Well, today's going to be a real fascinating discussion.
I call this my big fat panel because it's exploring the idea of obesity, what causes
obesity.
And we have assembled, I think, an all-star panel today of leading lights in various different
categories of knowledge that have been really doing great work in exploring why we have such a rise
in obesity over the years.
And each of these individuals I've interviewed in the past,
and we've never had them all together on one panel together.
But I thought if we're gonna tackle
the big elephant in the room,
which is causing so much dysfunction,
both on a health basis as well as a financial and
economic burden in this country and around the world, then we've got to
really dive into the specifics as to what is really going on with these seed
oil products and high PUFA products in general and their link to obesity. What
is the mechanism precisely what is driving this problem?
And so, just a brief introduction, and again, I'm not going to get all the accolades right,
you know, in just a short time, but Peter Dobromilsky, I met you through your blog,
Hyperlipid, where you've been doing great work in really getting into the weeds of explaining
the mechanisms. And I had a hard time following, but I had to keep of explaining the mechanisms and I had a
hard time following but I had to keep it was really I had to pause it and replay
but it was very fascinating stuff with your explanation for what what's going
on with the linoleic acid in the cells and Dr. Kate Shanahan of course you've
been the leading pioneer as a woman out there around
the world stage, sounding the alarm of this problem for a long time.
Saw you on Bill Maher's show and many, many other programs.
Fox, what was it, Jesse Waters you were just on, I saw.
And that's amazing stuff.
So a true pioneer on this topic of seed oils and also author of Fat Burn Fix and Deep Nutrition.
Of course, we got Tucker Goodrich who's a frequent,
if you are a listener or viewer of our radio show, you see Tucker on every week.
He is the proprietor of Yelling Stop, the blog,
and he too has been out there for a long time now talking about seed oils
and sounding the
alarm.
We have Brad Marshall with Fire in a Bottle, and he is someone that's been on my show exploring
how this linoleic acid is basically driving so much of what you call torpor, right?
A state of torpor that people are in, which is an interesting angle.
And so Brad has been raising low PUFA pork and low PUFA chicken experiments with really
interesting results and other types of, you know, experimentations. He's got a background in
genetics and biology. And we have Dr. Ray Peat, who's joining me from by phone today.
So he is also someone who's got a long history
of talking about these different issues.
And each person on this panel
brings a different perspective.
Kate Shanahan is an MD.
Peter Dobromilsky, you are in veterinarian, right?
Is that your?
Yeah. And so, everybody has different, and, you know,
Dr. Peat, you have a unique angle that I think a lot of people have been fascinated by. So,
I really want to welcome all of you to this discussion. Thank you.
It's an honor to be here. Yeah, thank you.
Very good. So, let's just start where I start off, which is to start with Peter, since youâ€¦that's
the order of introduction.
So, Peter, go ahead and tell us just, you know, your background a little bit and set
the table for what precisely is the mechanism.
If we're going to make this case to the world, we've got to figure out what precisely
is the mechanism for causing obesity and maybe there's multiple layers to this question.
Yeah, I would agree very much that I think
there are multiple layers to the question.
And my view has been for many years now
that obesity is primarily a signaling problem
and that there are layers to the signaling. The very most basic
layer of signaling, there is the mitochondria signaling to the cell what to do with the
available calories. And that signaling process goes right back to bacteria,
probably archaea as well, but nobody's ever looked at them.
So, but with bacteria, growth and reproduction
are inseparable from reactive oxygen species signaling.
And the method for producing the ROS by bacteria,
we really don't know about yet, but the mitochondrion is essentially bacterium and
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
I ended up with on a very theoretical basis. On a more practical basis,
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
hypothesis of what controlled obesity and that you could look at various populations
with very, very high carbohydrate intakes and there was no obesity. So I knew right from the beginning
that the insulin hypothesis of obesity was very attractive, very practical set of advice,
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.
And probably about 10-12 years ago, I sat down and tried to work out the difference in terms of how
fats and how carbohydrates were actually processed in the cell and in the mitochondria. And the
concept that it might be reactive oxygen species that were essential for signaling how many
calories a given cell should accept, more or less fell out of those back of the envelope doodles. And it went on from,
in slow steps from there over something like 60 blog posts
now, all of which essentially stem from those three or four.
So that's where I've ended up that
the seed oils signal differently within the cell from saturated fats and the fruit oils,
things like avocado oil or olive oil, are halfway house or closer to the monounsaturated
fats, which again are a normal signaling component of mammalian cells.
So we've got saturated fats and mixed with monounsaturated fats as a normal milieu
and C. doles mess that up.
I think that seems reasonable.
That's where I come from basically.
So I'll let someone else have a go.
Dr. Kate Sanihan, can you chime in with your, where you start with this question?
Yeah, absolutely.
So my conclusion is that a diet of seed oils builds body fat that makes people feel sick
and tired when they try to burn their body fat.
And because of that, we have people overeating,
as we know people are overeating
by somewhere around six to 800 calories on average,
although a lot of studies under-report that,
so not everybody is aware of that.
But so that drives overeating.
And then the other thing that it does
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
You know fueling on our body fat between meals and when you have too much PUFA in your body fat the polyunsaturated
fatty acid from these seed oils
It builds up in your body fat to a concentration that is
exceeds like all of, all of human history
by six times.
It used to be around 5%, now it's 30%.
And that dramatically changes the ability
of your mitochondria to generate energy.
It pretty much shuts them down
and threatens to kill your cells, right?
Because without energy, cells will die within six seconds.
They only have about six seconds supply of ATP energy.
And so what they do instead is they reach for another fuel.
And what do they reach for?
Sugar, because there's always some sugar in the bloodstream.
And what does that do if you haven't just eaten?
Well, it'll cause hypoglycemia, right?
It'll make you feel hypoglycemic.
And we have an epidemic of people experiencing hypoglycemia symptoms,? It'll make you feel hypoglycemic. And we have an epidemic of people experiencing
hypoglycemia symptoms. I can tell you this because pretty much every single one of my
patients who's overweight says, Oh yeah, my doctor, previous doctor, not me said I have
hypoglycemia and I have to eat right when I start to feel dizzy, when I start to feel
brain fog, when I faint, uh, it'll bring on seizures in some people.
This is a very serious endemic pandemic of hypoglycemia, and it's happening because our
body fat makes us feel sick and tired when we try to burn it, and it makes your mitochondria,
it kills your mitochondria. So I think that I've looked,
as far as like where do I fit in the context
of Jal's other theories here,
I feel like what every one of you says
is compatible with what I'm saying.
Like I feel like absolutely the signaling happens, right?
And reactive oxygen species play a huge role in all this.
And I mean, the other guys are gonna speak,
you haven't spoken yet to what your theories are,
but I'm obliquely familiar with all of them.
And I feel like it fits into that big picture.
So I feel like what I'm bringing to it is like,
synthesis for one thing, synthesis of the theories.
But for another thing, kind of, you know, it's all proof that we're all, we're all
right.
You're everyone that understands that seed oils are unhealthy.
You, for whatever reason, no matter how many different reasons you have, it's all,
it's correct.
For the most part, everyone that I've've heard I haven't heard anybody come up with any
Reason that seed oils are bad that is
completely untrue
Right. There's some there's some element to
Of truth, I think just about everything but I think the major mechanism is is is what I've said
It is that that big picture and just to give you a little bit of background,
I've actually, I was like reviewing like,
when I really got into this,
I don't know if you guys know,
but I went to Cornell for cellular
and molecular biochemistry in the 80s, in the late 80s.
And so back then I was, you know,
even though I wasn't a doctor
and I didn't know about PUFA,
I understood polyunsaturated fatty acids
and we're prone to oxidation and the spin states
of oxygen that will either allow
or prevent it from interacting.
And so I've kind of like was primed
for when I finally got into this,
when I was a doctor and I got sick
and nothing would make me feel better
to question the idea of saturated fat as being unhealthy.
And as soon as I saw that was literally
there was one research article that I saw
by Eva Sodergren and it was called,
it was her PhD thesis
and it was called Lipid Peroxidation in Vivo.
And when I saw that and the molecules of linoleic acid
and the reactions that happened in the body,
I knew immediately because I have all this background
that all of this would affect all of our cellular membranes,
our mitochondria, our fat cells, our brain cells, and all the
microstructures inside of our cells.
Because you can't have normal physiology when you've got reactive oxygen species flying
around and you get polymerization of the polyunsaturated fatty acids in the membranes, which destroys
an area of the membrane.
And this has to do with something called the permeability transition pore, where researchers
have found that burning PUFA causes this thing that they haven't really identified which
protein it is.
Some people say it's on the inner mitochondrial membrane, some people say it's on the outer
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
polyunsaturated fatty acids, you blow holes in the side of your mitochondria. I mean,
it's like, it's a major, major problem. It's like an explosion. And the different researchers
are doing their best to kind of identify, okay, this little bit and piece
of like broken, destroyed, damaged, trying, struggling to survive mitochondria has exactly
this thing on it.
But the big picture is what I said.
It's this is an inappropriate fuel.
It's as if we have traveled to, well, you know, in Star Trek, they call this thing the
M class planets, right, that
are compatible with life, right, right. And there was a recent movie, don't look up or
look up or one of those two, about the planet Earth blew up. And in 23,000 years, the rich
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?
We were on an M-class diet, compatible with life.
We have shifted to a diet that is not compatible.
That is how profound this switch to polyunsaturates
from mostly saturates is,
because we are constantly subjecting our bodies
to an unprecedented, uncontrollable amount
of oxidative stress and it just destroys life.
Very good.
Well said.
So Tucker Goodrich, I wanted to let you explain
how you see this problem of seed oils and
obesity.
Well, first off, I want to say it's an honor to be on this panel with everybody here.
I've gotten inspiration from all of them.
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
amazing to me how much I've learned in the interim and how much more I'm able to understand
what he wrote the first time around that I wasn't able to get.
Same goes for everybody else here. So I thank you all for the background I've gotten from all of you.
So my experience was somewhat, started out somewhat personal.
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
On a lark. I decided one day at the salad bar in my office to stop eating them
um
looking at the squeeze bottles of
Salad dressing at the end of the salad bar
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.
And to my surprise, my health increased dramatically and immediately.
An irritable bowel disease I had been suffering from for 16 years went away in two days.
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
Culminating in
Putting on my pants one morning to go to work buckling up my belt letting go and having them fall to the floor
Which was a fairly happy thing to have happen. Although the tailoring bills that followed that were
pretty severe
that followed that were pretty severe. So I got curious, why did this happen?
Why was, you know, it totally went against
what we're told to do.
We're told that these oils are part of a healthy diet
and that we should be consuming them
and that if we do so, we will lose weight and be healthy
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.
And I only recovered my health when I reversed that advice.
So I started, you know, at the time I was on Wall Street as a technology expert and
I was quite adept at researching and solving problems.
So I just turned that skill set to the scientific literature. And what I found over the
years, as you know, Peter and Kate have already mentioned, you know, it would be nice if there was
one thing going on here. It would make it a much easier story to explain to people.
make it a much easier story to explain to people. Unfortunately, that's not the case.
As Kate said, these are not something
that we've evolved to eat in the levels
that we are currently consuming them.
I came across one study that looked
at protein damage in the cell from the peroxidation of omega-6 fats.
And one chemical specifically they were looking at,
HNE, caused 24% of the proteins in the cell
to become damaged and dysfunctional.
That's an amazing impact on your body.
And it's not just mitochondria,
and it affects pretty much every cell process
around energy generation.
So, and that's after you eat them, right?
We also know from a number of studies
that even before these fats get into your body,
they have direct effects on your appetite.
They cause you to crave carbohydrates and sugar.
And if you look at what we are overeating, it's primarily carbohydrates and sugar.
That doesn't mean that they're causing obesity.
What it means is that we are eating a chemical that induces a state known as hyperphagia,
meaning overeating, and that what it stimulates us to eat is carbohydrates and sugar.
Sugar does have an independent effect,
particularly if you drink sugar,
but it's a much smaller effect than that of seed oils.
So once they get into your body,
they alter your fat storage pathways,
and in apparently everything from yeast
to nematodes, roundworms, to humans, they cause
your body to apparently store fat.
And once that fat goes into your adipocytes, your fat cells, the stored fats in your fat
cells then cause the fat cells to misfunction and become insulin resistant
so it's really you know if
It's quite amazing how many different effects these fats have on
Causing dysregulation of your body system, you know in a normal
Diet in the type of diet that we evolved to eat
We have of course a tendency to put on fat when times are good and to lose it when times are bad
But there are limits to that up and down right? I mean
400 pound people don't survive very long on the savannas of Africa
and
Eating a food that causes that to happen would be very anti-survival there,
and not having a regulatory system
would be very anti-survival there.
But what we are doing is inducing in ourself
a continuous state of dysregulation
causing this obesity epidemic.
So, Brad Marshall, you have a background
in molecular biology, you're also a pig farmer, so you get to see how pigs gain weight, and they're monogastric animals.
So, you take some very interesting perspectives on this question of how seed oils and high poofer products cause obesity.
Yeah, and I'm glad you brought that up.
Those are, like I say, the fact that I've raised pigs. So I've been kind of generally anti seed oils, you
know, ever since I read the oiling of America on the Weston
a price blog and like, I don't know the year 2002 or something.
And, and that so, so I started raising pigs
in around the year 2005.
And that really was one of the things
that I was trying to do because I knew that,
I knew the pigs were monogastric.
I also knew based on literature about raising pigs
from the 1800, late 1800s even, that says that, you know,
you can't feed pigs anything that contains too much
of the vegetable oils or you'll get soft pork.
And even back then it was known that American pork,
which was almost always corn finished,
sold at a discount in European markets because American
pork was known to be soft. And the Europeans finished their pork on barley, which has about
half of the linoleic acid of corn. And so it's been known at least since the 1800s that these
polyunsaturated fats kind of bioaccumulate in anything, or at least any monogastric that you feed them to. And so I was
sort of, you know, I was raising pastured pork, and it was all
GMO free. And I was doing everything I could to, you know,
keep keep my pork fat to not be soft. And so I have a lot of experiences
working with other farms.
And also with my own pigs on my own farm,
I realized that certain pigs genetically,
it didn't matter what you fed them,
they always had soft fat.
And so, I saw very firsthand
that the saturation of your own body fat,
there was a huge difference based on
what you fed the animal,
but also the genetics of the animal.
And so there was something happening internally
that could affect the body fat saturation.
And then obviously the externally,
what you fed them made a difference.
And so if you read fire in a bottle, a lot of, I talk a lot about an enzyme called SCD
one.
And what that does is it turns your stored body fat from a saturated fat into monounsaturated
fat.
And then also, um, of course the amount of dietary polyunsaturated fat. And so, because I think that, you know, sure,
the fat in your last meal, of course, plays a huge role in what your mitochondria are
actually oxidizing, but it's, it's sort of blended with your stored body fat before it
enters the mitochondria. And so you have these two different sort of pools of fat that at any point
in time you're, you're oxidizing. And so I've spent a
lot of time, you know, thinking about that. And that really is
where the the conversations about the torpor comes in and
the now and you know, and the torpor thing is, it's kind of an
analogy, you know, humans obviously don't- torpor
for those who don't know is a, is a, it's kind of an
alternative metabolic state that hibernating animals use before
they hibernate. But one of the things that they do is they have
to eat a lot of polyunsaturated fat to be able to go into torpor.
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
animals have very, very unsaturated body fat compared to, you know, an animal that is never going to
hibernate, even if they're monogastrics. And so then when you look at obese
humans over the last, you know, 70 years or however long, obviously polyunsaturated
fats have increased, but the amount of SCD1 has also increased. And so when you look at,
especially in the muscle tissue of obese humans,
there is an incredibly direct correlation
between the amount of SCD-1 produced in the muscle tissue
and the BMI of that human.
And so whenever you see a correlation
that's that direct in the real world,
I think that's interesting.
It, of course, doesn't necessarily prove causation.
But I've seen all of these parallels
between changes in body fat saturation and obesity,
in the exact same way that animals
who want to store fat for
hibernation do it is the exact same way that obese humans behave. And so that was
right. And of course all that started with me just trying to be trying to make
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,
Peter talks about, he's at a very low level
and I'm sort of like one level above that.
I'm a molecular biologist.
I like genes and, you know, genetic pathways, et cetera.
And one of the ways that my research keeps
bringing me back to is how we regenerate NAD+. Because if you
look at obese humans, it seems like we have too much. So NAD+,
it's an energy carrier,
an electron carrier.
It basically, as you break down your food,
whether or not it's carbohydrates or fats,
NAD plus takes a, picks up a hydrogen,
becomes NADH and a couple of electrons
and it takes it up and it drops it
into the mitochondria electron transport chain.
And that is how, and that's basically how we, an essential
part of how we turn our food into ATP. And so if there's not
enough NAD plus around, we simply can't run our metabolism
as quickly, it becomes a limiting factor. And if people
have heard of this, the Sirtuins, Sirtuins
require NAD plus and, and they remove acetyl groups from
things. And if you look at obese humans, they have a lot of
acetylated mitochondrial enzymes, such as complex one,
complex five, a whole bunch of them. And so, and so your
mitochondria don't work as efficiently if, if you have, if you have a lot of acetylated
enzymes, which is to say if you don't have enough NAD plus, and
you see this kind of irony in obese people that obviously
they have a lot of energy. You know, the person has plenty of
stored energy, but yet their cells are still low in ATP. Because, you know, they're not
convert, they're not efficiently converting, converting all of
that to, to ATP. And so, yeah, and there's a, there's an
enzyme called NNT. And so this will connect sort of what, yeah,
what Kate and I were saying about functional mitochondria back to what Peter was saying about ROS.
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
ROS from the mitochondria, we actually get NAD plus back. And
so what that looks like to me is, okay, so if you could get
your fat really unsaturated, then you won't make as much ROS
and that will give you less NAD+, and that will give you the ability to store body
fat and get ready for hibernation.
That's kind of the short version of it.
Dr. Robert R. Reilly Very good.
And Dr. Ray Peat, you get to pick who was right.
I'm just joking.
Give us your take on this question, please.
I've considered all of those over the years.
50 years ago, my dissertation in the biology department at the oxidative metabolic changes
that happened during reproductive aging.
And immediately I started running into the close interaction
between aging and polyunsaturated fat metabolism
producing age pigment, for example, and estrogen. Each one
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.
It accelerates the interaction, decomposing PUFA with aging under the influence of estrogen. And at that time,
I had to see the importance of the accumulating PUFA
with aging, but already the literature
was starting to claim that not only is PUFA in the food
good for preventing cancer and heart disease,
they said, but even preventing obesity. I've seen dozens of articles, more and
more over the years, showing in prevention of obesity with the other gross mistakes.
It causes cancer and causes heart disease
and reproductive aging
and all of the pro-inflammatory processes.
And all of that comes from the immense profitability
of selling products. Every time there's a super
profitable product, the science follows the profit absolutely going against the
facts in the case of PUFA and estrogen, but at least a dozen other substances.
And so you have to learn to disregard about 90 to 99% of the published medical
and even biochemical articles
as being nothing but reflections of advertising.
And I started looking at the physical properties that would account for the fact
that mammals in general, studies have been done on calves and human babies, at birth
they're generally so-called deficient in the essential fatty acids. Their tissues are
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
Celsius generally have that process of accumulating during their lifetime more and more of the plant-derived PUFA.
And in the process, their own metabolism is being damaged
and slowing down.
So from extremely high metabolic rate at birth
in the first two or three years,
as the PUFA accumulate in the tissues,
the metabolic rate slows down,
takes another big change towards inhibition of oxygen,
productive use at puberty.
And then when growth ceases in the 20s,
when you're no longer diluting those stored PUFA from
the environment, the rate of accumulation increases so that by middle and old age, the
metabolic rate is much slower, the brain and arteries and other tissues are starting to fill up with the largely
cholesterol esters of the polyunsaturated fats, also the stored
triglycerides, all of these become more polyunsaturated with aging.
And I think the basic reason for that is that
the double bonds, the more the double bonds the fat has,
the more affinity it has for water.
And so it has a greater tendency
to circulate free in the water and in
the process those same multiply unsaturated molecules block thyroid
function and release estrogen from the steroid-binding globulin,
making estrogen more available,
thyroid less available.
But the tendency is not only to not oxidize these
because they don't enter the cells for oxidation,
it takes a more saturated molecule
to get into the mitochondria and cells.
So the free-floating free amino acids
escape oxidative use
and are preferentially stored
as triglycerides and phospholipids and estrogens of cholesterol.
So all of the tissues lose function with aging as they accumulate these fats and that all along the route,
the metabolic rate is slowing down,
the temperature falls, it's somewhat defensive.
The cold temperature plants,
fish living at a cold temperature
are very highly polyunsaturated.
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.
And so the more cold organisms we eat,
the worse the problem is.
That was what led me to experiment with coconut oil.
And it's relatively high saturation,
goes with a higher metabolic rate.
And Pam Plona and other researchers have shown
that the more unsaturated an organism is,
for example, birds are much more saturated than mammals
and for a given weight, they have a much longer lifespan.
Pamphlon and others showed that that's a general principle
that life is shortened by the degree
of polyunsaturated fats in its tissues.
The physical property of being more water soluble
leading to the accumulation in the tissues
means that when you're under stress
and release stored fats,
both from triglycerides and phospholipids and esters,
these stress-induced free fatty acids
are going to be more polyunsaturated.
The older you are, the higher the accumulation, the more harmful
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
of free fatty acids in circulation stops the oxidation of glucose.
And it not only shifts the metabolic ratio,
but it actually lowers the metabolic rate.
Old people, old men, for example, at rest,
are burning actually more fat than the young men in the
same conditions, but the old man is laying down fat at the same time, burning fat faster
than young men, but getting a higher percent of body fat. You see the same thing with the waist to hip ratio,
deposition of unnecessary fat corresponds
to a lower oxidation of glucose
and a higher oxidation of fat or the respiratory quotient.
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
process. the mechanism behind the Randle cycle. When you're under stress, one way of
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
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.
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
atoms, you have to either produce more fat or more lactic acid or both. And generally
it's both of them. Diabetics have a chronically high lactic
acid production as well as high free fatty acids. So it starts with the
physical properties, the water solubility, and ends up with the problem of electron excess.
And making lactic acid and fat is the solution to that excess of electrons.
Well, very good. I really appreciate all of your answers.
And I have another question for everybody, but before I do,
I want to give everybody an opportunity to just raise your hand or speak up if you want
to ask a question to somebody else on the panel or ask for clarification
or a comment or anything, just if there's anything that's been said
so far that people want to respond to.
Well, the only thing I would like to add is on the
multifactoriality of this, based on piggybacking off of what
Tucker brought up, is that like there's so much going on here
that it's actually a detriment to the basically the cause
of helping other folks understand what the issues are.
There's like a saying in law that's like, if you want to get
away with murder, make sure that before you kill the person, you rob them and if possible, you rape them
and do as many other different things because then the attorney can get up there in front
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
that's kind of, you know, the problem.
That which is a fair point to make. But if we're going to
convince people that what we're saying here is correct, and I
think it is correct, at some point, we're going to have to
come up with a credible mechanism to explain what's
going on.
And as I said, it's a shame it's not a simple one, but, you know, we've, you know, a lot
of people in the United States are required to eat these foods essentially by law.
They're in the dietary guidelines.
They are fed to people in schools, in the military, in hospitals,
and we're going to have to have a solid evidentiary case to convince the authorities that they've
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
happening and what it, however complicated it may be, and it explains why, you know,
not just everybody in America or most people in America, but most people around the world
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
it, there's, I mean, you can tell me how I'm wrong, but I think it seems pretty simple to say
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
inflammatory effects of the PUFA in mitochondria and other tissues.
But I think that's a body metabolism as you can make it.
Yeah, which is true, but that's not going to convince a scientist.
He's going to want to know, okay, how does that happen?
Wait a second, though.
I mean, why wouldn't it convince a scientist if it's true?
How do you know it's true without seeing the mechanisms?
There are mechanisms.
I mean, I'm not making any of this up.
There's multiple mechanisms.
There's multiple steps in there.
But I mean, your body fat, if you eat too much PUFA,
it ends up in your body fat, that's step one, then between meals,
when your insulin is low,
and even if you're insulin resistant,
your body fat does release free fatty acids
into the circulation, those will get picked up by the cells
and utilized by the mitochondria,
and in excessive concentration,
that shuts down or reduces energy production
so that the cells then,
I mean this is all step by step,
I'm just taking you through the process
of every single one of these steps is not debated.
And then when, this one might be a little controversial,
when the cells are forced to burn PUFA,
that they, instead of shutting down,
they just put more GLute 4 transporters and
suck, slurp more sugar out of the bloodstream, that part is a missing
step. I haven't actually seen like too much evidence of that. I've seen indirect
evidence of that that I can point to, that the brain actually starts to tell
the liver to produce more sugar
to increase the blood sugar level.
That's how you become diabetic.
That's like another, that's why you raise
your blood sugar level when you're type two diabetic
because the brain says a normal blood sugar level
of 100 isn't enough, I want it to be 110 fasting
or 120 or 30.
But everything that I've said,
except for that one step of, you know,
what is the exact concentration of PUFA in the body fat
that makes the cells increase their glute four transporters
and slurp in more sugar from the bloodstream,
that's the only piece that's maybe missing,
but everything else is actually solid and no one in their
right mind, I think, would refute any of that.
So there is science, it's more than just one, a sound bite.
And that's the problem.
We have to force our scientists to actually listen to something more than, I mean, we
shouldn't have to, but we do have to, you know, get the people who are,
should be in this conversation to listen to the whole argument, not just a short sentence,
like cholesterol clogs your arteries or something simple, oversimplified like that and ridiculous.
Right.
Agreed.
Peter?
Quick word with Tucker or quick comment. I find your approach, your concept that PUFA make
endocannabinoids make you eat is very soundbite-y. Yeah?
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.
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
make them more insulin sensitive, so you do it diet-wise. But if you keep doing it,
six months down the road, they'll be intensely insulin resistant.
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.
That depends on your study. But the initial response is that putting polyunsaturated fats
into a rodent model makes them insulin sensitive. It happens to make them fat as well, but that's
the function of insulin. So making them insulin sensitive, I have no problem with that making them fat.
But the initial response, and in cell culture, you can feed polyunsaturates to cell cultures
without doing them any damage at all. You feed pure saturates to cell culture, and there's a
you're saturate to cell culture, and there's a reactive oxygen species driven catastrophe,
particularly if you're culture in 25 millimoles of glucose,
which is the standard culture medium,
and you add 400 millimoles of pure palmitic acid to that,
your cells will just die.
But you can add 400 millimoles of PUFA to it,
and there's no problem.
Acutely, the cells will be perfectly okay. And any
scientists that we ever try and convince will produce those papers and say, well, look at this.
And as you pointed out, Peter, there was a that's not a that's just just a moment,
as you've pointed out, Peter, that's not a physiological model, right? No,
all medic acid. Yeah. Right. Of course.
Yeah. Yeah. I mean, you can say, you can point to a lot of things that are irrelevant to the
argument and try to divert the argument, but that's, we have to, we can't let them do that.
We have to, we have to say, wait a second, that's irrelevant to our argument and how,
prove me wrong, right? Like you can say that too. You, every one of you can say,
you guys prove me wrong because I, I want to say that too. Every one of you can say, you guys prove me wrong
because I wanna run the conversation here.
You guys have been running the conversation for a long time.
We've been getting fatter and sicker.
So try to take what I'm asserting
and tell me where it's wrong
because I'm totally open to that.
And actually you said, Peter, what you brought up
is that like the insulin sensitivity?
That's totally in keeping with what I said.
It's indirect evidence of what I said, that when you force feed cells PUFA, they want
more sugar.
They're going to be drawing more sugar out of the bloodstream.
Well, you might measure that.
It might look like insulin sensitivity, right?
So that is exactly what I'm saying.
Yes, yes.
No, but my concept is that we get fat
because we're pathologically insulin sensitive. We're too sensitive. That's the problem that I see.
Yeah, and that is PUFA. I agree. It's as if obesity, we're trying to protect ourselves
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
radio show because I actually have seen a lot of, like, in my practice, it seems as
though it's the people who are not, you know, really obese who end up with cancer.
And, and you could make an argument there, you could explain
that not just cancer but also autoimmune disorders.
You could explain that as because perhaps they are burning the PUFA when they shouldn't
be and somebody, you know, and therefore exposing their DNA to oxidative damage and, you know,
getting cancer of course if you believe it's a genetic disease.
But regardless of the mechanism, you're creating the oxidative stress by burning the PUFA instead
of eating more, which would allow you to get more glucose, which is a safer thing to burn.
Because it doesn't have the double bonds, it doesn't have the polyunsaturated fatty
acids, and it doesn't have the double bonds, it doesn't have the polyunsaturated fatty acids
and it's safe to burn.
It's not the ideal fuel, but it's certainly better than,
so that obesity, basically overeating is a person
who's developing a habit of overeating
and to protect their cells
from having to burn the damaging PUFA.
And so it's like a metabolic choice there that their
body is making for them. And yeah, and I think that has, that's, PUFAs are so
bad that people will eat themselves almost to death and attempt to not have
to burn that and damage their mitochondria. Okay. Dr. Peat, do youâ€¦how do you sort out these different arguments?
I mean, I'm a layperson, so I'm, you know, I'm listening, and it all kind of seems
to be going in the same direction.
Do you have any thoughts on that?
Yeah. I think if you start trying to understand what the so-called Rangel cycle is all about,
you see that the interference of fat oxidation with the ability to oxidize and get energy
from glucose, that's the essential problem. The faster you oxidize fats, and that's promoted
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
production and full energy use of the oxygen towards fat synthesis and lactic acid synthesis.
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.
I think the Randle cycle is simpler.
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.
Well, you could put it the other way as well.
I mean, they influence each other, right?
You could put...
You could also say the glucose has the ability to influence the fat.
So it's a two-way street.
That means when you exaggerate the supply of glucose, you can actually lower the free
fatty acids and protect against all of the consequences of burning too much fat.
Right.
So, the Randle cycle is a regulatory process that, if I understand this correctly, that
determines what fuel the cell is going to use.
And of course, cells can use two fuels at once, obviously, but that's kind of the, if
you want, the seesaw that allows the cell to determine what fuel it's going to use.
But that use of type of fuel determines everything.
The electronic balance regulates the synthesis of fat.
And so the more fat you burn, the more fat than the young person is still making fat for deposition.
They become fatter because they are burning too much fat.
Dr. Pitt?
That is well established, but it just doesn't seem right to people, so they ignore it.
it just doesn't seem right to people, so they ignore it.
When you say that they're building, as you burn fat, you build fat,
is the presumption that you're building the fat
is coming from glucose,
because you're not burning the glucose,
so it's being converted to fat?
Was that your point?
When you burn fat,
you increase the ratio of NADH to
NAD. And that generates the fat from whatever it can get? Yeah, so the more fatty acids you burn,
the more fatty acids you synthesize. Yeah, and so, Dr. Peat, if I understand you,
and correct me if I'm wrong,
the argument about what is controlling the Randle cycle
is really kind of an argument about redox balance.
Would you say that's correct?
Yeah, yeah, absolutely.
Yeah.
So can I add slightly to that? And that is, I think we can all agree that the
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
to the cell and if the ROS make that input to the cell normal, the Randle cycle should simply sort
out what gets oxidized and what gets stored in an appropriate manner.
So total input to the cell was where my thinking
on ROS was coming from.
Randle cycle afterwards to sort out what's done
with the input to the cell.
Does that make sense?
Yes, Peter, I agree with that.
I think we wanna look at at it from the proper direction.
So the big picture is that when you are burning, when your body has a lot ofâ€”the big picture
is oxidative stress.
And having the physiology subjected to too much oxidative stress is going to have an
influence on things like the Randle cycle and the NAD to ratios
and everything else.
But it's the direction that we're going
is it's not the Randle cycle running everything.
It's the fact that we're eating so much more PUFA
and it's subjecting ourselves to extreme amounts
of oxidative stress, depleting our antioxidant systems.
That is going to
have an effect on the Randle cycle and on every other physiologic process.
Insulin sensitivity, the translocation of glucose into a cell or not, whether or not
liver, the liver is able to do any of the normal detoxification, it's gonna
have an impact on every process. And so what I want, what I'm, my point I'm trying
to make is that we can't take one little process that the body normally does
under normal circumstances and blame, you know, that for everything. The big
picture, we can't forget, I mean, it's kind of a little bit like missing the
forest for the trees, it seems to me, because the big picture is the forest of PUFA that
we're all living in, and it's just adulterating our physiology on every level, certainly what
you're talking about, but many other things.
That's the direction that I see things going and
the explanation that makes more sense to me. For almost a hundred
years, the oxidative stress and oxidative damage has been emphasized,
rate of living theory and so on,'s almost almost been a hundred percent neglect
of the reductive stress
process
that's what i'm talking about
reductive stress
precedes the reactive oxygen species production
the problem is reductive stress
that's promoted by not enough glucose oxidation,
too much PUFA.
Not enough glucose oxidation?
That's not making any sense to me,
because as humans, we're tooled to burn fat
way more than glucose.
So I just, I can't accept that.
Ironically, I'm literally, the current blog post I'm working on
is literally called, Reductive Stress Causes Oxidative Stress.
And so it's interesting.
Can you take a moment then and just define it so that the
people watching this can understand?
Yeah.
And so, oxidative stress, so NAD plus and NADH are a really good example of this and so
Any you know, they're almost the same molecule except one of them NADH obviously has an extra hydrogen and so
NADH is the reduced version of that molecule and NAD plus is the oxidized version. And so in a system where you have, well,
where a lot of things are oxidized, too many things are oxidized,
that's called oxidative stress. And so, um,
in, in the NAD system, if you had oxidative stress,
you'd have too much NAD plus and not enough NADH,
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.
You have too much NADH and not enough NAD+.
And that lack of NAD plus is called reductive stress,
and it is a real problem.
And one of the ways that you can get oxidative stress is,
well, kind of like I mentioned before,
if there's not enough NAD+, then your
mitochondrial enzymes become acetylated and they stop working. And I think that
that ends up driving this huge amount of reactive oxygen species coming out of
your mitochondria because like complex 5 is acetylated and it stops working efficiently.
And so you have no way to get the, you know,
the electrons entering the electron transport chain
to come all the way back down to make ATP
because Complex 5 isn't working.
And that's when you get this kind of massive
oxidative stress because all of these electrons
are trying to run through the electron transport chain
and they can't do it.
And so they're coming back out as reactive oxygen species.
Whereas if you're not in reductive stress,
if you have enough NAD+,
then complex five doesn't become acetylated
and the electrons can run through
and you don't end up with that kind of massive amount
of reactive oxygen species production. But that sounds like similar to what Dr. Peat is saying
about the Randle cycle is you need, you know, if you wind up with too much NADH, then,
you know, your metabolism just doesn't run right. Yeah, and experiments show that if you uncouple
the production of ATP by the electron transport chain,
if you waste oxygen, run glucose through the system
at a very high rate, excess site rate, for example,
will uncouple and become wasteful use of oxygen
and fuel.
That uncoupling is consuming oxygen at a high rate, but it's stopping random reactive oxygen
species production.
It gets rid of the dangerous electrons.
It gets rid of the harm of reductive stress.
Pasture oxidation reduces ROS.
Right, and the other thing I mentioned before
is the other way to get rid of the reductive stress
is if you're burning saturated
fat we have this system that removes ROS and it gives you back NAD plus and
that's the enzyme well really takes two enzymes it takes glutathione reductase
and then it takes this thing called NNT and so that actually uses ROS when
you're burnt when you're burning saturated fat
to give you back the NAD+.
But once you switch to burning PUFA,
you're not making the ROS in the same way
and the PUFA keeps you in that reductive stress.
I'm not buying the reductive stress, sorry.
The oxidative stress, I think what's happening is that when you've got so much oxidative
stress, you can have some backup in some aspects of the whole cell machinery, but I can't see
how it's driving.
Where is this reductive stress coming from? You know, PUFA causes
oxidative stress. So how do we go from oxidative stress to reductive stress? The only way you
can do it is by invoking like one or two single metabolic pathways as like these dominant
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
kind of explanation.
I'm sure it's something that can happen,
but I just don't think it's the dominant process.
And it matters because if we're trying to,
like say this is what's going on,
we can't like finger a metabolic process
that someone else, the opposition,
could say, well, easily say,
there's no way that process doesn't do that.
For example, there's an alternative explanation
for why the SCD enzyme is affected by PUFA
and that has to do with trying to maintain a certain amount,
trying to maintain the proper melting point of the fat.
And so if you have a high PUFA diet,
then you end up, people end up with more saturated fat
in their body tissues than normal.
And that's actually been one of the pieces of evidence
that the American Heart Association uses
to prove that saturated fat correlates with obesity
because they find people who are less healthy,
more metabolically deranged,
who have been eating the higher proportions of PUFA,
they have more saturated fat in their adipose tissue.
And they're saying it's, well, therefore,
it's because they eat more saturated fat, right? They're saying that that's what made them fat. And that is a
completely inside out convoluted way of looking at it. And we can't do that if we're going to be
right. But the, I mean, the, the evidence is quite clear that one of the major changes in the 20th
century, along with the increased consumption of seed oils, has been an increase in the adipose content of
polyunsaturated fats.
Eating polyunsaturated does not increase the amount of saturated fat that the body stores.
If it did, then Bradâ€”
Oh, it does.
Wait, wait.
Relatively, though.
If it didâ€”not relatively, so at all.
If it did have that effect, then Brad wouldn't have the problem with his pigs of having soft fat
Right. Well, no, I'm just a moment. It's all fat is due to the
storage of all in saturated fats
So look you take a look at the the composition of human adipose tissue through the past hundred years
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
have more saturated fat now than we did in the past compared to monounsaturated fat.
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
PUFA in our fat, but as a way to protect against that, the body has no choice how much PUFA
is going to end up in the adipose tissue, right?
That's just a reflection of the diet.
We can't change a polyunsaturated fat into a monounsaturated fat.
We have no, we have no capacity to do that.
But we can change sugar.
We do actually.
That does in fact happen.
All of the evidence I've seen is that there's definitely.
But not to a big degree if it does.
Because that's why we have this huge increase
in body fat, polyunsaturated fat as well.
So I need to touch it.
Well we've assessed because we've overwhelmed our regulatory mechanism.
Yeah, I would say there's a lot of evidence out there
that in obesity and diabetes,
the ratio of monounsaturated fat
to saturated fat increases.
There's, if you look up.
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
in obesity, I guess in diabetes too, the ratio of oleic acid to stearic acid goes up with
obesity. Well, stearic acid is just one of the many saturated fatty acids, right?
So we want to look at the total saturated fatty acid.
And we have other fatty acids besides stearic that we can make.
So that's what I'm talking about.
Right.
And yeah, it looks to me like average Americans now have
something like 10% less, well, like in the 1960s,
the studies that we have, there was one in Indiana
where saturated fat in lean adults
was something like 36% total saturates.
And if you look at obese people now,
it's something like, you know, 25 to 28% total saturates.
So it looks to me like saturated fat has decreased
specifically in obese people, but-
I'm not talking about that.
I'm talking about the ratio of saturated
to monounsaturated, which is the only thing
that our physiology can really make a big impact on.
We can easily turn a saturated fatty acid into a monounsaturated fatty acid. And we have stopped
doing that because we need to stop doing that because we have so much PUFA. So the ratio of
saturated to monounsaturated has changed in attempt to try and keep the melting point
of our body fat relatively constant.
So that's, it's a protective mechanism, right?
So we're trying to leave more, relatively more, we're trying to leave relatively more
of the saturates in our body fat because they will keep it more solid.
And if we were to desaturate that and have as much monounsaturated fat as we, you know,
we really ideally would want to, because that's the preferred fuel for mitochondria of the
three types, then we would have too much melty fat.
It would be, you know, there'd be too much unsaturated fatty acids in our fat.
So we're trying to keep it as saturated as possible
to protect against all the PUFA.
So you have to look at the ratio of the only things
that we can control, which is the total monounsaturated
and the total saturated.
Right, and that definitely happens.
So polyunsaturated fat at certain levels
absolutely does suppress the SCD1 enzyme,
the thing that makes saturated fat to monounsaturated fat.
The problem is at some further level of additional
and longer polyunsaturated fat, they go up in parallel.
The SCD1 starts increasing in parallel with increased polyunsaturated fat, and that's
when you start to see real obesity and real diabetes.
That's what I've seen.
Well, it might vary in different tissues.
If you're looking at the adipose versus the liver versus the muscle, so you can't make
a blanket statement about that.
Were you talking specifically about adipose?
Or was it?
I was talking specifically about adipose, yes.
Okay, yeah, so I mean, we don't wanna get too lost, though.
I mean, the big picture is that
I think we should try to come to
agreement as to whether or not oxidative stress is a bigger
issue than reductive stress. And I come down on the side of
oxidative stress is clearly the problem. And I don't know where
the reductive stress would be coming from these days,
honestly. So but I think if we can't agree on that, then we need to try to, because we have to
pick one.
We can't have both.
Well, you can't actually have both in the same cell at the same time.
And that's one of those sort of unfortunate truths, right?
Because what can happen is your pool...
But what's driving it is what I'm saying.
Your pool of...
What's driving it.
Right, right. And so I would argue that the,
specifically within the NAD plus NADH,
it's ultimately the reductive stress that's driving it.
But those are, but these are hard.
Because PUFAs cause oxidative stress
and we haven't changed our diet
in a way that would cause more reductive stress.
Well, the PUFAs cause in in the PUFAs cause reductive stress
in the NAD pool, but they cause oxidative stress
in like the glutathione pool, because, you know,
whenever you talk about, again,
it's like the cell tissue type.
Whenever you talk about reductive stress
and oxidative stress, it depends both
on the cellular sub-compartment.
Like, are we talking about in the mitochondria?
Are we talking about cytoplasm,
and then it depends on if we're talking about,
you know, NAD versus glutathione.
So you can have both in the same cell.
And that's, you know, unfortunately it's hard, right?
And it's confusing and it's 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, 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,
we're making it more complicated than it needs to be.
And so I think that, yes, there can be elements
and like there can be basically little kinks in the system
that is basically overall an oxidative stress problem
that can cause here and there reductive stress
because it's a seesaw, right?
So like you said, there's there, but the big picture
is PUFA is causing oxidative stress.
If we can't agree on that, then we can't agree
on why PUFA is bad, why seed oils are bad.
Well, here's what I would say.
I would say that if the biggest problem,
if the problem, you know, the overarching problem
is oxidative stress, then the suggestion would be
that if we were to take
lots of antioxidants, we could make the problem better. But most experiments that I've seen don't
suggest that's true. No, that's not what the suggestion would be. That is a fallacy. So
you have to understand that antioxidants, the term is so misused.
It's not like resveratrol has this
incredible antioxidant capacity.
I agree, I just mean like vitamin E.
I'm sure you know this, but we have
antioxidant enzymes, right?
I think you've probably written extensively
about one of them.
We have many antioxidant enzymes that,
because, antioxidation is you're taking something
that's from a very high energy state and you're bringing it down stepwise to a
safe energy level and it takes more than one enzyme to do that it takes more than
one step you can't just have vitamin C stepping in and solving all the problems
because it won't do that.
It won't bring it all the way down
to the proper energy level.
And then vitamin C needs to be regenerated.
And this is a fact that a lot of people don't realize,
but every antioxidant compound like vitamin C
can be pro-oxidant in a certain setting.
So you can't make a blanket statement about like, oh, well, we can just take antioxidants,
like everyone does, like everyone selling supplements.
I'm not saying you do, but everyone selling supplements says like, oh, you just need to
take this massive best antioxidant supplement, and then you won't have any issues with oxidation.
And as you pointed out, those studies never bear out and it's because it's
based on a fallacy.
In a healthy cell, the great bulk of the vitamin C inside the cell is in the form of dehydroascorbate.
It's the oxidized form which is active and protective. In reductive
stress, you lose that function of vitamin C. You lose the oxidative
function of vitamin C when the cell goes wrong and goes reductive stress. I'm sure there's a lot of consequences.
Can we just say that if you do anything which disables the electron transport chain,
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
chain with reactive oxygen species or by acetylating it or by adding ROS-derived polyunsaturated fatty acids to
the proteins of the electron transport chain, there is a component which is ROS-derived,
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
that they both occur together. I don't think it's either or and I think that reductive stress I
would view as a marker of dysfunction of the electron transport chain. Just trying to see whether you can get these two things
to be compatible.
Okay.
Dr. Peat, do you agree with that?
Yeah, and it's reductive stress that turns on fat synthesis
as well as lactic acid synthesis.
Right, okay.
So they're, I mean, one could almost say
they're two sides of a coin.
They're going on at the same time.
Right, I guess what we're saying is that.
And the process, the process is, um, what's going wrong is that you've got a dysfunction
in the regulatory system that's balancing those two processes.
Is that fair to say?
Yep.
And Dr. Peat, you're, in your opinion, part of that, what's going on there, is that you're not
burning enough glucose.
Is that correct?
Right.
I wrote a couple of newsletters on late 19th century experimenters with treating diabetes with huge amounts of sugar.
What it's doing essentially is shifting the Randle cycle, lowering free fatty acids,
stopping the interference with glucose oxidation, lowering fat production and lactic acid production, and getting respiration going.
Interesting. Now, one of the things that, you know, if we're going to get this message out,
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
have is that PUFA consumption is not a linear process. That you take a small amount and it has
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,
then it's actually seems to be beneficial
from a solely obesogenic standpoint.
Dr. Peat, do you have any thoughts on what's going on
with that process?
Because I've already seen there's a study that came out
by John Speakman in 2018 where he looked at fat causing
obesity compared to protein and glucose and you know he saw this clear pattern
that you know low levels of fat didn't produce much obesity moderate levels of
fat were the most obesogenic and then high levels of fat were the most obesogenic, and then high levels of fat, again,
obesity started going down.
Do you have any thoughts on what's driving that curve?
Yeah, when you have very large amounts
of either fat or glucose, you're sparing protein.
You're not oxidizing protein for energy.
Suppressing protein metabolism and
an excess of protein is a big problem that blocks thyroid function and oxidative metabolism,
for example, and contributes to aging.
contributes to aging.
Tucker, and you were talking about ketogenic high puffer diets.
Right.
The famous Bioserve's F3666,
it's 5% protein.
And we don't know whether that controls body weight in the rodent model through
ketogenesis and hypoinsulinemia or whether it's purely driven by the extremely low levels of
protein in the diet. So, from what Dr. Peat was saying, protein levels matter, and the standard ketogenic diet model
for rodent studies is massively hypoproteinemic.
It's borderline protein deficient.
Right, right, right.
Because otherwise you can't get them to generate ketones.
Ketones, that's the problem.
Even worse
if you supplement with normal levels of, what's the, what do you package triglycerides up in to
make VLDLs? Glycerol. Yeah, no, no, to make the actual capsule-y bit. Oh, the chylomicrons?
bit. Oh, the chylomicrons? No, I'm just, what on earth is the biochemical component?
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,
rather, so you end up with the,
so you end up with an accumulation of triglycerides
in the liver cells, which again,
is used to bump up the metabolism to ketones.
So, but if you supplement with, hang on a second,
it's on my desk.
Is it bile acid?
Barnitine?
No.
No, no, no.
Choline, choline.
Choline, right, of course.
And that's why choline deficiency causes fatty acid.
Choline deficiency.
Fatty liver.
Which means you can't export fats from liver cells.
Right, right, right, right, right.
Hence it's key to you.
So it's a bit of a nightmare for trying to,
come back to what Dr. Peat said,
was that you could be looking at the effect
of not metabolizing protein.
This is, so,
our model's not very good.
Right, that would make sense, and it would explain why that diet often but not always
causes fatty liver disease.
If you supplement with what do you call it?
Choline.
Then it doesn't, you can basically take Bioserve and add choline to it and no fatty liver.
So it's another non-physiological model for humans, effectively.
Yes. This discussion has been fascinating and there's so much things to think about,
but I do want to give our audience kind of a wrap up question for each of you to tackle briefly.
It's just kind of, I always like to make this, there's a lot of weeds we get into it and I
wanted that to happen. I want people to get into the nitty-gritty.
And then for those who, you know, they still want to know, okay, so what do you do about
that?
We've all explored different explanations as to why these seed oils and high PUFA products
are linked to the rise of obesity.
We've explained different theories about what's happening there.
You're not going to settle everything today, of course,
but I do want us to think in a thought experiment
at some point, if you were presenting a paper to Harvard,
how would we organize all this information
and come up with the best argument
against the Harvard establishment
for why they've gotten it wrong on these PUFA topics?
But that's for another time. Oh, that'sâ€¦
Yeah, go ahead. What's that?
I'll take that one. I would cite Mozaffarian et al. 2011, which was produced by the Harvard
School of Public Health, in which they show that the most fascinating, the most fattening food
by several fold is potatoes fried in seed oils. And then
they turned around and tried to hide the fact, but their own data shows that seed
oils are obesogenic and if you compare in humans a potato fried in butter or a
potato boiled to a potato fried in seed oils, they're not obesogenic, which kind of comes back to,
you know, Dr. Peat's fondness for glucose.
Glucose alone isn't a problem, it's only a problem
when it's accompanied with massive amounts of seed oils.
So yeah, that would be a very short presentation, I think.
I'd say, here's your paper, guys.
Ha ha ha.
There is at least one intervention study which can be interpreted in the same way as that.
A single meal feeding study which looked at how much you ate before you stopped, which
compared â€¦ their only saturated fat one was potato as opposed to the potatoes in Pufa
were what we call chips. what do you call them,
French fries over there?
Yeah.
French fries, yeah.
Yeah, of course chips, yeah.
But basically, it could be viewed in those terms.
And I mean, there was another interesting paper
that came out recently, I can't remember
the author, but they showed that even one of Peter's favorite obesogenic
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
toxin that dysregulates the Randle cycle and causes fat production, if you
blocked that process, then you blocked obesity. And that's a diet with a very,
that's very obesogenic, but has a very small amount of linoleic acid in it. And
at first it wouldn't, you wouldn't think amount of linoleic acid in it, and at first,
you wouldn't think that the linoleic acid
could be the driving factor of the obesity in that.
And interestingly enough, the intervention
that they used in those animals
was a very common human polymorphism
in the detoxification system for seed oils,
the ALDH2 star 2 mutation.
So yeah, that would be my little chat to Harvard.
Well, I just want to wrap it up with everybody, give a brief explanation as to what the best
dietary intervention that you have found in your own research or life to deal with the
obesogenic effects of seed oils and high
proof of consumption.
Just try to give us a brief little explanation without going, you know, we got to kind of
wrap it up here, but I want to give everybody kind of a homework to explore, you know.
We've given the problem, let's give a little bit of a solution for people who are wanting
to deal with obesity in their own life, and you've explained seed oils
causing it, so what do you do about it, in your opinion?
Peter?
I've got two points I would leave it with.
One is that, oh God, it's gonna go more than two points.
Okay, the first is low carb eating sidesteps
the problems of seed oils.
Okay, that's the first.
The second is that carbohydrate does not cause obesity
in the absence of seed oils.
The carbohydrate insulin model is incomplete.
And long term.
Does that mean if you're obese having eaten seed oils
and you stop eating seed oils and you eat lots of carbs,
it will not add to obesity or no, you're not saying that?
Once you've cleared your fat cells of it, yes.
You'd have to clear your fat cells
of the linoleic acid first.
That would be years, right, before you have to clear your fat cells of the linoleic acid first. But-
That would be years, right, before you could eat high-
That's why you should start with low carb.
And then sidestep the problem to begin with while you sort out the problem that you've
got.
Okay, I think that those two points, I'll leave it at those two.
Dr. Kate? Dr. Kate Connolly So, as you see, I have this summarized on
my Twitter profile.
Seed oils are death and deep nutrition is life.
Deep nutrition is what every traditional diet around the country does to some extent still,
but used to do. And we didn't have access to refined, it gets out the refined carbohydrates
which are empty calories. And then the rest of the edible world is really pretty much
open but you want to make sure you get enough protein. And the best way to do that, the
most like evolutionarily, well, based on on traditional diets every traditional diet was pretty rich in animal sources of protein
compared to plant sources of protein and
Always always in whole foods because we don't talk about it very much but protein
Processed protein powders are also extremely unhealthy
and Processed protein powders are also extremely unhealthy and
Because the processed and body is there partly a lot of the nutrition in there is destroyed
It's not the way our body is supposed to absorb protein and so on
Okay
Very good Tucker
Yeah, my Twitter hashtag for years has been
Yeah, my Twitter hashtag for years has been LCL6, low carb low sex, for exactly the reasons that Peter described.
I mean, you can clearly fix the problem just by lowering seed oils, but what seed oils
induces is an inability to properly process carbohydrates.
So clearly the most effective way to do it
is to reduce both.
Brad Marshall?
Yeah, I agree with most of what's been said.
I will say the other thing,
my initial kind of hack for this,
and I still agree with this,
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
sources of omega-6, including things like commercial chicken and pork, which can be
surprisingly high sources, and actually seek out foods that have a lot of stearic acid in them.
And the reason for that is that, well, there was a paper showing that supplementing stearic acid will,
in fact, increase your rate of fat oxidation. And I think that's, I have a guess as to why
this is. When you look at humans or animals that are doing lipogenesis, new fat making,
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
Mono unsaturated fat and what they have very very little of is is stearic acid
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
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
when those lipogenic genes are switched into the on position.
Dr. Ray Peat.
I think emphasis on body temperature should be greater.
The proof of lower your body temperature and turn on all of
the inflammatory things that tend to keep your temperature down and the
paying attention to the digestive and circulatory events when you eat polyunsaturated fats or too much protein.
The PUFA is already right in the bloodstream, turning down your metabolic rate by blocking
thyroid transport and function, and by activating the stress-related estrogen functions.
So even before you get to the cell, it's happening.
Very good.
So what would you recommend dietary interventions
for people with obesity caused by PUFA?
Raise your body temperature?
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.
Very good. I want to let all of you guys have an opportunity to tell us where we can find
your work, because I know a lot of people are going to want to do deep dives into your
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
and PETA, it'll come up as the first hit. And Dr. Kate, where can people find your work
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.
And there's plenty of information there
about what a traditional diet is, deep nutrition.
Very good, Tucker?
My blog is yelling-stop.blockspot.com
and I'm very active on Twitter at Tucker Goodrich.
And Brad? where would?
Yeah, so my work is all on fire in a bottle.
It's fireinabottle.net, but if you just duck, duck, go
or Google fire in a bottle, it'll come up.
And I am on Twitter at fire underscore bottle,
90% sure that's my correct Twitter handle.
Dr. Peat, do you have a website or newsletter?
Our newsletter is at raypeat's Newsletter, gmail.com, and the website is raypeat.com.
Very good.
It's been a real honor to listen to all of you today.
Wow, what a great time of discussion and learning, and I know our audience is going
to be really thrilled to just see these types of mechanisms explored. This is something
that you don't see happening in academia. I can assure you that. There's nobody doing
this right now in universities having a kind of symposium about seed oil mechanisms. So,
this is the future of academia in the 21st century. It's online now. So thank you all
very much for joining me and it's been a real treat. So thanks again. Thank you, David. Yeah,
thank you very much, everybody. Thanks, David. Take care. Everybody. Bye for now.
Bye!