WEBVTT

0:00:00.000 --> 0:00:03.320
 Well, today's going to be a real fascinating discussion.

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 I call this my big fat panel because it's exploring the idea of obesity, what causes

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 obesity.

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 And we have assembled, I think, an all-star panel today of leading lights in various different

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 categories of knowledge that have been really doing great work in exploring why we have such a rise

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 in obesity over the years.

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 And each of these individuals I've interviewed in the past,

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 and we've never had them all together on one panel together.

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 But I thought if we're gonna tackle

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 the big elephant in the room,

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 which is causing so much dysfunction,

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 both on a health basis as well as a financial and

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 economic burden in this country and around the world, then we've got to

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 really dive into the specifics as to what is really going on with these seed

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 oil products and high PUFA products in general and their link to obesity. What

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 is the mechanism precisely what is driving this problem?

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 And so, just a brief introduction, and again, I'm not going to get all the accolades right,

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 you know, in just a short time, but Peter Dobromilsky, I met you through your blog,

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 Hyperlipid, where you've been doing great work in really getting into the weeds of explaining

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 the mechanisms. And I had a hard time following, but I had to keep of explaining the mechanisms and I had a

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 hard time following but I had to keep it was really I had to pause it and replay

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 but it was very fascinating stuff with your explanation for what what's going

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 on with the linoleic acid in the cells and Dr. Kate Shanahan of course you've

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 been the leading pioneer as a woman out there around

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 the world stage, sounding the alarm of this problem for a long time.

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 Saw you on Bill Maher's show and many, many other programs.

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 Fox, what was it, Jesse Waters you were just on, I saw.

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 And that's amazing stuff.

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 So a true pioneer on this topic of seed oils and also author of Fat Burn Fix and Deep Nutrition.

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 Of course, we got Tucker Goodrich who's a frequent,

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 if you are a listener or viewer of our radio show, you see Tucker on every week.

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 He is the proprietor of Yelling Stop, the blog,

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 and he too has been out there for a long time now talking about seed oils

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 and sounding the

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 alarm.

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 We have Brad Marshall with Fire in a Bottle, and he is someone that's been on my show exploring

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 how this linoleic acid is basically driving so much of what you call torpor, right?

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 A state of torpor that people are in, which is an interesting angle.

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 And so Brad has been raising low PUFA pork and low PUFA chicken experiments with really

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 interesting results and other types of, you know, experimentations. He's got a background in

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 genetics and biology. And we have Dr. Ray Peat, who's joining me from by phone today.

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 So he is also someone who's got a long history

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 of talking about these different issues.

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 And each person on this panel

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 brings a different perspective.

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 Kate Shanahan is an MD.

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 Peter Dobromilsky, you are in veterinarian, right?

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 Is that your?

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 Yeah. And so, everybody has different, and, you know,

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 Dr. Peat, you have a unique angle that I think a lot of people have been fascinated by. So,

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 I really want to welcome all of you to this discussion. Thank you.

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 It's an honor to be here. Yeah, thank you.

0:03:40.960 --> 0:03:47.240
 Very good. So, let's just start where I start off, which is to start with Peter, since you…that's

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 the order of introduction.

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 So, Peter, go ahead and tell us just, you know, your background a little bit and set

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 the table for what precisely is the mechanism.

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 If we're going to make this case to the world, we've got to figure out what precisely

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 is the mechanism for causing obesity and maybe there's multiple layers to this question.

0:04:05.360 --> 0:04:09.280
 Yeah, I would agree very much that I think

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 there are multiple layers to the question.

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 And my view has been for many years now

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 that obesity is primarily a signaling problem

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 and that there are layers to the signaling. The very most basic

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 layer of signaling, there is the mitochondria signaling to the cell what to do with the

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 available calories. And that signaling process goes right back to bacteria,

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 probably archaea as well, but nobody's ever looked at them.

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 So, but with bacteria, growth and reproduction

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 are inseparable from reactive oxygen species signaling.

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 And the method for producing the ROS by bacteria,

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 we really don't know about yet, but the mitochondrion is essentially bacterium and

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 from my point of view, it has brought with it the signaling system that it had when it was a free bacterium, and it uses that to talk to the cell. So that's where

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 I ended up with on a very theoretical basis. On a more practical basis,

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 I started low-carb 20 years ago. I realized when I started low-carb that there were great big glaring holes in the low-carb

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 hypothesis of what controlled obesity and that you could look at various populations

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 with very, very high carbohydrate intakes and there was no obesity. So I knew right from the beginning

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 that the insulin hypothesis of obesity was very attractive, very practical set of advice,

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 but couldn't be fundamentally the only explanation. So I looked at that for many years, thought that there has to be more to it.

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 And probably about 10-12 years ago, I sat down and tried to work out the difference in terms of how

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 fats and how carbohydrates were actually processed in the cell and in the mitochondria. And the

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 concept that it might be reactive oxygen species that were essential for signaling how many

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 calories a given cell should accept, more or less fell out of those back of the envelope doodles. And it went on from,

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 in slow steps from there over something like 60 blog posts

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 now, all of which essentially stem from those three or four.

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 So that's where I've ended up that

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 the seed oils signal differently within the cell from saturated fats and the fruit oils,

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 things like avocado oil or olive oil, are halfway house or closer to the monounsaturated

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 fats, which again are a normal signaling component of mammalian cells.

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 So we've got saturated fats and mixed with monounsaturated fats as a normal milieu

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 and C. doles mess that up.

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 I think that seems reasonable.

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 That's where I come from basically.

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 So I'll let someone else have a go.

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 Dr. Kate Sanihan, can you chime in with your, where you start with this question?

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 Yeah, absolutely.

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 So my conclusion is that a diet of seed oils builds body fat that makes people feel sick

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 and tired when they try to burn their body fat.

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 And because of that, we have people overeating,

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 as we know people are overeating

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 by somewhere around six to 800 calories on average,

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 although a lot of studies under-report that,

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 so not everybody is aware of that.

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 But so that drives overeating.

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 And then the other thing that it does

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 is it changes your, it totally retools your metabolism. We're supposed to all be fat burners. We're supposed to spend most of our time

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 You know fueling on our body fat between meals and when you have too much PUFA in your body fat the polyunsaturated

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 fatty acid from these seed oils

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 It builds up in your body fat to a concentration that is

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 exceeds like all of, all of human history

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 by six times.

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 It used to be around 5%, now it's 30%.

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 And that dramatically changes the ability

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 of your mitochondria to generate energy.

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 It pretty much shuts them down

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 and threatens to kill your cells, right?

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 Because without energy, cells will die within six seconds.

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 They only have about six seconds supply of ATP energy.

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 And so what they do instead is they reach for another fuel.

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 And what do they reach for?

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 Sugar, because there's always some sugar in the bloodstream.

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 And what does that do if you haven't just eaten?

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 Well, it'll cause hypoglycemia, right?

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 It'll make you feel hypoglycemic.

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 And we have an epidemic of people experiencing hypoglycemia symptoms,? It'll make you feel hypoglycemic. And we have an epidemic of people experiencing

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 hypoglycemia symptoms. I can tell you this because pretty much every single one of my

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 patients who's overweight says, Oh yeah, my doctor, previous doctor, not me said I have

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 hypoglycemia and I have to eat right when I start to feel dizzy, when I start to feel

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 brain fog, when I faint, uh, it'll bring on seizures in some people.

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 This is a very serious endemic pandemic of hypoglycemia, and it's happening because our

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 body fat makes us feel sick and tired when we try to burn it, and it makes your mitochondria,

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 it kills your mitochondria. So I think that I've looked,

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 as far as like where do I fit in the context

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 of Jal's other theories here,

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 I feel like what every one of you says

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 is compatible with what I'm saying.

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 Like I feel like absolutely the signaling happens, right?

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 And reactive oxygen species play a huge role in all this.

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 And I mean, the other guys are gonna speak,

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 you haven't spoken yet to what your theories are,

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 but I'm obliquely familiar with all of them.

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 And I feel like it fits into that big picture.

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 So I feel like what I'm bringing to it is like,

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 synthesis for one thing, synthesis of the theories.

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 But for another thing, kind of, you know, it's all proof that we're all, we're all

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 right.

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 You're everyone that understands that seed oils are unhealthy.

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 You, for whatever reason, no matter how many different reasons you have, it's all,

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 it's correct.

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 For the most part, everyone that I've've heard I haven't heard anybody come up with any

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 Reason that seed oils are bad that is

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 completely untrue

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 Right. There's some there's some element to

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 Of truth, I think just about everything but I think the major mechanism is is is what I've said

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 It is that that big picture and just to give you a little bit of background,

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 I've actually, I was like reviewing like,

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 when I really got into this,

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 I don't know if you guys know,

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 but I went to Cornell for cellular

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 and molecular biochemistry in the 80s, in the late 80s.

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 And so back then I was, you know,

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 even though I wasn't a doctor

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 and I didn't know about PUFA,

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 I understood polyunsaturated fatty acids

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 and we're prone to oxidation and the spin states

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 of oxygen that will either allow

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 or prevent it from interacting.

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 And so I've kind of like was primed

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 for when I finally got into this,

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 when I was a doctor and I got sick

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 and nothing would make me feel better

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 to question the idea of saturated fat as being unhealthy.

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 And as soon as I saw that was literally

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 there was one research article that I saw

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 by Eva Sodergren and it was called,

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 it was her PhD thesis

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 and it was called Lipid Peroxidation in Vivo.

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 And when I saw that and the molecules of linoleic acid

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 and the reactions that happened in the body,

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 I knew immediately because I have all this background

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 that all of this would affect all of our cellular membranes,

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 our mitochondria, our fat cells, our brain cells, and all the

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 microstructures inside of our cells.

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 Because you can't have normal physiology when you've got reactive oxygen species flying

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 around and you get polymerization of the polyunsaturated fatty acids in the membranes, which destroys

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 an area of the membrane.

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 And this has to do with something called the permeability transition pore, where researchers

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 have found that burning PUFA causes this thing that they haven't really identified which

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 protein it is.

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 Some people say it's on the inner mitochondrial membrane, some people say it's on the outer

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 mitochondrial membrane, some people say it's on the outer mitochondrial membrane. Some people say it's like one membrane, one protein or another. What it is, is that when you burn

0:13:50.920 --> 0:13:54.920
 polyunsaturated fatty acids, you blow holes in the side of your mitochondria. I mean,

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 it's like, it's a major, major problem. It's like an explosion. And the different researchers

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 are doing their best to kind of identify, okay, this little bit and piece

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 of like broken, destroyed, damaged, trying, struggling to survive mitochondria has exactly

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 this thing on it.

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 But the big picture is what I said.

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 It's this is an inappropriate fuel.

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 It's as if we have traveled to, well, you know, in Star Trek, they call this thing the

0:14:23.520 --> 0:14:25.960
 M class planets, right, that

0:14:25.960 --> 0:14:31.220
 are compatible with life, right, right. And there was a recent movie, don't look up or

0:14:31.220 --> 0:14:37.160
 look up or one of those two, about the planet Earth blew up. And in 23,000 years, the rich

0:14:37.160 --> 0:14:47.640
 people end up on another M class planet. So M class planet, it's compatible with life. Well, we were on it, you can apply that to diet, right?

0:14:47.640 --> 0:14:50.940
 We were on an M-class diet, compatible with life.

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 We have shifted to a diet that is not compatible.

0:14:54.720 --> 0:14:59.720
 That is how profound this switch to polyunsaturates

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 from mostly saturates is,

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 because we are constantly subjecting our bodies

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 to an unprecedented, uncontrollable amount

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 of oxidative stress and it just destroys life.

0:15:16.120 --> 0:15:16.960
 Very good.

0:15:18.880 --> 0:15:19.720
 Well said.

0:15:19.720 --> 0:15:23.440
 So Tucker Goodrich, I wanted to let you explain

0:15:23.440 --> 0:15:25.760
 how you see this problem of seed oils and

0:15:25.760 --> 0:15:26.760
 obesity.

0:15:26.760 --> 0:15:34.640
 Well, first off, I want to say it's an honor to be on this panel with everybody here.

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 I've gotten inspiration from all of them.

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 When we talked to Dr. Peat the previous time, I mentioned that I think every time I go back and read his stuff, it's

0:15:48.680 --> 0:15:56.920
 amazing to me how much I've learned in the interim and how much more I'm able to understand

0:15:56.920 --> 0:16:01.040
 what he wrote the first time around that I wasn't able to get.

0:16:01.040 --> 0:16:11.400
 Same goes for everybody else here. So I thank you all for the background I've gotten from all of you.

0:16:11.400 --> 0:16:15.760
 So my experience was somewhat, started out somewhat personal.

0:16:15.760 --> 0:16:26.000
 I was a little bit overweight and very sick, and almost on a, you know know after doing some reading about the problems with seed oils

0:16:26.640 --> 0:16:32.160
 On a lark. I decided one day at the salad bar in my office to stop eating them

0:16:32.720 --> 0:16:33.760
 um

0:16:33.760 --> 0:16:35.760
 looking at the squeeze bottles of

0:16:36.560 --> 0:16:38.560
 Salad dressing at the end of the salad bar

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 I'm thinking that those must be the cheapest nastiest oils known to man to make it into that salad bar in an office cafeteria.

0:16:46.720 --> 0:16:53.640
 And to my surprise, my health increased dramatically and immediately.

0:16:53.640 --> 0:16:59.020
 An irritable bowel disease I had been suffering from for 16 years went away in two days.

0:16:59.020 --> 0:17:05.900
 And over the next couple of months, I lost all of my excess weight which I had been fighting for some time to no useful effect

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 Culminating in

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 Putting on my pants one morning to go to work buckling up my belt letting go and having them fall to the floor

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 Which was a fairly happy thing to have happen. Although the tailoring bills that followed that were

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 pretty severe

0:17:23.580 --> 0:17:28.420
 that followed that were pretty severe. So I got curious, why did this happen?

0:17:28.420 --> 0:17:33.420
 Why was, you know, it totally went against

0:17:34.300 --> 0:17:35.500
 what we're told to do.

0:17:35.500 --> 0:17:39.200
 We're told that these oils are part of a healthy diet

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 and that we should be consuming them

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 and that if we do so, we will lose weight and be healthy

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 and I only recovered my health when I reversed that advice. consuming them and that if we do so, we will lose weight and be healthy.

0:17:45.400 --> 0:17:49.680
 And I only recovered my health when I reversed that advice.

0:17:49.680 --> 0:17:57.240
 So I started, you know, at the time I was on Wall Street as a technology expert and

0:17:57.240 --> 0:18:00.560
 I was quite adept at researching and solving problems.

0:18:00.560 --> 0:18:07.920
 So I just turned that skill set to the scientific literature. And what I found over the

0:18:07.920 --> 0:18:14.880
 years, as you know, Peter and Kate have already mentioned, you know, it would be nice if there was

0:18:15.520 --> 0:18:22.800
 one thing going on here. It would make it a much easier story to explain to people.

0:18:24.160 --> 0:18:26.680
 make it a much easier story to explain to people. Unfortunately, that's not the case.

0:18:26.680 --> 0:18:34.400
 As Kate said, these are not something

0:18:34.400 --> 0:18:37.000
 that we've evolved to eat in the levels

0:18:37.000 --> 0:18:39.960
 that we are currently consuming them.

0:18:39.960 --> 0:18:42.000
 I came across one study that looked

0:18:42.000 --> 0:18:47.260
 at protein damage in the cell from the peroxidation of omega-6 fats.

0:18:47.260 --> 0:18:49.980
 And one chemical specifically they were looking at,

0:18:49.980 --> 0:18:54.740
 HNE, caused 24% of the proteins in the cell

0:18:54.740 --> 0:18:57.860
 to become damaged and dysfunctional.

0:18:57.860 --> 0:19:00.860
 That's an amazing impact on your body.

0:19:00.860 --> 0:19:03.700
 And it's not just mitochondria,

0:19:03.700 --> 0:19:06.560
 and it affects pretty much every cell process

0:19:06.560 --> 0:19:09.080
 around energy generation.

0:19:09.080 --> 0:19:12.680
 So, and that's after you eat them, right?

0:19:14.520 --> 0:19:17.720
 We also know from a number of studies

0:19:17.720 --> 0:19:20.080
 that even before these fats get into your body,

0:19:20.080 --> 0:19:24.020
 they have direct effects on your appetite.

0:19:24.020 --> 0:19:28.240
 They cause you to crave carbohydrates and sugar.

0:19:28.240 --> 0:19:32.800
 And if you look at what we are overeating, it's primarily carbohydrates and sugar.

0:19:32.800 --> 0:19:34.900
 That doesn't mean that they're causing obesity.

0:19:34.900 --> 0:19:40.400
 What it means is that we are eating a chemical that induces a state known as hyperphagia,

0:19:40.400 --> 0:19:46.720
 meaning overeating, and that what it stimulates us to eat is carbohydrates and sugar.

0:19:46.720 --> 0:19:48.900
 Sugar does have an independent effect,

0:19:48.900 --> 0:19:50.840
 particularly if you drink sugar,

0:19:50.840 --> 0:19:53.640
 but it's a much smaller effect than that of seed oils.

0:19:53.640 --> 0:19:56.880
 So once they get into your body,

0:19:56.880 --> 0:19:59.520
 they alter your fat storage pathways,

0:19:59.520 --> 0:20:03.560
 and in apparently everything from yeast

0:20:03.560 --> 0:20:09.920
 to nematodes, roundworms, to humans, they cause

0:20:09.920 --> 0:20:13.320
 your body to apparently store fat.

0:20:13.320 --> 0:20:21.160
 And once that fat goes into your adipocytes, your fat cells, the stored fats in your fat

0:20:21.160 --> 0:20:26.200
 cells then cause the fat cells to misfunction and become insulin resistant

0:20:27.400 --> 0:20:29.400
 so it's really you know if

0:20:31.520 --> 0:20:36.360
 It's quite amazing how many different effects these fats have on

0:20:37.380 --> 0:20:41.560
 Causing dysregulation of your body system, you know in a normal

0:20:42.320 --> 0:20:45.300
 Diet in the type of diet that we evolved to eat

0:20:45.480 --> 0:20:51.280
 We have of course a tendency to put on fat when times are good and to lose it when times are bad

0:20:51.520 --> 0:20:54.280
 But there are limits to that up and down right? I mean

0:20:54.880 --> 0:20:58.360
 400 pound people don't survive very long on the savannas of Africa

0:20:59.360 --> 0:21:01.360
 and

0:21:01.480 --> 0:21:05.880
 Eating a food that causes that to happen would be very anti-survival there,

0:21:05.880 --> 0:21:08.200
 and not having a regulatory system

0:21:08.200 --> 0:21:10.260
 would be very anti-survival there.

0:21:10.260 --> 0:21:12.880
 But what we are doing is inducing in ourself

0:21:12.880 --> 0:21:15.520
 a continuous state of dysregulation

0:21:15.520 --> 0:21:17.460
 causing this obesity epidemic.

0:21:20.280 --> 0:21:22.880
 So, Brad Marshall, you have a background

0:21:22.880 --> 0:21:28.500
 in molecular biology, you're also a pig farmer, so you get to see how pigs gain weight, and they're monogastric animals.

0:21:28.500 --> 0:21:35.500
 So, you take some very interesting perspectives on this question of how seed oils and high poofer products cause obesity.

0:21:36.500 --> 0:21:40.500
 Yeah, and I'm glad you brought that up.

0:21:40.500 --> 0:21:52.600
 Those are, like I say, the fact that I've raised pigs. So I've been kind of generally anti seed oils, you

0:21:52.600 --> 0:21:57.120
 know, ever since I read the oiling of America on the Weston

0:21:57.120 --> 0:22:02.720
 a price blog and like, I don't know the year 2002 or something.

0:22:04.480 --> 0:22:07.980
 And, and that so, so I started raising pigs

0:22:07.980 --> 0:22:09.520
 in around the year 2005.

0:22:10.400 --> 0:22:13.720
 And that really was one of the things

0:22:13.720 --> 0:22:16.600
 that I was trying to do because I knew that,

0:22:16.600 --> 0:22:17.980
 I knew the pigs were monogastric.

0:22:17.980 --> 0:22:22.980
 I also knew based on literature about raising pigs

0:22:23.060 --> 0:22:27.040
 from the 1800, late 1800s even, that says that, you know,

0:22:27.040 --> 0:22:31.680
 you can't feed pigs anything that contains too much

0:22:31.680 --> 0:22:36.200
 of the vegetable oils or you'll get soft pork.

0:22:36.200 --> 0:22:40.200
 And even back then it was known that American pork,

0:22:40.200 --> 0:22:42.900
 which was almost always corn finished,

0:22:42.900 --> 0:22:46.320
 sold at a discount in European markets because American

0:22:46.320 --> 0:22:51.840
 pork was known to be soft. And the Europeans finished their pork on barley, which has about

0:22:51.840 --> 0:23:00.080
 half of the linoleic acid of corn. And so it's been known at least since the 1800s that these

0:23:00.080 --> 0:23:09.040
 polyunsaturated fats kind of bioaccumulate in anything, or at least any monogastric that you feed them to. And so I was

0:23:09.040 --> 0:23:15.280
 sort of, you know, I was raising pastured pork, and it was all

0:23:15.280 --> 0:23:19.680
 GMO free. And I was doing everything I could to, you know,

0:23:19.680 --> 0:23:26.080
 keep keep my pork fat to not be soft. And so I have a lot of experiences

0:23:26.080 --> 0:23:27.680
 working with other farms.

0:23:28.600 --> 0:23:31.880
 And also with my own pigs on my own farm,

0:23:31.880 --> 0:23:35.400
 I realized that certain pigs genetically,

0:23:35.400 --> 0:23:36.760
 it didn't matter what you fed them,

0:23:36.760 --> 0:23:38.460
 they always had soft fat.

0:23:38.460 --> 0:23:42.200
 And so, I saw very firsthand

0:23:42.200 --> 0:23:46.040
 that the saturation of your own body fat,

0:23:46.040 --> 0:23:48.680
 there was a huge difference based on

0:23:50.200 --> 0:23:51.260
 what you fed the animal,

0:23:51.260 --> 0:23:54.000
 but also the genetics of the animal.

0:23:54.000 --> 0:23:57.000
 And so there was something happening internally

0:23:57.000 --> 0:23:59.880
 that could affect the body fat saturation.

0:23:59.880 --> 0:24:02.000
 And then obviously the externally,

0:24:02.000 --> 0:24:03.320
 what you fed them made a difference.

0:24:03.320 --> 0:24:09.360
 And so if you read fire in a bottle, a lot of, I talk a lot about an enzyme called SCD

0:24:09.360 --> 0:24:10.360
 one.

0:24:10.360 --> 0:24:17.120
 And what that does is it turns your stored body fat from a saturated fat into monounsaturated

0:24:17.120 --> 0:24:18.120
 fat.

0:24:18.120 --> 0:24:28.840
 And then also, um, of course the amount of dietary polyunsaturated fat. And so, because I think that, you know, sure,

0:24:28.840 --> 0:24:35.700
 the fat in your last meal, of course, plays a huge role in what your mitochondria are

0:24:35.700 --> 0:24:40.760
 actually oxidizing, but it's, it's sort of blended with your stored body fat before it

0:24:40.760 --> 0:24:47.960
 enters the mitochondria. And so you have these two different sort of pools of fat that at any point

0:24:47.960 --> 0:24:52.240
 in time you're, you're oxidizing. And so I've spent a

0:24:52.240 --> 0:24:55.800
 lot of time, you know, thinking about that. And that really is

0:24:55.800 --> 0:25:00.680
 where the the conversations about the torpor comes in and

0:25:00.680 --> 0:25:04.480
 the now and you know, and the torpor thing is, it's kind of an

0:25:04.480 --> 0:25:08.440
 analogy, you know, humans obviously don't- torpor

0:25:08.440 --> 0:25:12.640
 for those who don't know is a, is a, it's kind of an

0:25:12.680 --> 0:25:18.440
 alternative metabolic state that hibernating animals use before

0:25:18.440 --> 0:25:21.600
 they hibernate. But one of the things that they do is they have

0:25:21.600 --> 0:25:24.960
 to eat a lot of polyunsaturated fat to be able to go into torpor.

0:25:31.160 --> 0:25:38.800
 And then as they approach torpor, they increase the amount of SCD-1 that they make. And so, hibernating animals eat a lot of PUFA and they have a lot of SCD-1. And so, hibernating

0:25:38.800 --> 0:25:46.400
 animals have very, very unsaturated body fat compared to, you know, an animal that is never going to

0:25:46.400 --> 0:25:52.040
 hibernate, even if they're monogastrics. And so then when you look at obese

0:25:52.040 --> 0:25:58.840
 humans over the last, you know, 70 years or however long, obviously polyunsaturated

0:25:58.840 --> 0:26:05.960
 fats have increased, but the amount of SCD1 has also increased. And so when you look at,

0:26:06.840 --> 0:26:09.820
 especially in the muscle tissue of obese humans,

0:26:09.820 --> 0:26:12.080
 there is an incredibly direct correlation

0:26:12.080 --> 0:26:17.080
 between the amount of SCD-1 produced in the muscle tissue

0:26:17.880 --> 0:26:21.540
 and the BMI of that human.

0:26:21.540 --> 0:26:23.380
 And so whenever you see a correlation

0:26:23.380 --> 0:26:25.340
 that's that direct in the real world,

0:26:25.340 --> 0:26:27.200
 I think that's interesting.

0:26:27.200 --> 0:26:31.620
 It, of course, doesn't necessarily prove causation.

0:26:31.620 --> 0:26:36.620
 But I've seen all of these parallels

0:26:36.700 --> 0:26:40.500
 between changes in body fat saturation and obesity,

0:26:41.620 --> 0:26:43.300
 in the exact same way that animals

0:26:43.300 --> 0:26:45.040
 who want to store fat for

0:26:45.040 --> 0:26:51.960
 hibernation do it is the exact same way that obese humans behave. And so that was

0:26:51.960 --> 0:26:58.060
 right. And of course all that started with me just trying to be trying to make

0:26:58.060 --> 0:27:09.120
 the pork fat firm on my pigs that I was raising and it has sort of gone from there. But, and so now on the blog, I'm digging, you know,

0:27:09.280 --> 0:27:12.200
 Peter talks about, he's at a very low level

0:27:12.200 --> 0:27:14.820
 and I'm sort of like one level above that.

0:27:14.820 --> 0:27:16.120
 I'm a molecular biologist.

0:27:16.120 --> 0:27:21.120
 I like genes and, you know, genetic pathways, et cetera.

0:27:21.160 --> 0:27:26.000
 And one of the ways that my research keeps

0:27:26.000 --> 0:27:33.040
 bringing me back to is how we regenerate NAD+. Because if you

0:27:33.040 --> 0:27:41.680
 look at obese humans, it seems like we have too much. So NAD+,

0:27:41.680 --> 0:27:45.000
 it's an energy carrier,

0:27:45.500 --> 0:27:46.660
 an electron carrier.

0:27:46.660 --> 0:27:49.580
 It basically, as you break down your food,

0:27:49.580 --> 0:27:51.860
 whether or not it's carbohydrates or fats,

0:27:51.860 --> 0:27:55.500
 NAD plus takes a, picks up a hydrogen,

0:27:55.500 --> 0:27:58.140
 becomes NADH and a couple of electrons

0:27:58.140 --> 0:28:00.540
 and it takes it up and it drops it

0:28:00.540 --> 0:28:03.620
 into the mitochondria electron transport chain.

0:28:03.620 --> 0:28:06.960
 And that is how, and that's basically how we, an essential

0:28:06.960 --> 0:28:11.440
 part of how we turn our food into ATP. And so if there's not

0:28:11.440 --> 0:28:17.120
 enough NAD plus around, we simply can't run our metabolism

0:28:17.120 --> 0:28:21.400
 as quickly, it becomes a limiting factor. And if people

0:28:21.400 --> 0:28:25.280
 have heard of this, the Sirtuins, Sirtuins

0:28:25.280 --> 0:28:29.000
 require NAD plus and, and they remove acetyl groups from

0:28:29.000 --> 0:28:31.760
 things. And if you look at obese humans, they have a lot of

0:28:31.760 --> 0:28:37.080
 acetylated mitochondrial enzymes, such as complex one,

0:28:37.080 --> 0:28:42.160
 complex five, a whole bunch of them. And so, and so your

0:28:42.160 --> 0:28:49.360
 mitochondria don't work as efficiently if, if you have, if you have a lot of acetylated

0:28:49.360 --> 0:28:53.200
 enzymes, which is to say if you don't have enough NAD plus, and

0:28:53.200 --> 0:28:57.640
 you see this kind of irony in obese people that obviously

0:28:57.640 --> 0:29:01.880
 they have a lot of energy. You know, the person has plenty of

0:29:01.920 --> 0:29:07.120
 stored energy, but yet their cells are still low in ATP. Because, you know, they're not

0:29:07.120 --> 0:29:12.000
 convert, they're not efficiently converting, converting all of

0:29:12.000 --> 0:29:17.600
 that to, to ATP. And so, yeah, and there's a, there's an

0:29:17.600 --> 0:29:24.560
 enzyme called NNT. And so this will connect sort of what, yeah,

0:29:24.600 --> 0:29:30.000
 what Kate and I were saying about functional mitochondria back to what Peter was saying about ROS.

0:29:30.000 --> 0:29:45.680
 What this enzyme NNT does is it basically takes the ROS and it returns NAD+. it's kind of a magical device that in the process of removing

0:29:45.680 --> 0:29:52.880
 ROS from the mitochondria, we actually get NAD plus back. And

0:29:52.880 --> 0:29:55.800
 so what that looks like to me is, okay, so if you could get

0:29:55.800 --> 0:30:01.080
 your fat really unsaturated, then you won't make as much ROS

0:30:01.120 --> 0:30:07.000
 and that will give you less NAD+, and that will give you the ability to store body

0:30:07.000 --> 0:30:10.200
 fat and get ready for hibernation.

0:30:10.200 --> 0:30:13.120
 That's kind of the short version of it.

0:30:13.120 --> 0:30:15.520
 Dr. Robert R. Reilly Very good.

0:30:15.520 --> 0:30:19.280
 And Dr. Ray Peat, you get to pick who was right.

0:30:19.280 --> 0:30:20.280
 I'm just joking.

0:30:20.280 --> 0:30:25.000
 Give us your take on this question, please.

0:30:25.000 --> 0:30:32.720
 I've considered all of those over the years.

0:30:32.720 --> 0:30:45.000
 50 years ago, my dissertation in the biology department at the oxidative metabolic changes

0:30:46.500 --> 0:30:49.300
 that happened during reproductive aging.

0:30:50.980 --> 0:30:55.980
 And immediately I started running into the close interaction

0:30:57.240 --> 0:31:02.240
 between aging and polyunsaturated fat metabolism

0:31:04.460 --> 0:31:10.740
 producing age pigment, for example, and estrogen. Each one

0:31:10.740 --> 0:31:32.000
 intensifies the other and you can overlap those with oxygen deprivation in itself or or exoradiation or any sort of stress that uses or wastes oxygen.

0:31:32.000 --> 0:31:45.560
 It accelerates the interaction, decomposing PUFA with aging under the influence of estrogen. And at that time,

0:31:46.680 --> 0:31:51.680
 I had to see the importance of the accumulating PUFA

0:31:53.560 --> 0:31:58.120
 with aging, but already the literature

0:31:58.120 --> 0:32:03.120
 was starting to claim that not only is PUFA in the food

0:32:04.000 --> 0:32:06.960
 good for preventing cancer and heart disease,

0:32:06.960 --> 0:32:16.040
 they said, but even preventing obesity. I've seen dozens of articles, more and

0:32:16.040 --> 0:32:25.000
 more over the years, showing in prevention of obesity with the other gross mistakes.

0:32:26.200 --> 0:32:30.240
 It causes cancer and causes heart disease

0:32:31.160 --> 0:32:32.840
 and reproductive aging

0:32:34.080 --> 0:32:38.320
 and all of the pro-inflammatory processes.

0:32:38.320 --> 0:32:43.320
 And all of that comes from the immense profitability

0:32:44.000 --> 0:32:48.320
 of selling products. Every time there's a super

0:32:48.320 --> 0:32:57.120
 profitable product, the science follows the profit absolutely going against the

0:32:57.120 --> 0:33:06.160
 facts in the case of PUFA and estrogen, but at least a dozen other substances.

0:33:09.200 --> 0:33:14.200
 And so you have to learn to disregard about 90 to 99% of the published medical

0:33:14.640 --> 0:33:17.500
 and even biochemical articles

0:33:17.500 --> 0:33:21.940
 as being nothing but reflections of advertising.

0:33:22.900 --> 0:33:31.080
 And I started looking at the physical properties that would account for the fact

0:33:31.080 --> 0:33:41.280
 that mammals in general, studies have been done on calves and human babies, at birth

0:33:41.280 --> 0:33:47.760
 they're generally so-called deficient in the essential fatty acids. Their tissues are

0:33:47.760 --> 0:34:13.200
 making mead acids, taken as a deficiency of the plant-derived PUFA. And so I saw that the fact that animals generally close to 100 degrees Fahrenheit, 37 degrees

0:34:13.200 --> 0:34:28.080
 Celsius generally have that process of accumulating during their lifetime more and more of the plant-derived PUFA.

0:34:28.520 --> 0:34:32.840
 And in the process, their own metabolism is being damaged

0:34:32.840 --> 0:34:33.780
 and slowing down.

0:34:33.780 --> 0:34:37.880
 So from extremely high metabolic rate at birth

0:34:37.880 --> 0:34:40.280
 in the first two or three years,

0:34:40.280 --> 0:34:43.960
 as the PUFA accumulate in the tissues,

0:34:43.960 --> 0:34:46.040
 the metabolic rate slows down,

0:34:46.920 --> 0:34:51.920
 takes another big change towards inhibition of oxygen,

0:34:55.560 --> 0:34:58.200
 productive use at puberty.

0:34:58.200 --> 0:35:03.200
 And then when growth ceases in the 20s,

0:35:04.440 --> 0:35:10.200
 when you're no longer diluting those stored PUFA from

0:35:10.200 --> 0:35:18.400
 the environment, the rate of accumulation increases so that by middle and old age, the

0:35:18.400 --> 0:35:31.360
 metabolic rate is much slower, the brain and arteries and other tissues are starting to fill up with the largely

0:35:31.360 --> 0:35:38.980
 cholesterol esters of the polyunsaturated fats, also the stored

0:35:38.980 --> 0:35:45.000
 triglycerides, all of these become more polyunsaturated with aging.

0:35:45.900 --> 0:35:49.920
 And I think the basic reason for that is that

0:35:49.920 --> 0:35:54.920
 the double bonds, the more the double bonds the fat has,

0:35:57.060 --> 0:36:01.260
 the more affinity it has for water.

0:36:01.260 --> 0:36:04.640
 And so it has a greater tendency

0:36:04.640 --> 0:36:08.360
 to circulate free in the water and in

0:36:08.360 --> 0:36:17.000
 the process those same multiply unsaturated molecules block thyroid

0:36:17.000 --> 0:36:25.000
 function and release estrogen from the steroid-binding globulin,

0:36:27.480 --> 0:36:29.600
 making estrogen more available,

0:36:30.600 --> 0:36:32.800
 thyroid less available.

0:36:32.800 --> 0:36:37.800
 But the tendency is not only to not oxidize these

0:36:39.640 --> 0:36:43.840
 because they don't enter the cells for oxidation,

0:36:43.840 --> 0:36:47.080
 it takes a more saturated molecule

0:36:47.080 --> 0:36:50.940
 to get into the mitochondria and cells.

0:36:51.840 --> 0:36:55.600
 So the free-floating free amino acids

0:36:56.880 --> 0:37:00.960
 escape oxidative use

0:37:00.960 --> 0:37:04.440
 and are preferentially stored

0:37:04.440 --> 0:37:11.800
 as triglycerides and phospholipids and estrogens of cholesterol.

0:37:11.800 --> 0:37:25.000
 So all of the tissues lose function with aging as they accumulate these fats and that all along the route,

0:37:25.040 --> 0:37:28.340
 the metabolic rate is slowing down,

0:37:28.340 --> 0:37:33.340
 the temperature falls, it's somewhat defensive.

0:37:34.420 --> 0:37:38.840
 The cold temperature plants,

0:37:38.840 --> 0:37:41.640
 fish living at a cold temperature

0:37:41.640 --> 0:37:44.640
 are very highly polyunsaturated.

0:37:51.120 --> 0:38:05.000
 That's necessary just for physical flexibility. A cold fish is stiff because if it has saturated fat, but the polyunsaturated fats keep it liquid at refrigerator temperature.

0:38:06.600 --> 0:38:11.600
 And so the more cold organisms we eat,

0:38:13.480 --> 0:38:15.200
 the worse the problem is.

0:38:16.440 --> 0:38:20.320
 That was what led me to experiment with coconut oil.

0:38:21.660 --> 0:38:25.000
 And it's relatively high saturation,

0:38:27.960 --> 0:38:30.240
 goes with a higher metabolic rate.

0:38:30.240 --> 0:38:35.240
 And Pam Plona and other researchers have shown

0:38:35.400 --> 0:38:40.400
 that the more unsaturated an organism is,

0:38:43.480 --> 0:38:49.400
 for example, birds are much more saturated than mammals

0:38:49.400 --> 0:38:54.040
 and for a given weight, they have a much longer lifespan.

0:38:54.040 --> 0:38:59.040
 Pamphlon and others showed that that's a general principle

0:38:59.040 --> 0:39:02.880
 that life is shortened by the degree

0:39:02.880 --> 0:39:05.000
 of polyunsaturated fats in its tissues.

0:39:09.040 --> 0:39:14.040
 The physical property of being more water soluble

0:39:14.240 --> 0:39:18.200
 leading to the accumulation in the tissues

0:39:19.280 --> 0:39:23.120
 means that when you're under stress

0:39:23.120 --> 0:39:25.000
 and release stored fats,

0:39:27.280 --> 0:39:32.280
 both from triglycerides and phospholipids and esters,

0:39:34.600 --> 0:39:38.480
 these stress-induced free fatty acids

0:39:39.340 --> 0:39:42.720
 are going to be more polyunsaturated.

0:39:42.720 --> 0:39:49.480
 The older you are, the higher the accumulation, the more harmful

0:39:49.480 --> 0:40:09.320
 these free fatty acids become with aging. And the diabetes, obesity, and cancer, inflammatory degenerative diseases, all of these are linked through both the presence

0:40:09.320 --> 0:40:25.000
 of free fatty acids in circulation stops the oxidation of glucose.

0:40:27.400 --> 0:40:32.400
 And it not only shifts the metabolic ratio,

0:40:32.920 --> 0:40:36.440
 but it actually lowers the metabolic rate.

0:40:37.320 --> 0:40:42.320
 Old people, old men, for example, at rest,

0:40:43.440 --> 0:40:49.000
 are burning actually more fat than the young men in the

0:40:49.000 --> 0:40:59.360
 same conditions, but the old man is laying down fat at the same time, burning fat faster

0:40:59.360 --> 0:41:09.440
 than young men, but getting a higher percent of body fat. You see the same thing with the waist to hip ratio,

0:41:10.840 --> 0:41:15.840
 deposition of unnecessary fat corresponds

0:41:16.340 --> 0:41:21.340
 to a lower oxidation of glucose

0:41:21.340 --> 0:41:25.360
 and a higher oxidation of fat or the respiratory quotient.

0:41:25.360 --> 0:41:52.500
 And that's a general thing that the respiratory quotient in diabetes and all of these stress fat oxidation, high estrogen, and old age and any kind of sickness correspond to that

0:41:52.500 --> 0:42:11.600
 process. the mechanism behind the Randle cycle. When you're under stress, one way of

0:42:11.600 --> 0:42:32.080
 keeping some energy process production going is to get rid of the excess NADH so that you can produce more oxidation, so forming lactic acid which

0:42:32.080 --> 0:42:50.000
 leaves the cell, that consumes some NADH and allows some energy to continue to be produced. But fat synthesis is the other electron sink that gets rid of excess electrons.

0:42:50.000 --> 0:43:07.000
 So you burn fat, oxidize fatty acids, and you're increasing the NADH, raising the reductive properties of the cell and to get rid of those excess NADH reductive

0:43:10.800 --> 0:43:17.800
 atoms, you have to either produce more fat or more lactic acid or both. And generally

0:43:22.000 --> 0:43:27.240
 it's both of them. Diabetics have a chronically high lactic

0:43:27.240 --> 0:43:36.280
 acid production as well as high free fatty acids. So it starts with the

0:43:36.280 --> 0:43:47.000
 physical properties, the water solubility, and ends up with the problem of electron excess.

0:43:47.000 --> 0:43:58.000
 And making lactic acid and fat is the solution to that excess of electrons.

0:43:58.000 --> 0:44:02.000
 Well, very good. I really appreciate all of your answers.

0:44:02.000 --> 0:44:05.060
 And I have another question for everybody, but before I do,

0:44:05.060 --> 0:44:09.300
 I want to give everybody an opportunity to just raise your hand or speak up if you want

0:44:09.300 --> 0:44:14.600
 to ask a question to somebody else on the panel or ask for clarification

0:44:14.600 --> 0:44:19.020
 or a comment or anything, just if there's anything that's been said

0:44:19.020 --> 0:44:21.100
 so far that people want to respond to.

0:44:23.100 --> 0:44:25.840
 Well, the only thing I would like to add is on the

0:44:25.840 --> 0:44:29.120
 multifactoriality of this, based on piggybacking off of what

0:44:29.120 --> 0:44:32.360
 Tucker brought up, is that like there's so much going on here

0:44:33.320 --> 0:44:37.780
 that it's actually a detriment to the basically the cause

0:44:37.800 --> 0:44:40.700
 of helping other folks understand what the issues are.

0:44:41.080 --> 0:44:43.240
 There's like a saying in law that's like, if you want to get

0:44:43.240 --> 0:44:50.960
 away with murder, make sure that before you kill the person, you rob them and if possible, you rape them

0:44:50.960 --> 0:44:56.760
 and do as many other different things because then the attorney can get up there in front

0:44:56.760 --> 0:45:05.680
 of the jury and say, well, what is it you're saying he did? And it just gets confusing and people just give up. And

0:45:05.680 --> 0:45:08.400
 that's kind of, you know, the problem.

0:45:09.960 --> 0:45:14.400
 That which is a fair point to make. But if we're going to

0:45:15.640 --> 0:45:19.200
 convince people that what we're saying here is correct, and I

0:45:19.200 --> 0:45:21.880
 think it is correct, at some point, we're going to have to

0:45:21.880 --> 0:45:25.520
 come up with a credible mechanism to explain what's

0:45:25.520 --> 0:45:26.520
 going on.

0:45:26.520 --> 0:45:35.540
 And as I said, it's a shame it's not a simple one, but, you know, we've, you know, a lot

0:45:35.540 --> 0:45:39.680
 of people in the United States are required to eat these foods essentially by law.

0:45:39.680 --> 0:45:41.920
 They're in the dietary guidelines.

0:45:41.920 --> 0:45:48.040
 They are fed to people in schools, in the military, in hospitals,

0:45:48.040 --> 0:45:55.200
 and we're going to have to have a solid evidentiary case to convince the authorities that they've

0:45:55.200 --> 0:46:09.680
 been wrong for the last 60 or 70 years and that they need to change this pattern. And unless we can, you know, point to the studies that show that this is what is actually

0:46:09.680 --> 0:46:17.660
 happening and what it, however complicated it may be, and it explains why, you know,

0:46:17.660 --> 0:46:21.360
 not just everybody in America or most people in America, but most people around the world

0:46:21.360 --> 0:46:32.320
 have suddenly decided to overeat and get fat, right? You can make it complicated, but I think that you can also, you can make it simple, and I think

0:46:32.320 --> 0:46:36.560
 it, there's, I mean, you can tell me how I'm wrong, but I think it seems pretty simple to say

0:46:37.120 --> 0:46:46.240
 that a seed oil diet makes us build body fat that makes us feel sick and tired when we try and burn it because of the

0:46:46.240 --> 0:46:50.320
 inflammatory effects of the PUFA in mitochondria and other tissues.

0:46:50.320 --> 0:46:54.360
 But I think that's a body metabolism as you can make it.

0:46:54.360 --> 0:46:59.080
 Yeah, which is true, but that's not going to convince a scientist.

0:46:59.080 --> 0:47:01.360
 He's going to want to know, okay, how does that happen?

0:47:01.360 --> 0:47:03.040
 Wait a second, though.

0:47:03.040 --> 0:47:06.840
 I mean, why wouldn't it convince a scientist if it's true?

0:47:06.840 --> 0:47:09.860
 How do you know it's true without seeing the mechanisms?

0:47:11.320 --> 0:47:12.240
 There are mechanisms.

0:47:12.240 --> 0:47:13.760
 I mean, I'm not making any of this up.

0:47:13.760 --> 0:47:15.680
 There's multiple mechanisms.

0:47:15.680 --> 0:47:17.800
 There's multiple steps in there.

0:47:17.800 --> 0:47:22.420
 But I mean, your body fat, if you eat too much PUFA,

0:47:22.420 --> 0:47:26.460
 it ends up in your body fat, that's step one, then between meals,

0:47:26.460 --> 0:47:28.540
 when your insulin is low,

0:47:28.540 --> 0:47:31.780
 and even if you're insulin resistant,

0:47:31.780 --> 0:47:34.480
 your body fat does release free fatty acids

0:47:34.480 --> 0:47:37.440
 into the circulation, those will get picked up by the cells

0:47:37.440 --> 0:47:39.960
 and utilized by the mitochondria,

0:47:39.960 --> 0:47:43.060
 and in excessive concentration,

0:47:43.060 --> 0:47:46.960
 that shuts down or reduces energy production

0:47:46.960 --> 0:47:48.840
 so that the cells then,

0:47:48.840 --> 0:47:50.260
 I mean this is all step by step,

0:47:50.260 --> 0:47:51.720
 I'm just taking you through the process

0:47:51.720 --> 0:47:54.120
 of every single one of these steps is not debated.

0:47:54.120 --> 0:47:57.500
 And then when, this one might be a little controversial,

0:47:57.500 --> 0:48:00.860
 when the cells are forced to burn PUFA,

0:48:00.860 --> 0:48:04.880
 that they, instead of shutting down,

0:48:04.880 --> 0:48:07.800
 they just put more GLute 4 transporters and

0:48:07.800 --> 0:48:14.000
 suck, slurp more sugar out of the bloodstream, that part is a missing

0:48:14.000 --> 0:48:19.200
 step. I haven't actually seen like too much evidence of that. I've seen indirect

0:48:19.200 --> 0:48:23.840
 evidence of that that I can point to, that the brain actually starts to tell

0:48:23.840 --> 0:48:26.240
 the liver to produce more sugar

0:48:26.240 --> 0:48:28.680
 to increase the blood sugar level.

0:48:28.680 --> 0:48:31.640
 That's how you become diabetic.

0:48:31.640 --> 0:48:34.760
 That's like another, that's why you raise

0:48:34.760 --> 0:48:37.280
 your blood sugar level when you're type two diabetic

0:48:37.280 --> 0:48:40.480
 because the brain says a normal blood sugar level

0:48:40.480 --> 0:48:43.300
 of 100 isn't enough, I want it to be 110 fasting

0:48:43.300 --> 0:48:44.840
 or 120 or 30.

0:48:44.840 --> 0:48:47.360
 But everything that I've said,

0:48:47.360 --> 0:48:49.940
 except for that one step of, you know,

0:48:49.940 --> 0:48:52.840
 what is the exact concentration of PUFA in the body fat

0:48:52.840 --> 0:48:57.140
 that makes the cells increase their glute four transporters

0:48:57.140 --> 0:48:59.000
 and slurp in more sugar from the bloodstream,

0:48:59.000 --> 0:49:02.600
 that's the only piece that's maybe missing,

0:49:02.600 --> 0:49:07.160
 but everything else is actually solid and no one in their

0:49:07.160 --> 0:49:09.860
 right mind, I think, would refute any of that.

0:49:09.860 --> 0:49:13.800
 So there is science, it's more than just one, a sound bite.

0:49:13.800 --> 0:49:15.480
 And that's the problem.

0:49:15.480 --> 0:49:20.800
 We have to force our scientists to actually listen to something more than, I mean, we

0:49:20.800 --> 0:49:26.240
 shouldn't have to, but we do have to, you know, get the people who are,

0:49:26.240 --> 0:49:31.480
 should be in this conversation to listen to the whole argument, not just a short sentence,

0:49:31.480 --> 0:49:36.640
 like cholesterol clogs your arteries or something simple, oversimplified like that and ridiculous.

0:49:36.640 --> 0:49:37.640
 Right.

0:49:37.640 --> 0:49:38.640
 Agreed.

0:49:38.640 --> 0:49:39.640
 Peter?

0:49:39.640 --> 0:49:49.120
 Quick word with Tucker or quick comment. I find your approach, your concept that PUFA make

0:49:49.120 --> 0:49:57.840
 endocannabinoids make you eat is very soundbite-y. Yeah?

0:49:57.840 --> 0:50:06.400
 Well it's a great soundbite. Kate put it in her book. They give you the munchies. That's probably the best soundbite we have.

0:50:15.280 --> 0:50:28.560
 The problem I have is that I think we are talking about a process and I don't think it happens immediately. And there is a ton of research where if you feed poofers to laboratory rodents, you will invariably

0:50:28.560 --> 0:50:35.040
 make them more insulin sensitive, so you do it diet-wise. But if you keep doing it,

0:50:36.560 --> 0:50:40.080
 six months down the road, they'll be intensely insulin resistant.

0:50:41.600 --> 0:50:48.600
 Their fat cells may be still insulin sensitive or they may be insulin resistant. Their fat cells may be still insulin sensitive or they may be insulin resistant.

0:50:48.600 --> 0:50:57.040
 That depends on your study. But the initial response is that putting polyunsaturated fats

0:50:57.040 --> 0:51:03.200
 into a rodent model makes them insulin sensitive. It happens to make them fat as well, but that's

0:51:03.200 --> 0:51:07.680
 the function of insulin. So making them insulin sensitive, I have no problem with that making them fat.

0:51:08.880 --> 0:51:16.880
 But the initial response, and in cell culture, you can feed polyunsaturates to cell cultures

0:51:16.880 --> 0:51:22.400
 without doing them any damage at all. You feed pure saturates to cell culture, and there's a

0:51:21.980 --> 0:51:26.980
 you're saturate to cell culture, and there's a reactive oxygen species driven catastrophe,

0:51:27.900 --> 0:51:30.700
 particularly if you're culture in 25 millimoles of glucose,

0:51:30.700 --> 0:51:32.620
 which is the standard culture medium,

0:51:32.620 --> 0:51:36.080
 and you add 400 millimoles of pure palmitic acid to that,

0:51:36.080 --> 0:51:37.620
 your cells will just die.

0:51:37.620 --> 0:51:41.560
 But you can add 400 millimoles of PUFA to it,

0:51:41.560 --> 0:51:43.720
 and there's no problem.

0:51:43.720 --> 0:51:46.480
 Acutely, the cells will be perfectly okay. And any

0:51:46.480 --> 0:51:50.880
 scientists that we ever try and convince will produce those papers and say, well, look at this.

0:51:52.000 --> 0:51:57.440
 And as you pointed out, Peter, there was a that's not a that's just just a moment,

0:51:57.440 --> 0:52:00.640
 as you've pointed out, Peter, that's not a physiological model, right? No,

0:52:01.040 --> 0:52:05.680
 all medic acid. Yeah. Right. Of course.

0:52:05.680 --> 0:52:10.400
 Yeah. Yeah. I mean, you can say, you can point to a lot of things that are irrelevant to the

0:52:10.400 --> 0:52:15.520
 argument and try to divert the argument, but that's, we have to, we can't let them do that.

0:52:15.520 --> 0:52:20.640
 We have to, we have to say, wait a second, that's irrelevant to our argument and how,

0:52:20.640 --> 0:52:24.960
 prove me wrong, right? Like you can say that too. You, every one of you can say,

0:52:24.960 --> 0:52:26.240
 you guys prove me wrong because I, I want to say that too. Every one of you can say, you guys prove me wrong

0:52:26.240 --> 0:52:29.100
 because I wanna run the conversation here.

0:52:29.100 --> 0:52:30.760
 You guys have been running the conversation for a long time.

0:52:30.760 --> 0:52:32.060
 We've been getting fatter and sicker.

0:52:32.060 --> 0:52:36.060
 So try to take what I'm asserting

0:52:36.060 --> 0:52:37.880
 and tell me where it's wrong

0:52:37.880 --> 0:52:40.760
 because I'm totally open to that.

0:52:40.760 --> 0:52:43.800
 And actually you said, Peter, what you brought up

0:52:43.800 --> 0:52:47.080
 is that like the insulin sensitivity?

0:52:47.080 --> 0:52:48.800
 That's totally in keeping with what I said.

0:52:48.800 --> 0:52:53.440
 It's indirect evidence of what I said, that when you force feed cells PUFA, they want

0:52:53.440 --> 0:52:54.440
 more sugar.

0:52:54.440 --> 0:52:56.360
 They're going to be drawing more sugar out of the bloodstream.

0:52:56.360 --> 0:52:57.640
 Well, you might measure that.

0:52:57.640 --> 0:53:00.560
 It might look like insulin sensitivity, right?

0:53:00.560 --> 0:53:03.200
 So that is exactly what I'm saying.

0:53:03.200 --> 0:53:04.200
 Yes, yes.

0:53:04.200 --> 0:53:06.800
 No, but my concept is that we get fat

0:53:06.800 --> 0:53:13.040
 because we're pathologically insulin sensitive. We're too sensitive. That's the problem that I see.

0:53:13.840 --> 0:53:21.840
 Yeah, and that is PUFA. I agree. It's as if obesity, we're trying to protect ourselves

0:53:21.840 --> 0:53:30.600
 by building fat, right? We're trying to protect ourselves from burning PUFA by becoming obese, right? And I brought this up with, with, on David's

0:53:30.600 --> 0:53:36.680
 radio show because I actually have seen a lot of, like, in my practice, it seems as

0:53:36.680 --> 0:53:41.720
 though it's the people who are not, you know, really obese who end up with cancer.

0:53:41.720 --> 0:53:45.320
 And, and you could make an argument there, you could explain

0:53:45.320 --> 0:53:49.400
 that not just cancer but also autoimmune disorders.

0:53:49.400 --> 0:53:55.120
 You could explain that as because perhaps they are burning the PUFA when they shouldn't

0:53:55.120 --> 0:54:02.400
 be and somebody, you know, and therefore exposing their DNA to oxidative damage and, you know,

0:54:02.400 --> 0:54:06.120
 getting cancer of course if you believe it's a genetic disease.

0:54:06.120 --> 0:54:12.760
 But regardless of the mechanism, you're creating the oxidative stress by burning the PUFA instead

0:54:12.760 --> 0:54:21.000
 of eating more, which would allow you to get more glucose, which is a safer thing to burn.

0:54:21.000 --> 0:54:24.600
 Because it doesn't have the double bonds, it doesn't have the polyunsaturated fatty

0:54:24.600 --> 0:54:25.000
 acids, and it doesn't have the double bonds, it doesn't have the polyunsaturated fatty acids

0:54:25.000 --> 0:54:26.760
 and it's safe to burn.

0:54:26.760 --> 0:54:30.080
 It's not the ideal fuel, but it's certainly better than,

0:54:30.080 --> 0:54:34.880
 so that obesity, basically overeating is a person

0:54:34.880 --> 0:54:36.720
 who's developing a habit of overeating

0:54:36.720 --> 0:54:38.720
 and to protect their cells

0:54:38.720 --> 0:54:41.960
 from having to burn the damaging PUFA.

0:54:41.960 --> 0:54:46.140
 And so it's like a metabolic choice there that their

0:54:46.140 --> 0:54:53.200
 body is making for them. And yeah, and I think that has, that's, PUFAs are so

0:54:53.200 --> 0:54:59.480
 bad that people will eat themselves almost to death and attempt to not have

0:54:59.480 --> 0:55:11.400
 to burn that and damage their mitochondria. Okay. Dr. Peat, do you…how do you sort out these different arguments?

0:55:11.400 --> 0:55:15.320
 I mean, I'm a layperson, so I'm, you know, I'm listening, and it all kind of seems

0:55:15.320 --> 0:55:17.600
 to be going in the same direction.

0:55:17.600 --> 0:55:19.240
 Do you have any thoughts on that?

0:55:19.240 --> 0:55:30.880
 Yeah. I think if you start trying to understand what the so-called Rangel cycle is all about,

0:55:30.880 --> 0:55:40.160
 you see that the interference of fat oxidation with the ability to oxidize and get energy

0:55:40.160 --> 0:55:52.960
 from glucose, that's the essential problem. The faster you oxidize fats, and that's promoted

0:55:52.960 --> 0:56:11.680
 by the unsaturation degree, the faster you oxidize fats, the slower you oxidize glucose. And that shifts the whole electronic balance, for example, away from carbon dioxide

0:56:11.680 --> 0:56:19.680
 production and full energy use of the oxygen towards fat synthesis and lactic acid synthesis.

0:56:19.680 --> 0:56:28.800
 I would, I think that's an overstatement of what the Randle cycle actually does. I think that's an overstatement of what the Randle cycle actually does.

0:56:28.800 --> 0:56:33.920
 I think the Randle cycle is simpler.

0:56:33.920 --> 0:56:51.240
 You can just, it's really just a description of the cell has an option to burn fat or sugar. And what... But the fat changes the ability of the cell to use sugar and go oxidize.

0:56:51.240 --> 0:56:52.800
 Well, you could put it the other way as well.

0:56:52.800 --> 0:56:54.840
 I mean, they influence each other, right?

0:56:54.840 --> 0:56:55.840
 You could put...

0:56:55.840 --> 0:56:58.280
 You could also say the glucose has the ability to influence the fat.

0:56:58.280 --> 0:57:01.080
 So it's a two-way street.

0:57:01.080 --> 0:57:07.760
 That means when you exaggerate the supply of glucose, you can actually lower the free

0:57:07.760 --> 0:57:16.240
 fatty acids and protect against all of the consequences of burning too much fat.

0:57:16.240 --> 0:57:18.040
 Right.

0:57:18.040 --> 0:57:26.760
 So, the Randle cycle is a regulatory process that, if I understand this correctly, that

0:57:26.760 --> 0:57:29.960
 determines what fuel the cell is going to use.

0:57:29.960 --> 0:57:34.680
 And of course, cells can use two fuels at once, obviously, but that's kind of the, if

0:57:34.680 --> 0:57:40.120
 you want, the seesaw that allows the cell to determine what fuel it's going to use.

0:57:40.120 --> 0:57:46.680
 But that use of type of fuel determines everything.

0:57:46.680 --> 0:57:53.460
 The electronic balance regulates the synthesis of fat.

0:57:53.460 --> 0:58:11.600
 And so the more fat you burn, the more fat than the young person is still making fat for deposition.

0:58:12.320 --> 0:58:15.760
 They become fatter because they are burning too much fat.

0:58:16.720 --> 0:58:17.280
 Dr. Pitt?

0:58:18.080 --> 0:58:24.880
 That is well established, but it just doesn't seem right to people, so they ignore it.

0:58:25.000 --> 0:58:26.000
 it just doesn't seem right to people, so they ignore it.

0:58:29.760 --> 0:58:32.800
 When you say that they're building, as you burn fat, you build fat,

0:58:32.800 --> 0:58:35.120
 is the presumption that you're building the fat

0:58:35.120 --> 0:58:37.000
 is coming from glucose,

0:58:38.160 --> 0:58:39.680
 because you're not burning the glucose,

0:58:39.680 --> 0:58:41.320
 so it's being converted to fat?

0:58:41.320 --> 0:58:42.440
 Was that your point?

0:58:43.520 --> 0:58:44.960
 When you burn fat,

0:58:44.960 --> 0:58:49.520
 you increase the ratio of NADH to

0:58:49.520 --> 0:58:58.000
 NAD. And that generates the fat from whatever it can get? Yeah, so the more fatty acids you burn,

0:58:58.000 --> 0:59:07.000
 the more fatty acids you synthesize. Yeah, and so, Dr. Peat, if I understand you,

0:59:07.000 --> 0:59:09.160
 and correct me if I'm wrong,

0:59:09.160 --> 0:59:12.800
 the argument about what is controlling the Randle cycle

0:59:12.800 --> 0:59:17.800
 is really kind of an argument about redox balance.

0:59:17.800 --> 0:59:19.320
 Would you say that's correct?

0:59:19.320 --> 0:59:21.160
 Yeah, yeah, absolutely.

0:59:21.160 --> 0:59:22.000
 Yeah.

0:59:23.280 --> 0:59:31.360
 So can I add slightly to that? And that is, I think we can all agree that the

0:59:31.360 --> 0:59:51.000
 Randle cycle partitions what you do with calories. What I was looking at for from the ROS point of view was looking at normalizing the total calorie intake

0:59:51.000 --> 1:00:01.240
 to the cell and if the ROS make that input to the cell normal, the Randle cycle should simply sort

1:00:01.240 --> 1:00:05.100
 out what gets oxidized and what gets stored in an appropriate manner.

1:00:06.160 --> 1:00:10.740
 So total input to the cell was where my thinking

1:00:10.740 --> 1:00:12.800
 on ROS was coming from.

1:00:12.800 --> 1:00:16.080
 Randle cycle afterwards to sort out what's done

1:00:16.080 --> 1:00:17.720
 with the input to the cell.

1:00:18.960 --> 1:00:20.480
 Does that make sense?

1:00:20.480 --> 1:00:22.040
 Yes, Peter, I agree with that.

1:00:22.040 --> 1:00:25.760
 I think we wanna look at at it from the proper direction.

1:00:25.760 --> 1:00:32.760
 So the big picture is that when you are burning, when your body has a lot of—the big picture

1:00:32.760 --> 1:00:35.000
 is oxidative stress.

1:00:35.000 --> 1:00:41.000
 And having the physiology subjected to too much oxidative stress is going to have an

1:00:41.000 --> 1:00:45.640
 influence on things like the Randle cycle and the NAD to ratios

1:00:45.640 --> 1:00:46.800
 and everything else.

1:00:46.800 --> 1:00:49.640
 But it's the direction that we're going

1:00:49.640 --> 1:00:52.040
 is it's not the Randle cycle running everything.

1:00:52.040 --> 1:00:57.040
 It's the fact that we're eating so much more PUFA

1:00:57.600 --> 1:01:01.120
 and it's subjecting ourselves to extreme amounts

1:01:01.120 --> 1:01:04.480
 of oxidative stress, depleting our antioxidant systems.

1:01:04.480 --> 1:01:05.160
 That is going to

1:01:05.160 --> 1:01:12.040
 have an effect on the Randle cycle and on every other physiologic process.

1:01:12.040 --> 1:01:20.120
 Insulin sensitivity, the translocation of glucose into a cell or not, whether or not

1:01:20.120 --> 1:01:26.700
 liver, the liver is able to do any of the normal detoxification, it's gonna

1:01:26.700 --> 1:01:31.580
 have an impact on every process. And so what I want, what I'm, my point I'm trying

1:01:31.580 --> 1:01:37.400
 to make is that we can't take one little process that the body normally does

1:01:37.400 --> 1:01:44.020
 under normal circumstances and blame, you know, that for everything. The big

1:01:44.020 --> 1:01:47.440
 picture, we can't forget, I mean, it's kind of a little bit like missing the

1:01:47.440 --> 1:01:52.640
 forest for the trees, it seems to me, because the big picture is the forest of PUFA that

1:01:52.640 --> 1:01:59.560
 we're all living in, and it's just adulterating our physiology on every level, certainly what

1:01:59.560 --> 1:02:04.200
 you're talking about, but many other things.

1:02:04.200 --> 1:02:06.720
 That's the direction that I see things going and

1:02:06.720 --> 1:02:12.120
 the explanation that makes more sense to me. For almost a hundred

1:02:12.120 --> 1:02:20.360
 years, the oxidative stress and oxidative damage has been emphasized,

1:02:20.360 --> 1:02:27.440
 rate of living theory and so on,'s almost almost been a hundred percent neglect

1:02:27.440 --> 1:02:29.320
 of the reductive stress

1:02:29.320 --> 1:02:30.200
 process

1:02:30.200 --> 1:02:32.600
 that's what i'm talking about

1:02:32.600 --> 1:02:34.560
 reductive stress

1:02:34.560 --> 1:02:39.980
 precedes the reactive oxygen species production

1:02:39.980 --> 1:02:43.920
 the problem is reductive stress

1:02:43.920 --> 1:02:47.760
 that's promoted by not enough glucose oxidation,

1:02:47.760 --> 1:02:48.900
 too much PUFA.

1:02:51.680 --> 1:02:53.640
 Not enough glucose oxidation?

1:02:53.640 --> 1:02:54.880
 That's not making any sense to me,

1:02:54.880 --> 1:02:57.820
 because as humans, we're tooled to burn fat

1:02:57.820 --> 1:02:58.880
 way more than glucose.

1:02:58.880 --> 1:03:01.300
 So I just, I can't accept that.

1:03:05.320 --> 1:03:10.360
 Ironically, I'm literally, the current blog post I'm working on

1:03:10.360 --> 1:03:14.080
 is literally called, Reductive Stress Causes Oxidative Stress.

1:03:14.760 --> 1:03:15.920
 And so it's interesting.

1:03:16.320 --> 1:03:19.320
 Can you take a moment then and just define it so that the

1:03:19.320 --> 1:03:20.120
 people watching this can understand?

1:03:20.120 --> 1:03:20.440
 Yeah.

1:03:20.440 --> 1:03:28.460
 And so, oxidative stress, so NAD plus and NADH are a really good example of this and so

1:03:29.920 --> 1:03:36.840
 Any you know, they're almost the same molecule except one of them NADH obviously has an extra hydrogen and so

1:03:37.360 --> 1:03:47.920
 NADH is the reduced version of that molecule and NAD plus is the oxidized version. And so in a system where you have, well,

1:03:47.920 --> 1:03:50.780
 where a lot of things are oxidized, too many things are oxidized,

1:03:50.780 --> 1:03:54.460
 that's called oxidative stress. And so, um,

1:03:55.180 --> 1:03:57.980
 in, in the NAD system, if you had oxidative stress,

1:03:57.980 --> 1:04:01.380
 you'd have too much NAD plus and not enough NADH,

1:04:01.380 --> 1:04:06.120
 but what you see in most obese and diabetic humans is the opposite. You have too much NADH and not enough NADH, but what you see in most obese and diabetic humans is the opposite.

1:04:06.120 --> 1:04:08.520
 You have too much NADH and not enough NAD+.

1:04:10.880 --> 1:04:14.760
 And that lack of NAD plus is called reductive stress,

1:04:14.760 --> 1:04:16.040
 and it is a real problem.

1:04:16.040 --> 1:04:21.040
 And one of the ways that you can get oxidative stress is,

1:04:21.360 --> 1:04:23.080
 well, kind of like I mentioned before,

1:04:23.080 --> 1:04:25.760
 if there's not enough NAD+, then your

1:04:25.760 --> 1:04:31.920
 mitochondrial enzymes become acetylated and they stop working. And I think that

1:04:31.920 --> 1:04:37.640
 that ends up driving this huge amount of reactive oxygen species coming out of

1:04:37.640 --> 1:04:45.000
 your mitochondria because like complex 5 is acetylated and it stops working efficiently.

1:04:45.320 --> 1:04:49.680
 And so you have no way to get the, you know,

1:04:49.680 --> 1:04:53.420
 the electrons entering the electron transport chain

1:04:53.420 --> 1:04:55.760
 to come all the way back down to make ATP

1:04:55.760 --> 1:04:58.260
 because Complex 5 isn't working.

1:04:58.260 --> 1:05:00.680
 And that's when you get this kind of massive

1:05:02.040 --> 1:05:04.420
 oxidative stress because all of these electrons

1:05:04.420 --> 1:05:07.040
 are trying to run through the electron transport chain

1:05:07.040 --> 1:05:08.000
 and they can't do it.

1:05:08.000 --> 1:05:11.840
 And so they're coming back out as reactive oxygen species.

1:05:11.840 --> 1:05:15.520
 Whereas if you're not in reductive stress,

1:05:15.520 --> 1:05:17.600
 if you have enough NAD+,

1:05:17.600 --> 1:05:21.200
 then complex five doesn't become acetylated

1:05:21.200 --> 1:05:22.920
 and the electrons can run through

1:05:22.920 --> 1:05:26.080
 and you don't end up with that kind of massive amount

1:05:26.080 --> 1:05:32.720
 of reactive oxygen species production. But that sounds like similar to what Dr. Peat is saying

1:05:33.280 --> 1:05:38.720
 about the Randle cycle is you need, you know, if you wind up with too much NADH, then,

1:05:39.360 --> 1:05:47.400
 you know, your metabolism just doesn't run right. Yeah, and experiments show that if you uncouple

1:05:47.400 --> 1:05:52.400
 the production of ATP by the electron transport chain,

1:05:52.960 --> 1:05:57.960
 if you waste oxygen, run glucose through the system

1:05:59.240 --> 1:06:04.240
 at a very high rate, excess site rate, for example,

1:06:04.560 --> 1:06:09.000
 will uncouple and become wasteful use of oxygen

1:06:09.000 --> 1:06:10.440
 and fuel.

1:06:10.440 --> 1:06:20.800
 That uncoupling is consuming oxygen at a high rate, but it's stopping random reactive oxygen

1:06:20.800 --> 1:06:22.720
 species production.

1:06:22.720 --> 1:06:26.000
 It gets rid of the dangerous electrons.

1:06:26.000 --> 1:06:29.820
 It gets rid of the harm of reductive stress.

1:06:31.680 --> 1:06:36.680
 Pasture oxidation reduces ROS.

1:06:37.240 --> 1:06:39.340
 Right, and the other thing I mentioned before

1:06:39.340 --> 1:06:44.340
 is the other way to get rid of the reductive stress

1:06:44.440 --> 1:06:45.880
 is if you're burning saturated

1:06:45.880 --> 1:06:54.200
 fat we have this system that removes ROS and it gives you back NAD plus and

1:06:54.200 --> 1:06:58.720
 that's the enzyme well really takes two enzymes it takes glutathione reductase

1:06:58.720 --> 1:07:04.760
 and then it takes this thing called NNT and so that actually uses ROS when

1:07:04.760 --> 1:07:07.420
 you're burnt when you're burning saturated fat

1:07:07.420 --> 1:07:09.340
 to give you back the NAD+.

1:07:09.340 --> 1:07:11.460
 But once you switch to burning PUFA,

1:07:11.460 --> 1:07:14.340
 you're not making the ROS in the same way

1:07:14.340 --> 1:07:19.200
 and the PUFA keeps you in that reductive stress.

1:07:22.260 --> 1:07:24.560
 I'm not buying the reductive stress, sorry.

1:07:24.560 --> 1:07:30.720
 The oxidative stress, I think what's happening is that when you've got so much oxidative

1:07:30.720 --> 1:07:40.400
 stress, you can have some backup in some aspects of the whole cell machinery, but I can't see

1:07:40.400 --> 1:07:41.880
 how it's driving.

1:07:41.880 --> 1:07:46.640
 Where is this reductive stress coming from? You know, PUFA causes

1:07:46.640 --> 1:07:52.400
 oxidative stress. So how do we go from oxidative stress to reductive stress? The only way you

1:07:52.400 --> 1:07:59.720
 can do it is by invoking like one or two single metabolic pathways as like these dominant

1:07:59.720 --> 1:08:07.800
 pathways and controlling the cell energy partitioning. And it doesn't make sense to me. I'm sorry, it's just, it seems like a small picture

1:08:07.800 --> 1:08:10.700
 kind of explanation.

1:08:12.040 --> 1:08:14.280
 I'm sure it's something that can happen,

1:08:14.280 --> 1:08:18.220
 but I just don't think it's the dominant process.

1:08:18.220 --> 1:08:21.280
 And it matters because if we're trying to,

1:08:21.280 --> 1:08:23.760
 like say this is what's going on,

1:08:23.760 --> 1:08:27.640
 we can't like finger a metabolic process

1:08:27.640 --> 1:08:30.800
 that someone else, the opposition,

1:08:30.800 --> 1:08:33.760
 could say, well, easily say,

1:08:33.760 --> 1:08:37.320
 there's no way that process doesn't do that.

1:08:37.320 --> 1:08:40.320
 For example, there's an alternative explanation

1:08:40.320 --> 1:08:45.000
 for why the SCD enzyme is affected by PUFA

1:08:45.360 --> 1:08:50.360
 and that has to do with trying to maintain a certain amount,

1:08:50.760 --> 1:08:54.200
 trying to maintain the proper melting point of the fat.

1:08:54.200 --> 1:08:56.560
 And so if you have a high PUFA diet,

1:08:56.560 --> 1:09:00.160
 then you end up, people end up with more saturated fat

1:09:00.160 --> 1:09:03.460
 in their body tissues than normal.

1:09:03.460 --> 1:09:06.740
 And that's actually been one of the pieces of evidence

1:09:06.740 --> 1:09:08.520
 that the American Heart Association uses

1:09:08.520 --> 1:09:12.460
 to prove that saturated fat correlates with obesity

1:09:12.460 --> 1:09:14.740
 because they find people who are less healthy,

1:09:14.740 --> 1:09:16.020
 more metabolically deranged,

1:09:16.020 --> 1:09:18.660
 who have been eating the higher proportions of PUFA,

1:09:18.660 --> 1:09:21.720
 they have more saturated fat in their adipose tissue.

1:09:21.720 --> 1:09:24.300
 And they're saying it's, well, therefore,

1:09:24.300 --> 1:09:28.960
 it's because they eat more saturated fat, right? They're saying that that's what made them fat. And that is a

1:09:28.960 --> 1:09:37.120
 completely inside out convoluted way of looking at it. And we can't do that if we're going to be

1:09:37.120 --> 1:09:43.680
 right. But the, I mean, the, the evidence is quite clear that one of the major changes in the 20th

1:09:43.680 --> 1:09:50.360
 century, along with the increased consumption of seed oils, has been an increase in the adipose content of

1:09:50.360 --> 1:09:52.440
 polyunsaturated fats.

1:09:52.440 --> 1:09:57.800
 Eating polyunsaturated does not increase the amount of saturated fat that the body stores.

1:09:57.800 --> 1:09:58.800
 If it did, then Brad—

1:09:58.800 --> 1:09:59.800
 Oh, it does.

1:09:59.800 --> 1:10:00.800
 Wait, wait.

1:10:00.800 --> 1:10:01.800
 Relatively, though.

1:10:01.800 --> 1:10:03.640
 If it did—not relatively, so at all.

1:10:03.640 --> 1:10:07.880
 If it did have that effect, then Brad wouldn't have the problem with his pigs of having soft fat

1:10:08.320 --> 1:10:13.560
 Right. Well, no, I'm just a moment. It's all fat is due to the

1:10:14.240 --> 1:10:16.600
 storage of all in saturated fats

1:10:17.040 --> 1:10:23.520
 So look you take a look at the the composition of human adipose tissue through the past hundred years

1:10:24.120 --> 1:10:30.920
 and of human adipose tissue through the past 100 years. And when you look at the ratio of saturated to monounsaturated fat, you see that we actually

1:10:30.920 --> 1:10:36.440
 have more saturated fat now than we did in the past compared to monounsaturated fat.

1:10:36.440 --> 1:10:47.480
 And yes, you are, Tucker and Brad, you are both correct that now we have a low, we have more melty fat, we have more

1:10:47.480 --> 1:10:53.080
 PUFA in our fat, but as a way to protect against that, the body has no choice how much PUFA

1:10:53.080 --> 1:10:55.800
 is going to end up in the adipose tissue, right?

1:10:55.800 --> 1:10:58.960
 That's just a reflection of the diet.

1:10:58.960 --> 1:11:03.520
 We can't change a polyunsaturated fat into a monounsaturated fat.

1:11:03.520 --> 1:11:07.020
 We have no, we have no capacity to do that.

1:11:07.020 --> 1:11:08.100
 But we can change sugar.

1:11:08.100 --> 1:11:09.420
 We do actually.

1:11:09.420 --> 1:11:12.140
 That does in fact happen.

1:11:12.140 --> 1:11:14.940
 All of the evidence I've seen is that there's definitely.

1:11:14.940 --> 1:11:16.700
 But not to a big degree if it does.

1:11:16.700 --> 1:11:19.740
 Because that's why we have this huge increase

1:11:19.740 --> 1:11:23.980
 in body fat, polyunsaturated fat as well.

1:11:23.980 --> 1:11:24.820
 So I need to touch it.

1:11:24.820 --> 1:11:28.440
 Well we've assessed because we've overwhelmed our regulatory mechanism.

1:11:28.440 --> 1:11:30.720
 Yeah, I would say there's a lot of evidence out there

1:11:30.720 --> 1:11:35.720
 that in obesity and diabetes,

1:11:35.880 --> 1:11:38.600
 the ratio of monounsaturated fat

1:11:38.600 --> 1:11:40.920
 to saturated fat increases.

1:11:42.760 --> 1:11:44.600
 There's, if you look up.

1:11:44.600 --> 1:11:54.380
 No, not monounsaturated, total unsaturated, total unsaturated, but not monounsaturated. increases. If you look up the desaturase index, there's a ton of evidence that at least specifically

1:11:54.380 --> 1:12:03.700
 in obesity, I guess in diabetes too, the ratio of oleic acid to stearic acid goes up with

1:12:03.700 --> 1:12:10.040
 obesity. Well, stearic acid is just one of the many saturated fatty acids, right?

1:12:10.040 --> 1:12:13.480
 So we want to look at the total saturated fatty acid.

1:12:13.480 --> 1:12:17.040
 And we have other fatty acids besides stearic that we can make.

1:12:17.040 --> 1:12:19.240
 So that's what I'm talking about.

1:12:19.240 --> 1:12:20.240
 Right.

1:12:20.240 --> 1:12:25.000
 And yeah, it looks to me like average Americans now have

1:12:25.200 --> 1:12:30.200
 something like 10% less, well, like in the 1960s,

1:12:31.440 --> 1:12:33.640
 the studies that we have, there was one in Indiana

1:12:33.640 --> 1:12:35.840
 where saturated fat in lean adults

1:12:35.840 --> 1:12:39.040
 was something like 36% total saturates.

1:12:39.040 --> 1:12:41.620
 And if you look at obese people now,

1:12:41.620 --> 1:12:46.460
 it's something like, you know, 25 to 28% total saturates.

1:12:48.180 --> 1:12:53.180
 So it looks to me like saturated fat has decreased

1:12:53.820 --> 1:12:55.500
 specifically in obese people, but-

1:12:55.500 --> 1:12:57.680
 I'm not talking about that.

1:12:57.680 --> 1:13:00.180
 I'm talking about the ratio of saturated

1:13:00.180 --> 1:13:02.260
 to monounsaturated, which is the only thing

1:13:02.260 --> 1:13:05.280
 that our physiology can really make a big impact on.

1:13:05.280 --> 1:13:13.440
 We can easily turn a saturated fatty acid into a monounsaturated fatty acid. And we have stopped

1:13:13.440 --> 1:13:20.240
 doing that because we need to stop doing that because we have so much PUFA. So the ratio of

1:13:20.240 --> 1:13:28.240
 saturated to monounsaturated has changed in attempt to try and keep the melting point

1:13:28.240 --> 1:13:31.800
 of our body fat relatively constant.

1:13:31.800 --> 1:13:34.600
 So that's, it's a protective mechanism, right?

1:13:34.600 --> 1:13:40.320
 So we're trying to leave more, relatively more, we're trying to leave relatively more

1:13:40.320 --> 1:13:45.120
 of the saturates in our body fat because they will keep it more solid.

1:13:45.120 --> 1:13:50.380
 And if we were to desaturate that and have as much monounsaturated fat as we, you know,

1:13:50.380 --> 1:13:55.200
 we really ideally would want to, because that's the preferred fuel for mitochondria of the

1:13:55.200 --> 1:14:01.560
 three types, then we would have too much melty fat.

1:14:01.560 --> 1:14:06.900
 It would be, you know, there'd be too much unsaturated fatty acids in our fat.

1:14:06.900 --> 1:14:09.300
 So we're trying to keep it as saturated as possible

1:14:09.300 --> 1:14:11.780
 to protect against all the PUFA.

1:14:11.780 --> 1:14:13.640
 So you have to look at the ratio of the only things

1:14:13.640 --> 1:14:17.320
 that we can control, which is the total monounsaturated

1:14:17.320 --> 1:14:19.740
 and the total saturated.

1:14:19.740 --> 1:14:21.540
 Right, and that definitely happens.

1:14:21.540 --> 1:14:27.200
 So polyunsaturated fat at certain levels

1:14:27.200 --> 1:14:32.200
 absolutely does suppress the SCD1 enzyme,

1:14:32.400 --> 1:14:35.300
 the thing that makes saturated fat to monounsaturated fat.

1:14:35.300 --> 1:14:39.360
 The problem is at some further level of additional

1:14:39.360 --> 1:14:43.360
 and longer polyunsaturated fat, they go up in parallel.

1:14:44.480 --> 1:14:50.680
 The SCD1 starts increasing in parallel with increased polyunsaturated fat, and that's

1:14:50.680 --> 1:14:55.500
 when you start to see real obesity and real diabetes.

1:14:55.500 --> 1:14:56.500
 That's what I've seen.

1:14:56.500 --> 1:14:59.280
 Well, it might vary in different tissues.

1:14:59.280 --> 1:15:04.520
 If you're looking at the adipose versus the liver versus the muscle, so you can't make

1:15:04.520 --> 1:15:06.680
 a blanket statement about that.

1:15:06.680 --> 1:15:09.840
 Were you talking specifically about adipose?

1:15:09.840 --> 1:15:10.680
 Or was it?

1:15:10.680 --> 1:15:13.920
 I was talking specifically about adipose, yes.

1:15:13.920 --> 1:15:18.920
 Okay, yeah, so I mean, we don't wanna get too lost, though.

1:15:19.480 --> 1:15:21.440
 I mean, the big picture is that

1:15:23.560 --> 1:15:25.440
 I think we should try to come to

1:15:25.440 --> 1:15:28.320
 agreement as to whether or not oxidative stress is a bigger

1:15:28.320 --> 1:15:31.720
 issue than reductive stress. And I come down on the side of

1:15:31.760 --> 1:15:35.920
 oxidative stress is clearly the problem. And I don't know where

1:15:35.920 --> 1:15:38.600
 the reductive stress would be coming from these days,

1:15:38.760 --> 1:15:46.800
 honestly. So but I think if we can't agree on that, then we need to try to, because we have to

1:15:46.800 --> 1:15:47.800
 pick one.

1:15:47.800 --> 1:15:48.800
 We can't have both.

1:15:48.800 --> 1:15:53.120
 Well, you can't actually have both in the same cell at the same time.

1:15:53.120 --> 1:15:56.160
 And that's one of those sort of unfortunate truths, right?

1:15:56.160 --> 1:15:58.400
 Because what can happen is your pool...

1:15:58.400 --> 1:16:01.120
 But what's driving it is what I'm saying.

1:16:01.120 --> 1:16:02.120
 Your pool of...

1:16:02.120 --> 1:16:03.120
 What's driving it.

1:16:03.120 --> 1:16:05.900
 Right, right. And so I would argue that the,

1:16:05.900 --> 1:16:09.200
 specifically within the NAD plus NADH,

1:16:09.200 --> 1:16:11.660
 it's ultimately the reductive stress that's driving it.

1:16:11.660 --> 1:16:15.540
 But those are, but these are hard.

1:16:15.540 --> 1:16:17.840
 Because PUFAs cause oxidative stress

1:16:17.840 --> 1:16:19.580
 and we haven't changed our diet

1:16:19.580 --> 1:16:22.080
 in a way that would cause more reductive stress.

1:16:23.100 --> 1:16:26.880
 Well, the PUFAs cause in in the PUFAs cause reductive stress

1:16:26.880 --> 1:16:29.520
 in the NAD pool, but they cause oxidative stress

1:16:29.520 --> 1:16:32.880
 in like the glutathione pool, because, you know,

1:16:32.880 --> 1:16:34.960
 whenever you talk about, again,

1:16:34.960 --> 1:16:36.220
 it's like the cell tissue type.

1:16:36.220 --> 1:16:37.680
 Whenever you talk about reductive stress

1:16:37.680 --> 1:16:39.340
 and oxidative stress, it depends both

1:16:39.340 --> 1:16:42.680
 on the cellular sub-compartment.

1:16:42.680 --> 1:16:44.320
 Like, are we talking about in the mitochondria?

1:16:44.320 --> 1:16:45.440
 Are we talking about cytoplasm,

1:16:45.440 --> 1:16:48.220
 and then it depends on if we're talking about,

1:16:48.220 --> 1:16:51.380
 you know, NAD versus glutathione.

1:16:51.380 --> 1:16:55.400
 So you can have both in the same cell.

1:16:55.400 --> 1:16:58.960
 And that's, you know, unfortunately it's hard, right?

1:16:58.960 --> 1:17:00.720
 And it's confusing and it's hard to understand.

1:17:00.720 --> 1:17:01.560
 Well, it shouldn't be.

1:17:01.560 --> 1:17:02.520
 We have to make it simple.

1:17:02.520 --> 1:17:03.520
 Our job is to make it simple.

1:17:03.520 --> 1:17:06.080
 And I think if we're paying attention to the wrong thing, we're making it more complicated than it hard to understand. Well, it shouldn't be. We have to make it simple. Our job is to make it simple. And I think if we're paying attention to the wrong thing,

1:17:06.080 --> 1:17:08.280
 we're making it more complicated than it needs to be.

1:17:08.280 --> 1:17:11.100
 And so I think that, yes, there can be elements

1:17:11.100 --> 1:17:14.920
 and like there can be basically little kinks in the system

1:17:14.920 --> 1:17:18.580
 that is basically overall an oxidative stress problem

1:17:18.580 --> 1:17:21.700
 that can cause here and there reductive stress

1:17:21.700 --> 1:17:23.200
 because it's a seesaw, right?

1:17:23.200 --> 1:17:27.080
 So like you said, there's there, but the big picture

1:17:27.080 --> 1:17:29.520
 is PUFA is causing oxidative stress.

1:17:29.520 --> 1:17:32.440
 If we can't agree on that, then we can't agree

1:17:32.440 --> 1:17:34.920
 on why PUFA is bad, why seed oils are bad.

1:17:34.920 --> 1:17:35.880
 Well, here's what I would say.

1:17:35.880 --> 1:17:38.800
 I would say that if the biggest problem,

1:17:38.800 --> 1:17:41.200
 if the problem, you know, the overarching problem

1:17:41.200 --> 1:17:44.360
 is oxidative stress, then the suggestion would be

1:17:44.360 --> 1:17:45.440
 that if we were to take

1:17:45.440 --> 1:17:51.200
 lots of antioxidants, we could make the problem better. But most experiments that I've seen don't

1:17:51.200 --> 1:17:55.760
 suggest that's true. No, that's not what the suggestion would be. That is a fallacy. So

1:17:58.160 --> 1:18:05.000
 you have to understand that antioxidants, the term is so misused.

1:18:06.400 --> 1:18:09.600
 It's not like resveratrol has this

1:18:09.600 --> 1:18:11.800
 incredible antioxidant capacity.

1:18:11.800 --> 1:18:14.040
 I agree, I just mean like vitamin E.

1:18:14.040 --> 1:18:15.480
 I'm sure you know this, but we have

1:18:15.480 --> 1:18:16.920
 antioxidant enzymes, right?

1:18:16.920 --> 1:18:18.360
 I think you've probably written extensively

1:18:18.360 --> 1:18:19.180
 about one of them.

1:18:19.180 --> 1:18:22.680
 We have many antioxidant enzymes that,

1:18:22.680 --> 1:18:26.400
 because, antioxidation is you're taking something

1:18:26.400 --> 1:18:31.680
 that's from a very high energy state and you're bringing it down stepwise to a

1:18:31.680 --> 1:18:38.800
 safe energy level and it takes more than one enzyme to do that it takes more than

1:18:38.800 --> 1:18:43.760
 one step you can't just have vitamin C stepping in and solving all the problems

1:18:43.760 --> 1:18:45.760
 because it won't do that.

1:18:45.760 --> 1:18:47.100
 It won't bring it all the way down

1:18:47.100 --> 1:18:49.740
 to the proper energy level.

1:18:49.740 --> 1:18:52.120
 And then vitamin C needs to be regenerated.

1:18:52.120 --> 1:18:54.800
 And this is a fact that a lot of people don't realize,

1:18:54.800 --> 1:18:58.360
 but every antioxidant compound like vitamin C

1:18:59.440 --> 1:19:03.880
 can be pro-oxidant in a certain setting.

1:19:03.880 --> 1:19:08.700
 So you can't make a blanket statement about like, oh, well, we can just take antioxidants,

1:19:08.700 --> 1:19:10.560
 like everyone does, like everyone selling supplements.

1:19:10.560 --> 1:19:14.820
 I'm not saying you do, but everyone selling supplements says like, oh, you just need to

1:19:14.820 --> 1:19:21.780
 take this massive best antioxidant supplement, and then you won't have any issues with oxidation.

1:19:21.780 --> 1:19:27.360
 And as you pointed out, those studies never bear out and it's because it's

1:19:27.360 --> 1:19:31.160
 based on a fallacy.

1:19:31.160 --> 1:19:41.840
 In a healthy cell, the great bulk of the vitamin C inside the cell is in the form of dehydroascorbate.

1:19:41.840 --> 1:19:47.860
 It's the oxidized form which is active and protective. In reductive

1:19:47.860 --> 1:19:56.680
 stress, you lose that function of vitamin C. You lose the oxidative

1:19:56.680 --> 1:20:05.440
 function of vitamin C when the cell goes wrong and goes reductive stress. I'm sure there's a lot of consequences.

1:20:15.760 --> 1:20:16.640
 Can we just say that if you do anything which disables the electron transport chain,

1:20:30.880 --> 1:20:37.920
 you are not going to be able to convert NADH in bulk to NAD+. So you will, however you damage the electron transport chain, you will end up with reductive stress. Whether you are damaging the electron transport

1:20:37.920 --> 1:20:48.640
 chain with reactive oxygen species or by acetylating it or by adding ROS-derived polyunsaturated fatty acids to

1:20:48.640 --> 1:20:57.360
 the proteins of the electron transport chain, there is a component which is ROS-derived,

1:20:57.360 --> 1:21:08.560
 but the end result is reductive stress because you cannot get rid of the NADH or you cannot convert the NADH to NAD+. So I would maintain

1:21:08.560 --> 1:21:16.480
 that they both occur together. I don't think it's either or and I think that reductive stress I

1:21:16.480 --> 1:21:25.080
 would view as a marker of dysfunction of the electron transport chain. Just trying to see whether you can get these two things

1:21:25.080 --> 1:21:26.560
 to be compatible.

1:21:26.560 --> 1:21:27.400
 Okay.

1:21:29.200 --> 1:21:31.620
 Dr. Peat, do you agree with that?

1:21:31.620 --> 1:21:36.040
 Yeah, and it's reductive stress that turns on fat synthesis

1:21:36.040 --> 1:21:38.760
 as well as lactic acid synthesis.

1:21:41.340 --> 1:21:42.180
 Right, okay.

1:21:42.180 --> 1:21:44.420
 So they're, I mean, one could almost say

1:21:44.420 --> 1:21:45.900
 they're two sides of a coin.

1:21:45.900 --> 1:21:46.900
 They're going on at the same time.

1:21:46.900 --> 1:21:47.900
 Right, I guess what we're saying is that.

1:21:47.900 --> 1:21:54.700
 And the process, the process is, um, what's going wrong is that you've got a dysfunction

1:21:54.700 --> 1:21:58.300
 in the regulatory system that's balancing those two processes.

1:21:58.300 --> 1:22:00.660
 Is that fair to say?

1:22:00.660 --> 1:22:02.160
 Yep.

1:22:02.160 --> 1:22:09.040
 And Dr. Peat, you're, in your opinion, part of that, what's going on there, is that you're not

1:22:09.040 --> 1:22:11.120
 burning enough glucose.

1:22:11.120 --> 1:22:13.120
 Is that correct?

1:22:13.120 --> 1:22:14.120
 Right.

1:22:14.120 --> 1:22:27.000
 I wrote a couple of newsletters on late 19th century experimenters with treating diabetes with huge amounts of sugar.

1:22:27.000 --> 1:22:37.000
 What it's doing essentially is shifting the Randle cycle, lowering free fatty acids,

1:22:37.000 --> 1:22:49.200
 stopping the interference with glucose oxidation, lowering fat production and lactic acid production, and getting respiration going.

1:22:51.760 --> 1:22:56.960
 Interesting. Now, one of the things that, you know, if we're going to get this message out,

1:22:56.960 --> 1:23:06.880
 and we're going to convince scientists as to the validity of it, one of the things that we're going to have to explain better than I think we

1:23:06.880 --> 1:23:17.280
 have is that PUFA consumption is not a linear process. That you take a small amount and it has

1:23:17.280 --> 1:23:26.840
 little effect on obesity, and then you take a large amount and it also has little effect of obesity. And if you take a large amount in a ketogenic diet,

1:23:26.840 --> 1:23:30.920
 then it's actually seems to be beneficial

1:23:30.920 --> 1:23:34.480
 from a solely obesogenic standpoint.

1:23:34.480 --> 1:23:37.300
 Dr. Peat, do you have any thoughts on what's going on

1:23:37.300 --> 1:23:38.520
 with that process?

1:23:38.520 --> 1:23:42.520
 Because I've already seen there's a study that came out

1:23:42.520 --> 1:23:49.760
 by John Speakman in 2018 where he looked at fat causing

1:23:49.760 --> 1:23:56.840
 obesity compared to protein and glucose and you know he saw this clear pattern

1:23:56.840 --> 1:24:01.600
 that you know low levels of fat didn't produce much obesity moderate levels of

1:24:01.600 --> 1:24:05.720
 fat were the most obesogenic and then high levels of fat were the most obesogenic, and then high levels of fat, again,

1:24:05.720 --> 1:24:07.220
 obesity started going down.

1:24:07.220 --> 1:24:10.320
 Do you have any thoughts on what's driving that curve?

1:24:11.160 --> 1:24:13.960
 Yeah, when you have very large amounts

1:24:13.960 --> 1:24:18.960
 of either fat or glucose, you're sparing protein.

1:24:18.960 --> 1:24:23.540
 You're not oxidizing protein for energy.

1:24:24.480 --> 1:24:27.440
 Suppressing protein metabolism and

1:24:29.040 --> 1:24:38.000
 an excess of protein is a big problem that blocks thyroid function and oxidative metabolism,

1:24:38.000 --> 1:24:41.120
 for example, and contributes to aging.

1:24:41.480 --> 1:24:45.840
 contributes to aging.

1:24:50.280 --> 1:24:52.840
 Tucker, and you were talking about ketogenic high puffer diets.

1:24:52.840 --> 1:24:53.660
 Right.

1:24:53.660 --> 1:24:58.660
 The famous Bioserve's F3666,

1:24:59.620 --> 1:25:01.360
 it's 5% protein.

1:25:02.280 --> 1:25:08.640
 And we don't know whether that controls body weight in the rodent model through

1:25:09.600 --> 1:25:16.880
 ketogenesis and hypoinsulinemia or whether it's purely driven by the extremely low levels of

1:25:16.880 --> 1:25:26.760
 protein in the diet. So, from what Dr. Peat was saying, protein levels matter, and the standard ketogenic diet model

1:25:27.980 --> 1:25:32.060
 for rodent studies is massively hypoproteinemic.

1:25:34.760 --> 1:25:38.200
 It's borderline protein deficient.

1:25:38.200 --> 1:25:40.240
 Right, right, right.

1:25:40.240 --> 1:25:42.440
 Because otherwise you can't get them to generate ketones.

1:25:42.440 --> 1:25:44.680
 Ketones, that's the problem.

1:25:44.680 --> 1:25:45.200
 Even worse

1:25:45.200 --> 1:25:55.040
 if you supplement with normal levels of, what's the, what do you package triglycerides up in to

1:25:55.040 --> 1:26:02.480
 make VLDLs? Glycerol. Yeah, no, no, to make the actual capsule-y bit. Oh, the chylomicrons?

1:26:08.240 --> 1:26:09.520
 bit. Oh, the chylomicrons? No, I'm just, what on earth is the biochemical component?

1:26:16.400 --> 1:26:25.000
 Not carnitine, not carnosine, there's a ... it's gone now, it's not going to come back, but they make it deficient in F366, so the liver cells can't export chylomicrons or VLDLs,

1:26:25.160 --> 1:26:28.280
 rather, so you end up with the,

1:26:28.280 --> 1:26:33.280
 so you end up with an accumulation of triglycerides

1:26:33.720 --> 1:26:35.800
 in the liver cells, which again,

1:26:35.800 --> 1:26:39.000
 is used to bump up the metabolism to ketones.

1:26:39.000 --> 1:26:44.000
 So, but if you supplement with, hang on a second,

1:26:45.260 --> 1:26:46.100
 it's on my desk.

1:26:46.100 --> 1:26:46.940
 Is it bile acid?

1:26:46.940 --> 1:26:47.780
 Barnitine?

1:26:47.780 --> 1:26:48.600
 No.

1:26:48.600 --> 1:26:49.440
 No, no, no.

1:26:50.660 --> 1:26:52.120
 Choline, choline.

1:26:52.120 --> 1:26:53.360
 Choline, right, of course.

1:26:53.360 --> 1:26:56.080
 And that's why choline deficiency causes fatty acid.

1:26:56.080 --> 1:26:56.920
 Choline deficiency.

1:26:56.920 --> 1:26:57.760
 Fatty liver.

1:26:57.760 --> 1:27:00.060
 Which means you can't export fats from liver cells.

1:27:00.060 --> 1:27:01.580
 Right, right, right, right, right.

1:27:01.580 --> 1:27:02.400
 Hence it's key to you.

1:27:02.400 --> 1:27:05.300
 So it's a bit of a nightmare for trying to,

1:27:06.880 --> 1:27:08.740
 come back to what Dr. Peat said,

1:27:08.740 --> 1:27:12.240
 was that you could be looking at the effect

1:27:12.240 --> 1:27:14.080
 of not metabolizing protein.

1:27:14.080 --> 1:27:16.600
 This is, so,

1:27:19.420 --> 1:27:20.720
 our model's not very good.

1:27:23.320 --> 1:27:29.460
 Right, that would make sense, and it would explain why that diet often but not always

1:27:29.460 --> 1:27:31.520
 causes fatty liver disease.

1:27:31.520 --> 1:27:35.120
 If you supplement with what do you call it?

1:27:35.120 --> 1:27:36.120
 Choline.

1:27:36.120 --> 1:27:42.960
 Then it doesn't, you can basically take Bioserve and add choline to it and no fatty liver.

1:27:42.960 --> 1:27:48.160
 So it's another non-physiological model for humans, effectively.

1:27:48.160 --> 1:27:52.560
 Yes. This discussion has been fascinating and there's so much things to think about,

1:27:52.560 --> 1:27:57.840
 but I do want to give our audience kind of a wrap up question for each of you to tackle briefly.

1:27:57.840 --> 1:28:02.080
 It's just kind of, I always like to make this, there's a lot of weeds we get into it and I

1:28:02.080 --> 1:28:05.840
 wanted that to happen. I want people to get into the nitty-gritty.

1:28:05.840 --> 1:28:11.240
 And then for those who, you know, they still want to know, okay, so what do you do about

1:28:11.240 --> 1:28:12.240
 that?

1:28:12.240 --> 1:28:17.580
 We've all explored different explanations as to why these seed oils and high PUFA products

1:28:17.580 --> 1:28:19.960
 are linked to the rise of obesity.

1:28:19.960 --> 1:28:24.760
 We've explained different theories about what's happening there.

1:28:24.760 --> 1:28:26.600
 You're not going to settle everything today, of course,

1:28:26.600 --> 1:28:30.400
 but I do want us to think in a thought experiment

1:28:30.400 --> 1:28:33.040
 at some point, if you were presenting a paper to Harvard,

1:28:33.040 --> 1:28:35.160
 how would we organize all this information

1:28:35.160 --> 1:28:38.120
 and come up with the best argument

1:28:38.120 --> 1:28:40.160
 against the Harvard establishment

1:28:40.160 --> 1:28:43.480
 for why they've gotten it wrong on these PUFA topics?

1:28:43.480 --> 1:28:45.600
 But that's for another time. Oh, that's…

1:28:45.600 --> 1:28:46.960
 Yeah, go ahead. What's that?

1:28:46.960 --> 1:28:54.800
 I'll take that one. I would cite Mozaffarian et al. 2011, which was produced by the Harvard

1:28:54.800 --> 1:29:01.360
 School of Public Health, in which they show that the most fascinating, the most fattening food

1:29:02.000 --> 1:29:08.000
 by several fold is potatoes fried in seed oils. And then

1:29:08.000 --> 1:29:14.160
 they turned around and tried to hide the fact, but their own data shows that seed

1:29:14.160 --> 1:29:19.840
 oils are obesogenic and if you compare in humans a potato fried in butter or a

1:29:19.840 --> 1:29:27.080
 potato boiled to a potato fried in seed oils, they're not obesogenic, which kind of comes back to,

1:29:27.080 --> 1:29:30.140
 you know, Dr. Peat's fondness for glucose.

1:29:30.140 --> 1:29:32.480
 Glucose alone isn't a problem, it's only a problem

1:29:32.480 --> 1:29:35.280
 when it's accompanied with massive amounts of seed oils.

1:29:35.280 --> 1:29:39.520
 So yeah, that would be a very short presentation, I think.

1:29:39.520 --> 1:29:41.200
 I'd say, here's your paper, guys.

1:29:41.200 --> 1:29:42.040
 Ha ha ha.

1:29:43.840 --> 1:29:48.600
 There is at least one intervention study which can be interpreted in the same way as that.

1:29:48.600 --> 1:29:54.640
 A single meal feeding study which looked at how much you ate before you stopped, which

1:29:54.640 --> 1:30:04.120
 compared … their only saturated fat one was potato as opposed to the potatoes in Pufa

1:30:04.120 --> 1:30:07.480
 were what we call chips. what do you call them,

1:30:07.480 --> 1:30:08.560
 French fries over there?

1:30:08.560 --> 1:30:09.380
 Yeah.

1:30:09.380 --> 1:30:10.220
 French fries, yeah.

1:30:10.220 --> 1:30:12.160
 Yeah, of course chips, yeah.

1:30:12.160 --> 1:30:16.360
 But basically, it could be viewed in those terms.

1:30:16.360 --> 1:30:18.300
 And I mean, there was another interesting paper

1:30:18.300 --> 1:30:20.640
 that came out recently, I can't remember

1:30:23.560 --> 1:30:29.760
 the author, but they showed that even one of Peter's favorite obesogenic

1:30:29.760 --> 1:30:48.400
 diets, the SIRWIT diet, that if you blocked the effect of the oxidative products of the small amount of linoleic acid in that diet, right? The HNE, the

1:30:48.400 --> 1:30:54.400
 toxin that dysregulates the Randle cycle and causes fat production, if you

1:30:54.400 --> 1:31:00.220
 blocked that process, then you blocked obesity. And that's a diet with a very,

1:31:00.220 --> 1:31:04.880
 that's very obesogenic, but has a very small amount of linoleic acid in it. And

1:31:04.880 --> 1:31:06.420
 at first it wouldn't, you wouldn't think amount of linoleic acid in it, and at first,

1:31:06.420 --> 1:31:08.640
 you wouldn't think that the linoleic acid

1:31:08.640 --> 1:31:11.300
 could be the driving factor of the obesity in that.

1:31:11.300 --> 1:31:13.940
 And interestingly enough, the intervention

1:31:13.940 --> 1:31:15.760
 that they used in those animals

1:31:15.760 --> 1:31:19.560
 was a very common human polymorphism

1:31:19.560 --> 1:31:22.620
 in the detoxification system for seed oils,

1:31:23.660 --> 1:31:28.920
 the ALDH2 star 2 mutation.

1:31:28.920 --> 1:31:31.880
 So yeah, that would be my little chat to Harvard.

1:31:31.880 --> 1:31:37.340
 Well, I just want to wrap it up with everybody, give a brief explanation as to what the best

1:31:37.340 --> 1:31:44.640
 dietary intervention that you have found in your own research or life to deal with the

1:31:44.640 --> 1:31:46.520
 obesogenic effects of seed oils and high

1:31:46.520 --> 1:31:47.520
 proof of consumption.

1:31:47.520 --> 1:31:52.480
 Just try to give us a brief little explanation without going, you know, we got to kind of

1:31:52.480 --> 1:31:57.160
 wrap it up here, but I want to give everybody kind of a homework to explore, you know.

1:31:57.160 --> 1:32:01.760
 We've given the problem, let's give a little bit of a solution for people who are wanting

1:32:01.760 --> 1:32:07.240
 to deal with obesity in their own life, and you've explained seed oils

1:32:09.140 --> 1:32:13.240
 causing it, so what do you do about it, in your opinion?

1:32:13.240 --> 1:32:14.080
 Peter?

1:32:16.000 --> 1:32:20.080
 I've got two points I would leave it with.

1:32:20.080 --> 1:32:25.000
 One is that, oh God, it's gonna go more than two points.

1:32:25.320 --> 1:32:30.320
 Okay, the first is low carb eating sidesteps

1:32:30.800 --> 1:32:33.160
 the problems of seed oils.

1:32:33.160 --> 1:32:34.400
 Okay, that's the first.

1:32:35.380 --> 1:32:40.360
 The second is that carbohydrate does not cause obesity

1:32:40.360 --> 1:32:42.020
 in the absence of seed oils.

1:32:43.960 --> 1:32:47.140
 The carbohydrate insulin model is incomplete.

1:32:49.640 --> 1:32:50.480
 And long term.

1:32:50.480 --> 1:32:53.680
 Does that mean if you're obese having eaten seed oils

1:32:53.680 --> 1:32:56.800
 and you stop eating seed oils and you eat lots of carbs,

1:32:56.800 --> 1:32:58.920
 it will not add to obesity or no, you're not saying that?

1:32:58.920 --> 1:33:01.360
 Once you've cleared your fat cells of it, yes.

1:33:01.360 --> 1:33:02.640
 You'd have to clear your fat cells

1:33:02.640 --> 1:33:04.840
 of the linoleic acid first.

1:33:04.840 --> 1:33:05.400
 That would be years, right, before you have to clear your fat cells of the linoleic acid first. But-

1:33:05.400 --> 1:33:07.200
 That would be years, right, before you could eat high-

1:33:07.200 --> 1:33:10.160
 That's why you should start with low carb.

1:33:10.160 --> 1:33:15.480
 And then sidestep the problem to begin with while you sort out the problem that you've

1:33:15.480 --> 1:33:16.480
 got.

1:33:16.480 --> 1:33:21.480
 Okay, I think that those two points, I'll leave it at those two.

1:33:21.480 --> 1:33:27.640
 Dr. Kate? Dr. Kate Connolly So, as you see, I have this summarized on

1:33:27.640 --> 1:33:29.440
 my Twitter profile.

1:33:29.440 --> 1:33:33.200
 Seed oils are death and deep nutrition is life.

1:33:33.200 --> 1:33:40.240
 Deep nutrition is what every traditional diet around the country does to some extent still,

1:33:40.240 --> 1:33:48.520
 but used to do. And we didn't have access to refined, it gets out the refined carbohydrates

1:33:48.520 --> 1:33:56.520
 which are empty calories. And then the rest of the edible world is really pretty much

1:33:56.520 --> 1:34:03.040
 open but you want to make sure you get enough protein. And the best way to do that, the

1:34:03.040 --> 1:34:11.600
 most like evolutionarily, well, based on on traditional diets every traditional diet was pretty rich in animal sources of protein

1:34:12.080 --> 1:34:14.160
 compared to plant sources of protein and

1:34:14.600 --> 1:34:19.820
 Always always in whole foods because we don't talk about it very much but protein

1:34:20.220 --> 1:34:24.040
 Processed protein powders are also extremely unhealthy

1:34:24.720 --> 1:34:26.260
 and Processed protein powders are also extremely unhealthy and

1:34:26.260 --> 1:34:31.720
 Because the processed and body is there partly a lot of the nutrition in there is destroyed

1:34:31.720 --> 1:34:35.360
 It's not the way our body is supposed to absorb protein and so on

1:34:36.160 --> 1:34:37.480
 Okay

1:34:37.480 --> 1:34:39.480
 Very good Tucker

1:34:40.520 --> 1:34:44.120
 Yeah, my Twitter hashtag for years has been

1:34:49.040 --> 1:34:51.480
 Yeah, my Twitter hashtag for years has been LCL6, low carb low sex, for exactly the reasons that Peter described.

1:34:51.480 --> 1:34:59.520
 I mean, you can clearly fix the problem just by lowering seed oils, but what seed oils

1:34:59.520 --> 1:35:04.000
 induces is an inability to properly process carbohydrates.

1:35:04.000 --> 1:35:06.360
 So clearly the most effective way to do it

1:35:06.360 --> 1:35:07.580
 is to reduce both.

1:35:09.760 --> 1:35:10.680
 Brad Marshall?

1:35:11.720 --> 1:35:14.760
 Yeah, I agree with most of what's been said.

1:35:14.760 --> 1:35:16.660
 I will say the other thing,

1:35:19.160 --> 1:35:21.000
 my initial kind of hack for this,

1:35:21.000 --> 1:35:22.360
 and I still agree with this,

1:35:22.360 --> 1:35:26.800
 is to, obviously, one, stop eating seed oils or other sources of omega for this, and I still agree with this, is to obviously, one, stop eating seed oils or other

1:35:27.440 --> 1:35:31.680
 sources of omega-6, including things like commercial chicken and pork, which can be

1:35:31.680 --> 1:35:38.800
 surprisingly high sources, and actually seek out foods that have a lot of stearic acid in them.

1:35:39.440 --> 1:35:46.980
 And the reason for that is that, well, there was a paper showing that supplementing stearic acid will,

1:35:46.980 --> 1:35:51.880
 in fact, increase your rate of fat oxidation. And I think that's, I have a guess as to why

1:35:51.880 --> 1:36:00.380
 this is. When you look at humans or animals that are doing lipogenesis, new fat making,

1:36:00.380 --> 1:36:05.080
 what you see is they tend to have a lot of PUFA, they tend to have a lot of POOPA. They tend to have a lot of

1:36:05.760 --> 1:36:10.600
 Mono unsaturated fat and what they have very very little of is is stearic acid

1:36:10.600 --> 1:36:17.740
 So I think the body sees fat with very low stearic acid as oh, we should be making fat and I think the body sees

1:36:18.640 --> 1:36:26.280
 Situation with lots of stearic acid as we should be burning fat because stearic acid is really the one thing that is like totally obliterated

1:36:26.280 --> 1:36:30.900
 when those lipogenic genes are switched into the on position.

1:36:33.800 --> 1:36:34.920
 Dr. Ray Peat.

1:36:37.260 --> 1:36:42.260
 I think emphasis on body temperature should be greater.

1:36:44.480 --> 1:36:48.680
 The proof of lower your body temperature and turn on all of

1:36:48.680 --> 1:36:55.000
 the inflammatory things that tend to keep your temperature down and the

1:36:55.000 --> 1:37:09.680
 paying attention to the digestive and circulatory events when you eat polyunsaturated fats or too much protein.

1:37:09.680 --> 1:37:17.520
 The PUFA is already right in the bloodstream, turning down your metabolic rate by blocking

1:37:17.520 --> 1:37:25.000
 thyroid transport and function, and by activating the stress-related estrogen functions.

1:37:28.520 --> 1:37:31.460
 So even before you get to the cell, it's happening.

1:37:33.760 --> 1:37:34.760
 Very good.

1:37:34.760 --> 1:37:37.440
 So what would you recommend dietary interventions

1:37:37.440 --> 1:37:40.940
 for people with obesity caused by PUFA?

1:37:42.920 --> 1:37:44.280
 Raise your body temperature?

1:37:58.200 --> 1:38:08.080
 Yeah, and stearic acid and sugar, for example, do that. And avoiding too much fish and poultry and pork. Those are the major foods other than the direct seed oils.

1:38:08.080 --> 1:38:13.600
 Very good. I want to let all of you guys have an opportunity to tell us where we can find

1:38:13.600 --> 1:38:17.640
 your work, because I know a lot of people are going to want to do deep dives into your

1:38:17.640 --> 1:38:32.920
 websites and so forth. So, Peter, where can people find your work? Everything is on hyperlipid, h-y-p-e-r lipid. If you duck, duck, go hyperlipid

1:38:32.920 --> 1:38:38.720
 and PETA, it'll come up as the first hit. And Dr. Kate, where can people find your work

1:38:38.720 --> 1:38:45.000
 or anything you want to leave with? Well, it's drkate.com and there's plenty of information Dr. Kate D-R-C-A-T-E dot com.

1:38:46.800 --> 1:38:49.560
 And there's plenty of information there

1:38:49.560 --> 1:38:53.160
 about what a traditional diet is, deep nutrition.

1:38:53.160 --> 1:38:54.320
 Very good, Tucker?

1:38:55.740 --> 1:38:59.680
 My blog is yelling-stop.blockspot.com

1:38:59.680 --> 1:39:03.120
 and I'm very active on Twitter at Tucker Goodrich.

1:39:04.080 --> 1:39:06.560
 And Brad? where would?

1:39:06.560 --> 1:39:09.640
 Yeah, so my work is all on fire in a bottle.

1:39:09.640 --> 1:39:12.860
 It's fireinabottle.net, but if you just duck, duck, go

1:39:12.860 --> 1:39:14.780
 or Google fire in a bottle, it'll come up.

1:39:14.780 --> 1:39:19.780
 And I am on Twitter at fire underscore bottle,

1:39:20.900 --> 1:39:23.160
 90% sure that's my correct Twitter handle.

1:39:24.600 --> 1:39:27.520
 Dr. Peat, do you have a website or newsletter?

1:39:27.520 --> 1:39:37.080
 Our newsletter is at raypeat's Newsletter, gmail.com, and the website is raypeat.com.

1:39:37.080 --> 1:39:38.080
 Very good.

1:39:38.080 --> 1:39:40.720
 It's been a real honor to listen to all of you today.

1:39:40.720 --> 1:39:45.920
 Wow, what a great time of discussion and learning, and I know our audience is going

1:39:45.920 --> 1:39:52.240
 to be really thrilled to just see these types of mechanisms explored. This is something

1:39:52.240 --> 1:39:55.820
 that you don't see happening in academia. I can assure you that. There's nobody doing

1:39:55.820 --> 1:40:01.360
 this right now in universities having a kind of symposium about seed oil mechanisms. So,

1:40:01.360 --> 1:40:07.760
 this is the future of academia in the 21st century. It's online now. So thank you all

1:40:07.760 --> 1:40:13.200
 very much for joining me and it's been a real treat. So thanks again. Thank you, David. Yeah,

1:40:13.200 --> 1:40:43.920
 thank you very much, everybody. Thanks, David. Take care. Everybody. Bye for now.

1:40:42.230 --> 1:40:48.150
 Bye!