, your trigger, which

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is driving this dysfunction to begin

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with, whether it be mold and infection

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like a lime or what have you, and then to

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concurrently lower the toxic load on your

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body as much as possible.

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Then again, and that I think is where

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most people are going to struggle the

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most and where it is behoove, the correct

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word, then to work with a

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practitioner such as yourself.

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And then to start to start working

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through the other components of this

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dysfunction, sort of dealing with

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emotional issues, dealing with adverse

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childhood events, etc.

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And then to slowly reintroduce the

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nutrient-set support mitochondrial

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function, and to then

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hopefully get to the point where they

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have proper hormonal

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signaling and less despotic guts, etc.

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With that, it sort of has a hierarchy,

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sort of be a functional

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way to sort of approach.

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Yes.

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And what's very interesting is there that

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you mentioned supporting the mitochondria

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a little bit later in that process.

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And often one sort of gut reaction, one's

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knee jerk reaction is to start giving

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large numbers of mitochondrial nutrients

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very quickly like CoQ10,

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300 milligrams or whatever.

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And actually, if the mitochondria have

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down regulated intelligently and

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intentionally and unable to process those

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kinds of nutrients at

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the present time, it's just

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an inappropriate thing to do.

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I mean, you've always got to be

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supporting the mitochondria in a basic

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way, of course, but giving lots and lots

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of very specific nutrients at the

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beginning of that process when you're

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still in CDR1 or 2 is

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probably less efficient.

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Yeah.

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With the exception of something like

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methylene blue, which I'll ask you about

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in a bit, but otherwise, I see it.

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If you're bombarding a system that is

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electrical with too many electron donors,

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you're potentially just going to create a

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high reactive oxygen, just a high level

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of RRS between complex 4 and 5.

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So ultimately, you're going to end up

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doing more harm potentially than good.

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Yes.

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And a lot of it will be escaping through

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the UCPs, the uncoupling proteins, and

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it's creating heat rather than creating

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energy if it's getting into the

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mitochondria at all.

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So I work not only directly, but I have a

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lot to do with a lot of bodybuilders, and

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a lot of them use these various

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uncoupling agents to utilize

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from a fat loss perspective.

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And interestingly enough, there have been

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a few who have sort of shown some sort of

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signs of clinical remission

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by utilizing these compounds.

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Not that I would suggest, or I'm sure you

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would, that using something

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like DMP is in any way safe,

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these thermogenic compounds, if you

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overdo them even slightly,

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they can actually kill you.

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But yeah, it is interesting that by sort

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of uncoupling mitochondria deliberately,

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you can actually see an improvement in

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energy, which I suppose makes sense.

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But yeah, it comes with a lot of

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potential drawbacks.

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Anyway, that is rabbit hole in a tangent.

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Gillian, you've been a star.

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I think I'd like to close off with a few

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rapid fire questions, if that's okay.

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We can answer them.

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They're never rapid fire.

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But we can, yeah, just a few sort of

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off-the-cuff questions.

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Okay, so starting off, if you could fast

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forward mitochondrial medicine, say 10

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years, what

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breakthrough would you hope to see?

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Would you like to see?

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Oh goodness.

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I'd like to see a lot more simplicity.

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It's the simplicity

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beyond the complexity.

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And so I do hope that together with

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others, we can work towards that to make

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it a lot easier to overcome the cell

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danger response and restore patient's

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health, not have people

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stuck in ME for 20 and 30 years.

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I love that.

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I mean, someone like Ron Davis, Professor

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Davis in the States, the Open Medicine

Speaker:

Foundation, his son is in a...

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That's what gives him his motivation,

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unable to even take in

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sensations from around him.

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He sometimes can't even speak to him.

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This is so clearly a

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mitochondrial issue, and to be able to

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find simpler solutions would be

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absolutely tremendous.

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And affordable solutions as well.

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Yes, there we go.

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Unfortunately,

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medicine, I think, is still in that place

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where health is bought.

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And these problems aren't complex.

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I mean, they are complex to solve, but I

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feel there are so many

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solutions that are readily available.

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They just aren't accessible to 99.9% of

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the population at the moment.

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And that's a bit of a tragedy, and it's

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definitely what is a

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stumbling block for most,

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because it really, when you sort of

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understand the basics of it, like I do,

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and I'm nothing special, you do realize

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how simple these issues, broadly

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speaking, are to solve, at least

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initially.

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Obviously, if you're dealing with

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something more complicated, like a long

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code, where there's potentially a spike

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protein involvement, then

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it gets more complicated.

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But there are definitely solutions.

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They've just got to be accessible.

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Your answer is definitely,

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yeah, it's great.

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I was going to be obnoxious and say

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something like mitochondrial

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transplants, which I think...

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No, no, no.

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The body is too intelligent to need that

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kind of intervention.

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Yeah.

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I'm just excited.

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Aubrey de Grey and his

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attempts over the years.

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Thank you.

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Thanks very much.

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What can I say?

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It's a biochemist in me.

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I just want to see what happens when

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someone prods

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something or something else.

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Okay, next one.

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Red light therapy is thought to improve

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mitochondrial function.

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And I suppose it does,

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at least peripherally.

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Do you think it's effective at helping to

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improve CDR or is it not that...

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Yes, absolutely.

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I think that photobio-modulation is

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massively important.

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And that, along with the light, as I

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mentioned earlier, sometimes patients

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can't take a lot of supplements and they

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can't even take a lot of...

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Obviously, transdermal nutrients,

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electrolytes, and so on can help.

Speaker:

But sometimes you really do have to start

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with these more sort of

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extracorporeal types of therapy.

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And I think the red light, perhaps just

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an umbrella above the person's head,

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perhaps just for three minutes.

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Once every couple of days, I've seen that

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make a huge difference as well.

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It's got to be the right frequency.

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And there are specialists like Dr.

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Damien Downing, who I know you're

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interviewing very soon, who have spent

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many, many years looking into that and

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have a whole range of

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products related to that.

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It would be very, very important really

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not to waste your money on the wrong

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frequency, but there are specialists

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available who can give one

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that kind of information.

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Yeah, there definitely are.

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Vegas mode stimulators.

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There are a few out there.

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Are you a fan of these?

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Do you think they're effective?

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I haven't used them myself.

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Items like the Sensate, again, through

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working closely with Dr.

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Damien, because I am a member of the BSCM

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as well on the committee.

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So I attend every event of theirs, and

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he's seen benefits from that.

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And I do have colleagues who also have

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done, but I haven't

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recommended them myself.

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Not yet.

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Fair enough.

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And the last one, and maybe

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this one is a bit obscure.

Speaker:

So if needs be, we can cut it down.

Speaker:

But what do you think about

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mitochondrial support peptides?

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Things like MoTSI or SS31?

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I don't know if you've come across these

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or if you've got any thoughts on them.

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Do you think they're effective?

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Have you utilized them in practice?

Speaker:

Dr.

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Holtz-Dolfen states, for example, as a

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great specialist in those.

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I haven't used them, and they're

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difficult to access here.

Speaker:

And I think he would really need to, A,

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B, and M, D, I would

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say really to use them.

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I think even in the states, they've, the

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FDA has removed a lot of them from the

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market now, perhaps

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without any justification.

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But it's a bit of a hot potato.

Speaker:

I would much prefer to start with

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something simpler, like I was just

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explaining previously, the right balance

Speaker:

of minerals, checking the

Speaker:

patient's sodium status.

Speaker:

COTS is so often just a matter of getting

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the potassium and the

Speaker:

sodium ratios right.

Speaker:

Starting with the basics, and often I do

Speaker:

find people have been

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through the most incredible

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odysseys, perhaps even using apheresis,

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which is filtering of the blood, the

Speaker:

entire blood, attempting to remove the

Speaker:

antibodies and aspects such as I've just

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mentioned, have not

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been touched on at all.

Speaker:

So diet, of course, is

Speaker:

so important as well.

Speaker:

So using the, as I say, simpler, sort of

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more accessible

Speaker:

techniques would be my preference.

Speaker:

But I'd be very prepared to sort of take

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part in seminars and

Speaker:

learn more about the peptides.

Speaker:

I just haven't done that yet.

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Yeah, they're definitely interesting.

Speaker:

And things like MODC, sort of which

Speaker:

enhance insulin sensitivity and promote

Speaker:

the sort of mitochondrial biogenesis, it

Speaker:

acts on the folate AMPK pathway.

Speaker:

And it's also thought to

Speaker:

be an exercise mimetic.

Speaker:

And I think Downstreamer that promotes

Speaker:

some PGC1R for activation.

Speaker:

And then you have things like SS31, which

Speaker:

more instead of that sort of the

Speaker:

biogenesis aspect, it, let's see if I can

Speaker:

get this right, it binds to cardiolipine

Speaker:

and I think it improves the membrane

Speaker:

health and the structure thereof, thereby

Speaker:

sort of reducing ROS

Speaker:

and improving ATP output.

Speaker:

So they definitely are interesting and

Speaker:

there's definitely some

Speaker:

therapeutic potential there.

Speaker:

But I think, as you alluded to, it's,

Speaker:

I think the FDA has, I hate this term,

Speaker:

clamped down on a lot of them because of

Speaker:

the gray market aspect.

Speaker:

And I think people have just

Speaker:

had too much access to them.

Speaker:

And yeah, I don't think they're inherent

Speaker:

inherently a problem.

Speaker:

But I think when you start looking at

Speaker:

things like where they're sourced, they

Speaker:

can become an issue.

Speaker:

A lot of them come from, they're not even

Speaker:

compounded, they just come from the Far

Speaker:

East or whatever where they're just

Speaker:

manufactured and you don't

Speaker:

know what you get alongside them.

Speaker:

The endotoxin load,

Speaker:

obviously, yeah, the endotoxin load, the

Speaker:

lipopolysaccharide

Speaker:

load, heavy metals, etc.

Speaker:

But they are, when they use correctly,

Speaker:

they definitely are incredible.

Speaker:

Okay, last one.

Speaker:

What are your thoughts on methylene blue?

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I don't use it myself.

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I do have some concerns when I listen to

Speaker:

what it does to the MAO pathway

Speaker:

or enzyme.

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MAO, A, I think.

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And B, yeah.

Speaker:

Is it B?

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Yes.

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An enough dosage to be fair.

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Yes, I sort of, again, I'm a little bit

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perhaps cautious that way.

Speaker:

And I would prefer to see it used by

Speaker:

doctors and not too widely accessible

Speaker:

just because of the risks that appear to

Speaker:

be in the dosage and so on.

Speaker:

But I'm very happy to

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work in teams where people,

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which I do prefer to do, actually, I

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always prefer to work in

Speaker:

multidisciplinary teams and there might

Speaker:

be a doctor included.

Speaker:

I know that Dr.

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Klinghardt, for example, does use it and

Speaker:

other doctors who I know as well.

Speaker:

So they're willing to be guided by them,

Speaker:

but I don't recommend it myself.

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Yeah, again, it's a

Speaker:

very interesting molecule.

Speaker:

And obviously, being an electron donor

Speaker:

and being able to bypass some of those

Speaker:

block complexes, I think for the right

Speaker:

person, it's definitely a good option.

Speaker:

And somebody who's already got healthy

Speaker:

liver mitochondrial function, it's

Speaker:

definitely not warranted.

Speaker:

And it can actually, again, cause

Speaker:

electron leakage with excessive use.

Speaker:

I think one of the things it's able to do

Speaker:

is to switch from ferrous ion to the

Speaker:

ferric ion, i.e. from the 3 to the 2 plus

Speaker:

stage and the methanolabemia, which is a

Speaker:

problem as well, and for which it was

Speaker:

originally used and still is.

Speaker:

It just makes me wonder whether there are

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other ways of encouraging better ion

Speaker:

transport and releasing the trapped ion

Speaker:

and creating the right form of ion for

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the body to utilize rather than

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necessarily using that.

Speaker:

But I'm open to learning more about it.

Speaker:

Yeah, no, it is an interesting molecule.

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And there's a large amount of data there

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around its use and sort of regulating

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things like ferroptosis, which is another

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rabbit hole for another day.

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But yeah, I think for a lot of people in

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this who are struggling with CDR, the

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point you touched on with regards to it

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being an MAOI, yeah, an monoamine oxidase

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inhibitor, is very on point because,

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yeah, I mean, if you're going to inhibit

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MAO, you're going to sort of increase

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histamine levels potentially, which is

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going to cause all sorts of

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people all sorts of issues.

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So I think a little

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knowledge can be a dangerous thing.

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And it's ultimately up to the individual

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to educate themselves thoroughly if they

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do choose to use these

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sorts of compounds, but

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causing the serotonin

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syndrome as well, which patients

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generally do disclose everything to one,

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but not always

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absolutely every last thing.

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Sometimes they forget.

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And if they are an SSRI,

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it can potentially be fatal.

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Yeah, I think it's ultimately a bit of a

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done in Kruger at the

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end of the days, isn't it?

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You sort of, little

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knowledges can be a dangerous thing.

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Jolynn, you've been a star and this

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conversation has been

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delightful and informative.

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Thank you so much.

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And I'll thank you.

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It's been up and delighted to be here.

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Thank you.

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If people want to work with you, if they

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want to find out more about the AONM, I

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think I got there, where

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would you like to point them?

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Where can they find you?

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Well, the Academy of Nutritional Medicine

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AONM is readily

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accessible at the url aonm.org.

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And all our tests and

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our events are there.

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I hold a bit like you, you know, a

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podcast about a

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webinar about once a week.

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And I'm always there and have an email,

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Jolynn, with 1L, interestingly, at

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aonm.org, where I can

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always be reached as well.

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So thank you so, so much.

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It's absolutely stunning for different

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speakers you have available.

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And I'm going to go back now over all of

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your recordings and listen to them

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because it sounds as though you have

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amazing topics that you've covered and

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are planning to cover.

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Thank you.

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That's very kind of you.

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Thank you.

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We'll chat soon.

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Thank you.

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Bye bye.

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About the Podcast

vP life
Discussions on the latest in longevity science, health and functional medicine
vP Life, brought to you by vitalityPRO, provides you with expert advice from leading voices in the functional and integrative medicine world.

Irrespective of the guest and topic, our discussions will aim to educate and provide you with the tools and information you need to create change in your life.

About your host

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Robert Underwood