The Jordan Harbinger Show - 1234: Layne Norton | Debunking Diet Soda Panic and Seed Oil Hysteria
Episode Date: November 4, 2025Protein sources, seed oil panic, aspartame fears — nutritional scientist Dr. Layne Norton dismantles the internet's favorite fitness myths here!Full show notes and resources can be found he...re: jordanharbinger.com/1234What We Discuss with Dr. Layne Norton:Total protein intake matters more than source. Once you consume 30-40 grams of protein in a sitting, the specific source becomes largely irrelevant since the muscle-building signal gets saturated.Aspartame fears are scientifically unfounded. Despite popular panic, artificial sweeteners don't cause insulin spikes, increase hunger, or cause diabetes. Cancer risks only appear at 10,000x normal consumption in lab rats.Context over absolutes defines expert communication. Real experts rarely use words like "always," "never," "best," or "worst." They provide nuance, acknowledge uncertainty, and present opposing viewpoints before explaining their position.Emotional manipulation drives supplement marketing. The more exclamation points and extreme claims in marketing, the less likely it's legitimate. Extraordinary claims require extraordinary evidence, not just assertion.Listen to how fitness experts (or any experts, for that matter) speak, not just what they say. Train yourself to recognize measured, contextual language that acknowledges complexity. When you spot fear-mongering or absolute statements, investigate deeper and demand evidence before accepting claims.And much more...And if you're still game to support us, please leave a review here — even one sentence helps! Sign up for Six-Minute Networking — our free networking and relationship development mini course — at jordanharbinger.com/course!Subscribe to our once-a-week Wee Bit Wiser newsletter today and start filling your Wednesdays with wisdom!Do you even Reddit, bro? Join us at r/JordanHarbinger!This Episode is Brought to You by Our Fine Sponsors: Quiltmind: 10% off 1st year: joingelt.com/jhsArticle: $50 off first purchase of $100 or more: article.com/jordanBetterHelp: 10% off first month: betterhelp.com/jordanAirbnb: airbnb.com/hostAG1: Welcome kit: drinkag1.com/jordanSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
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This episode is sponsored in part by Conspiruality Podcast.
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Aspartame does not cause an insulin or glucose response.
It does not increase hunger.
If anything, it reduces energy intake.
No, it does not cause type 2 diabetes.
It does not cause you to be hungry.
People will say, well, they cause cancer.
Yeah, if you give it to a lab rat at 10,000 times the dose you should normally consume,
then, yes, you see some weird things.
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Y'all caught me mid-crunch on some Quest protein chips.
Don't judge me.
It's field research.
Today on the show, not all protein is created equal, or is it?
We're diving deep into the great protein debate with Dr. Lane Norton, PhD in Nutritional Sciences,
world champion powerlifter, and a guy who's probably corrected more bad diet advice on the
internet than your entire group chat combined.
We're tackling questions today, such as, does it matter if your protein comes from
chicken, collagen, or a scoop of way from a plastic tub, how much protein is too much before your
kidneys start in intervention, and what does the 2025 evidence actually say about stuff
like diet soda, aspartame, those mysterious non-nutrative sweeteners that everyone on TikTok
ironically swears is melting your brain will also bust some of the biggest fitness miss that
just refused to die, like whether fasting unlocks autophagy, superpowers, seed oils, causing
cancer, and a whole lot more. Lane just took home the 2024 IPF Masters won world title at 43,
so we'll talk a little bit about longevity, recovery, and what surprised him about his own physiology
after decades of training and coaching. Oh, and if you've ever wondered whether food labels are
basically a bunch of lies. You know, if the government's nutrition guidelines are secretly
big food fan fiction, or if you're literally pissing away your money on creatine, this episode is for
you. So crack open a protein shake, toss out your detox teas, and get ready for a no BS evidence-first
conversation with the man who lives and dies by the data, not diet drama, Dr. Lane Norton. Here we go.
Has all protein created equal? If I'm eating Quest protein, they don't sponsor me or anything,
so if you shit all over the product, it's fine. But if I'm eating these like,
protein Doritos, basically, from Quest.
Is that kind of as good as drinking a glass of milk, or am I delusional when I do that?
Yeah.
You're worrying about the margins.
Yeah, okay.
If you get enough total protein in the day, that's by far the biggest lever.
Okay.
And if you get enough total protein at a meal, the source becomes much less important.
Basically, sources of protein are much more important when you're at lower protein doses.
But once you get up to like over 30, 40 grams at a sitting, it's just not going to matter.
you've got enough that the signal gets saturated.
I see.
Yeah, I rarely do that, although I did, like, you know,
if you go to like, all you can eat Korean barbecue
and you're eating, I don't know, 400 grams of ribi,
you're probably overloading the circuits a little bit.
But generally, I try to eat a few hours spaced apart,
but I don't want meat and milk every two, three hours.
I'm an investor in David Protein,
and people will be like,
this is not as good as whole food.
I'm like, I never said it was supposed to replace whole food,
but I'm saying, like,
you got to think about what people replace this stuff with.
which we'll talk about with seed oils.
But if you're replacing chicken breast and rice and vegetables with a protein bar,
I can make the argument that's not as quote unquote good,
although I think the overall food matrix of your diet is what determines how healthy you are.
But people, they're eating that protein bar instead of getting McDonald's or takeout or delivery
or doing it out of convenience.
I don't know anybody who's like, I have the time and the ability to cook,
but I am choosing to have a protein bar because it just tastes so great and I love it so much.
Like, nobody's doing that.
That's a really good point. Usually when I eat something like this, it's because I have a show or I'm about to get on a call or I'm in a call and everyone's just going to have to watch me eat this whatever and get it down because otherwise I don't get enough protein during the day. People are always like, how do you eat 180 grams of protein per day? And it's like slowly, like the eating of an elephant, right? No, I don't have a steak for lunch and dinner. I just eat small little bits throughout the day. And if I'm driving or in the passenger seat of a car, I might have to eat protein.
because I don't want more chocolate. I just can't handle it. It's disgusting at this point.
Like two protein bars a day, three, four, it's disgusting at a certain point. So it doesn't really
matter as much if I'm getting my protein from chicken or powdered collagen in a can as long as I
keep a balance of real food and fake food, so to speak?
Well, collagen specifically is not a great source of protein, especially for muscle.
For muscle, it's actually probably the single worst protein you can possibly consume. It's very
low in essential amino acids, it's very low in leucine, which is the amino acid responsible for
initiating muscle protein synthesis. I know people say it improves the hair, skin, and nails, or
like tendons and stuff. I would tell people that the data just doesn't make sense. There's some
human randomized control trials that show better outcomes, but it doesn't increase connective
tissue synthesis. There's a ton of research on this now showing it doesn't increase connective
tissue synthesis, or at least it doesn't increase it more than weigh protein. So I think if collagen
has a beneficial effect, it's simply because you're getting some amino acids compared to nothing.
And you probably just better off if you worry about your hair, skin, and nails, just take
way protein and wear sunscreen. That makes sense. Shoot, all right, because in the last few months,
I was like, oh, I got this collagen protein, and my wife likes it because hair, skin nails, like you
said, and then it's, oh, okay, well, I'll just replace my dimatized weight protein with this.
And, yeah, back to the other stuff, I suppose.
Especially for muscle tissue.
Yeah, pre-workout.
It's pretty horrible protein source.
There's a study looking at 30 grams of collagen didn't stimulate muscle protein synthesis,
and I'm not aware of any protein source that 30 grams other than collagen doesn't
stimulate muscle protein synthesis.
Yeah.
It's pretty poor.
So I work out after having a shake, these people who work out fasted, I don't know
who these people are. I can't do it. I will keel over. So I started drinking the collagen before the
workout. Before that, I did drink weight protein. I guess I'm going back to the way protein,
and I never thought about that. I just thought it was the same thing. I don't know. They don't
tell you that it doesn't do anything, right? That's not of the can. And again, like, it's more
about what your overall diet is like. That's the much more bigger determinant of health.
People can get really lost in the margins with this stuff. Yeah, when it specifically comes to
muscle metabolism, muscle protein synthesis.
It's just a very poor quality source of protein.
What about high protein diets and kidney damage?
People will say, you're getting 180 grams of protein per day.
That's bad for you.
Or my dad did the Atkins diet, which is not what I'm doing.
But his doctor said, you can only stay on it for a couple of months.
I keep hearing that less so in 2025, but certainly even just a few years ago,
almost everybody said, you're giving yourself kidney damage.
which I do blood work like every few months.
I'm fine so far.
People, unfortunately, when something gets published in a textbook, people receive it as the
word of God.
And a long time ago, in dietetic and nutrition textbooks, it was claimed that you want
to avoid high protein diets because they might be hard on the kidneys.
And this was based on some epidemiological studies, which is basically just like looking at
correlations, which is not sufficient to prove causation, and also looking at some animal data.
And I will say like weak, pretty weak data at the time. But it got published in textbooks,
and now we have been stuck with that dogma for over 50 years. The reality is we now have
multiple meta-analyses, which for those listening who aren't familiar with what a meta-analysis is,
it is a study of studies. So you attempt to combine the results from a bunch of different studies,
the similar designs and look at what is the overall effect.
So probably, the top protein metabolism researcher in the world is a guy named Stu Phillips,
and he was the lead on a meta-analysis in 2018 that showed that high-protein diets do not
negatively impact healthy kidneys.
There was another meta-analysis similar to that one, looking at human randomized control
trials, which is what we use to establish causality.
I think a lot of people quote studies and then I'll get an email that says there was this in 2015 by this and then I chat GPT that and they're like basically there's reasons you should give certain studies credence and others not or like some like you said epidemiological are not looking at causation and like people like me don't understand really what that means right off the bad I'm not even looking for that if it's a study I believe it I don't know if I shouldn't do that. Yeah so that is a big issue is when different studies get cited the average person is
not equipped. Most undergraduate scientists aren't equipped. A lot of PhDs, quite frankly,
from what I've seen are not equipped, to actually understand what studies should get more weight
versus others. When it comes to epidemiology, what we were talking about is there's two different
basic kinds of epidemiology. There's what's called cross-sectional, and then there's what's called
longitudinal. Cross-sectional is, for example, we looked at the incidence of, I'm just going to make up
stuff, may or may not be accurate. We looked at the instance of type 2 diabetes amongst people
who drink diet soda. And we found that people who drink diet soda have higher rates of type 2 diabetes.
Okay. All right. The average person hears that and goes, see, diet soda causes type 2 diabetes.
If you are doing a correlation, you can have also what's called reverse causality. What is it
to say that people who have type 2 diabetes are just more likely to drink diet soda?
What's to stop that from being the correct association?
And also, there are tons of confounding variables in these
because you are not having a treatment in these studies.
You are just looking at people's behavior
and attempting to correlate things.
And I will tell you, most of these correlations are pretty weak
in these nutritional epidemiology studies.
And you can Google spurious correlations
and you can find correlations that are literally almost perfect,
one to one, and make absolutely no sense.
I think something was like, there's almost a perfect correlation between the number of people who die by becoming trangled in their bed sheets and the U.S. spending on space exploration.
So basically the more the more the U.S. spends on space exploration, the more people die getting tangled in their bed sheets?
Or the more people who get tangled and die in their bed sheets, the more the U.S. spends on space exploration.
I could have gotten the specific correlation wrong, but stuff like that.
So it's clearly unrelated.
It's just coincidentally correlated.
I mean, we got to think it's unrelated, you know.
I can't imagine what the causality would be there, right?
Now, I'm not saying that all epidemiology is garbage.
I'm not saying that at all.
I'm just saying that you always have to understand
that there could be a lot of moderating variables
and confounding variables.
So that's cross-sectional.
Then if we look at something like longitudinal,
which are called cohort studies,
they're typically rated a higher quality of evidence
than cross-sectional.
And the reason is, now you're still not having a treatment,
but you're looking at groups of people
and you're tracking those people over time
and you're looking at the incidence of different things over time.
So let's take the same sort of subject.
We followed people for 10 years,
and we looked at the amount of people who consume diet soda
and the incidence of type 2 diabetes,
and we found that people who consumed diet soda
were 30% more likely to develop type 2 diabetes.
Okay, a little bit stronger evidence,
because now you are looking at,
okay, if there is no difference at baseline between these groups,
then it's a little bit bit,
stronger argument that maybe there's some causality here because you're tracking them over time.
However, the reverse causality issue still applies. And the reason it does is because there may be
just inherent characteristics of those people, whether it be genetic, environmental. People
don't do things in isolation. They tend to do group behavior. So what if people who tend to drink
more diet soda just more unhealthy overall? Like they do more unhealthy?
the overall behaviors. You can't establish that from cohort studies. So what we do is what's called
randomized control trials. And it is the randomization, the random part of that is very important.
And people need to understand. Reason randomization is important is now instead of you self-selecting
into a group, right, I choose to drink diet soda versus I choose not to avoid diet soda or
health conscious people who just drink water.
They probably have a bunch of other health-promoting behaviors.
But if we have a randomized control trial where we just take, say, 100 people and say,
all right, 50 of you are doing regular soda and 50 of you are doing diet soda and you don't
get to choose.
Then what we can assume is that any difference in baseline characteristics amongst the
participants will be randomly distributed over the treatment groups.
And so then if there is a difference between the treatment.
we can assume that it was because of the treatment and not because of some confounding variable.
Does that make sense?
Yeah, it does.
And I think a lot of people, again, myself included until recently, didn't really understand that.
I mean, if you take a group of people, like you said, that are all from like the same place or the same income bracket or the same ethnicity, whatever it is, you're going to end up with these correlations where you can't just point to the one thing and say that this is it.
Isn't that kind of why the bigger the study, often the more reliable it is, right?
If you're measuring, I don't know, the circumference of someone's head, you can get a sample
size of 20 people.
It's potentially going to be off by a lot.
But if you get 150,000 people, it's probably going to be a lot more accurate.
As long as those 150,000 people don't all live in Nuremberg, Germany.
So we call that sampling bias.
Now, the issue is when you're dealing with humans, when you're doing human studies, you can't
get everything all in one study. You can't get like high control, high subject number, and long
duration. Because the reality is, I think people have this impression that people that are involved in
research studies are just like this group of people who just like sit around twilling their thumbs
waiting for research studies to go, hey, you, and they go, okay, great, I'll just put all my entire
life on hold. You can just poke and prod me. No, there are people like you. There are people like
me, they're people like your average person who has a life, who has stuff to do, and the more
control you try to put under their life, the less likely they are to be included in the study.
I see. So it's like, you cannot have caffeine for a year. And I'm like, I'm out. Yeah, exactly.
So a great example could be, let's say your personal belief was a diet soda was bad for you.
Guess what? When you get randomized to the diet soda group, you go, okay, I'm not doing that.
Yeah. So the researchers have dropouts. And that's why when you look at like,
epidemiological studies or cohort data, you'll see some of them have tens of thousands,
hundreds of thousands, even millions of participants, because especially if it's not very
invasive stuff that they're looking at, they're just like having a food recall and then looking
at body weight, for example, you can get tons of participants from that. But if you're wanting
very detailed dietary recalls, or you want to say, like, we're going to provide all the food
to participants, or let's go really extreme.
We're going to put them in a metabolic ward where we are tracking every single thing that
they eat.
They can't eat anything outside of what people provide for them.
Who wants to stay in food jail for six months?
Right.
Yeah.
The compensation has to be like a lot.
Yeah.
If you want a long-term study with high subject number, it's going to be very free
living and very low control.
If you want high subject number with high control, it is going to be very short-neutral.
duration. If you want long duration, high control, it's going to be very low subject number. And if you
want all those things together, it's going to be in lab rats. Right. Right. Right. Who have no choice.
The reality is that this is why I don't get super excited about single studies. And I very rarely
come out and say, this study's good, this study's bad. Data is just data. There are bad
interpretations of data and there are really bad social media hot takes that I see all the freaking
time, but the data is just the data. And how it's collected, the methods that are used,
how it's analyzed, that is going to tell me how much weight I give that for something.
There's so many scientists who, like, they'll say we're testing this in their hypothesis or
their introduction, and I'll read the methods and I'll go, that study is not equipped to answer
the question that you're asking. Okay, the data, I can use it as a piece of a puzzle.
but it's not telling me what you say it's telling me
because it either wasn't collected the right way,
it wasn't the right population,
you didn't have the right control group.
So when it comes to randomize control trials,
which is the highest form of evidence
because it has high control,
you just don't get that many that are over 12 weeks long.
You don't get them with thousands of people.
You just don't, because when you're trying
to implement control on people,
they don't want to be involved in that for very long.
But that is the highest form of evidence.
And it seems like the problem with that is
then you have to extrapolate the answers.
So over the three weeks that we did this high control, high random, whatever study, these people exhibited slightly higher, I don't know, let's say like A1C, right, or some other thing.
Okay, so if you do this for years and you have A1C that's that high all the time, you're definitely going to take 10 years off your life.
And it's, ah, therefore, diet soda or whatever is bad for you.
And it's like, well, wait a minute.
If you do that study for three weeks, you don't know that.
Because when you do it with rats or if you did it with, I don't know, a prison population that didn't have a choice, unethical, whatever.
let's just cite, it's hypothetical.
Maybe there are A1C goes down after four weeks, and it just normalizes.
But you don't know that because your study was three weeks long, so all that extrapolating
that you did is actually just bullshit, right?
Correct.
I want to come back to your original question because I was talking about meta-analysis,
but there was a meta-analysis of human randomized control trials of protein intake
and kidney function showing that, again, it did not negatively affect kidney function.
And also, I'll circle it back to just give people the quick, short answer when it comes
to diet soda and say, like...
That was my next question.
I was like, okay, everyone's like, so is it bad for you or not?
God damn it.
Yeah.
Yeah, so type 2 diabetes, there was actually this study out of Australia that I don't even think it was published yet,
but I think it was presented at a scientific conference, so it hasn't gone through peer review yet,
but it wouldn't surprise me.
I think it's something like a 38% increased risk of type 2 diabetes amongst people who drink diet soda.
You go, aha.
Okay, but the problem is in the human randomized control trials, we see the exact opposite.
People who drink diet soda in place of regular soda lose weight and they have better cardiovascular
metabolic health outcomes. And they actually lose a little bit more weight than people who
substitute with water. I think that is likely because if you're used to drinking sugar, sweet
and you switch to water, you may still be seeking out that sweet taste elsewhere. Whereas if you
sub it with a diet soda, maybe that just fills that gap and you're less likely to seek it out
somewhere else. Antitotally personally, that is exactly it. I grew up drinking pop, we called it,
in Michigan. I drank a ton of it. And nobody was like, hey, you shouldn't drink two liters of
Coca-Cola per day because Midwest diet, whatever, and I got fat, surprise.
I basically cut it out as a teenager because I was like,
girls don't like dudes with giant guts generally in high school.
And then I started getting in shape and I was working out.
And a lot of the guys are like, don't drink soda and work out.
Then I go to college and it's like an all-you-can-eat buffet or whatever.
I'm like, ah, I love soda.
But they have Diet Coke.
I'll just drink that.
And I stopped drinking anything with sugar.
And even to this day, I love a good Diet Coke.
I know everyone's going to die young, whatever.
That's why you're here.
but I don't eat chocolate, I don't have desserts, I don't do any of that because if I have a sweet tooth craving,
I go and get like a diet orange cream Coke zero or whatever, have a few tips of that and I'm like,
I don't want anything else with sugar in it for the rest of the day, and I drink that throughout the day.
And yeah, I don't get any calories from it.
Now, if it was super bad for you in some other way, that would definitely be a problem,
but it sounds like there's just not that much evidence for that.
So specifically with type 2 diabetes, again, I've traced this logic all the way out.
So again, we see the opposite thing in the randomized control trial.
So why would we see opposite, the explanation will be reverse causality?
And that is exactly what it is.
So if you look at people who drink diet soda, the reason that they are more likely to have type 2 diabetes is not because diet soda causes them to have type 2 diabetes.
People who drink diet soda are more likely to be overweight to begin with.
And they're more likely to make diet attempts.
So what they are doing is this is a selection.
selection bias where they're looking at, okay, well, these people who drink more diet soda,
yeah, because they're trying to lose weight, okay? And if they compare people who drink diet soda
versus people who just drink water, who don't drink regular soda, diet soda drinkers have a lower
overall diet quality and consume more calories on average than people who just drink water.
Now, some people may say, see, diet soda makes you hungry because it releases insulin and it causes
a hunger response in the brain. That's been roundly debunked.
there's the only sweetener that's a little bit weird is saccharin, which is sweet and low.
I would tell people like, it's probably better than regular sugar on balance, but it's the
worst of the sweeteners.
There does seem to be some weird effects with that in terms of some glycemic responses and
whatnot.
But aspartame, sucralose, monk fruit, stevia, there was two meta-analysis that came out,
one on those sweeteners overall showing no effect on insulin, blood glucose,
responses, any kind of like endocrine hormone, basically the conclusion of the study in this,
again, meta-analysis of randomized control trials. So this is combining our highest quality
evidence showing that their takeaway was it has the same effects as water. And then there was one
recently looking at aspartame and insulin secretion, hunger responses, and basically showed the
same thing. Aspartame does not cause an insulin or glucose response. It's a insulin or glucose response. It's
not increase hunger, if anything, it reduces energy intake. So, no, it does not cause type
two diabetes. It does not cause you to be hungry. If it did cause you to be hungry, then that
would actually suggest that these artificial sweeteners are great fat burners, because in randomized
control trials, these people lose weight when they switch from sugar-sweetened beverages to artificially
sweetened beverages, and they lose more weight than people that consume water in place of
sugar-sweetened beverages. So if you're going to say that the diet soda made you
hungry and you were eating more calories, but they still lost weight, then doesn't that mean
that they're great fat burners? So this logic falls apart. People will say, well, they cause cancer.
Yeah, if you give it to a lab rat at 10,000 times the dose you should normally consume,
then yes, you see some weird things. But let's take aspartame, for example, because that's one of the
most tested compounds in history. Aspartame is a dipeptide, two amino acids,
phenylalanine and aspartic acid combined with a methyl ester group.
It is metabolized into three things.
It is metabolized into phenylalanine, aspartic acid, both of which are amino acids.
It's so funny to see these graphics.
Some of these social media people will be like, oh, phenolalaline is a neurotoxin.
Yeah, if you apply it directly to brain cells, it's a neurotoxin.
We have this thing called the blood-brain barrier.
And oh, by the way, you get 30 times more phenolalaline in a stake.
If you're worried about the amino acids that are literally in every protein you consume that you get 20 to 30 times more of in any protein source, then why are you worried about diet soda if you're not worried about those protein sources?
So then there's other thing it's metabolized into is methanol. People go, aha, see, it's the methanol. Okay, well, let's break this down. The reason that this is important to understand, Aspartame has never in any research study been shown to enter the bloodstream or be found in.
in any tissue, it is rapidly and completely metabolized into those three components. So if it is
bad for you, it is exerting its effects through one of those three things. Now, I think we can
just set the amino acids to the side, because like I said, if you're worried about those,
and you've got to be worried about any protein intake whatsoever. So let's look at the methanol.
First of all, if we look at the things that aspartame is claimed to do to you, that's very different
than the side effects from too much methanol,
which is basically like central nervous toxicity,
cardiopulmonary failure, and death and blindness.
Methadol itself is not necessarily toxic,
but it's metabolized into formate or formic acid,
which is toxic.
Now, in a study looking at aspartame consumption,
they gave what would have been the equivalent
of 26 Diet Cokes over an eight-hour period,
which I think even the highest consumers of
diet sort of probably aren't hitting that mark.
There were a couple guys in law school who I think were damn close.
But other than that, during finals week, other than that, I think we're probably okay.
And they noted that there was no real increase in blood methanol levels, no increase in the
blood levels of formic acid or formate.
You get more methanol in a glass of orange juice or tomato juice, quite a bit more
methanol.
You get more methanol in a lot of servings of fruits and vegetables.
And yet fruits and vegetables are associated with better overall metabolic health.
And once again, even at very high doses of aspartame intake, you don't see rises in methanol.
Now, there was one study, Rivers and Rats, and they looked at a massive dose.
Basically the equivalent of, once you equate for human equivalent dosing in animals,
a massive dose equivalent to about 100 Diet Coke one time, which, by the way, you'd actually die from electrolyte dilution,
from drinking that much fluid
before you would even get these negative effects.
But I digress. Anyways, in that study,
they did note in blood levels of methanol,
but no rise in formate.
So even that was not sufficient
to take those blood levels up enough
to get to a level of formate
that would cause negative effects.
And again, even if it did,
people say, well, what about over time?
You're thinking about bioaccumulation, right?
but there's more discussion about microplastics now.
There's things like lead, mercury, those things take a long time to process out of the body.
They can accumulate.
Okay, fair enough.
Methadol is processed out of your body in hours.
So if it is exerting these negative effects, it has to be acute.
And again, if a spurtame's causing cancer, please explain how it's doing this.
And whenever I bring this to people, once I go through all this data, they just go to,
well, it's man-made synthetic.
Right.
The appeal to nature fallacy, right?
That natural things are better.
Yeah, the naturalism fallacy, which I'll tell you, arsenic's natural, snake venomous natural.
A lot of poisonous plants are natural.
Cyanide in the apple seeds, no one stays away from apples because of that.
And even an apple juice, I don't think they bother taking the seeds out.
They just squash it because there's a little bit of cyanide in your apple juice.
Whatever, man, you'll be fine.
And the reality is, like, when it comes to toxic.
the dosage makes the poison. You could have something that is thought of as a very toxic compound. If it's at a
low enough dose, you will be okay. It won't have negative effects. You can also have something that
people view as being inert. Take water. Good old dihydrogen monoxide. If you drink around 10 times
the amount of water that's recommended, you could actually die from electrolyte dilution. Anything can be
toxic at a high enough dose.
What is that called again, the LD50 or the RD50?
You know what I'm talking about?
Yeah, so LD50 is basically like the dosage of a compound that will kill approximately
50% of the population.
There's a bell curve response.
Speaking of getting enough protein, look, I'm not saying you need to eat like Lane Norton
to hit your goals.
But if your idea of a balanced diet is three cold brews in a protein bar that tastes like
drywall, you might want to rethink that.
Personally, I'm team.
Whatever doesn't make me chew for 10 minutes.
straight. Now, chew on this. We'll be right back. If you're wondering how I manage to book all these
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Now, back to Lane Norton.
I remember Neil deGrasse Tyson was on talking about, we did it with Ben and Jerry's or something,
because I was like, what's that pesticide that everyone freaks out?
And it's like, they use, yeah, they use glyphosate and then it goes in here and then it goes in there.
In order to eat enough Ben and Jerry, or whatever ice cream it was, to get enough glyphosate from the vanilla beans or whatever it is,
you would have to eat so much of this,
you would be dead from the sugar
before you had enough
of that pesticide in your system.
Like, not even close.
Like, it would take you, like,
three years of only eating ice cream
to get enough glyphosated,
and then he got other problems.
Yeah, well, then you have the Gary Breckas
of the world saying,
you want to avoid synthetic vitamin B12
because it has,
it's cyanocabalaman,
and the cyanos stands for cyanide.
So I did the calculation on this
to hit the LD50
of,
cyanide from cyanocombole, which, by the way, you still wouldn't be toxic because cyanide is only
dangerous. People don't understand. There's a difference between a free form of a chemical and a bonded
form of a chemical. Okay? So, for example, chloride gas kill you. Sodium chloride, that's salt.
Let's put it on our food. Right. Exactly. So these things are not the same.
bonded cyanocobalaman, the cyanide group is totally stable and not dangerous at all.
Now, even if it was, let's say it actually was, I think he was talking about Celsius drinks.
Maybe that was that, but whatever was, you would have needed 43,000 servings at one time to hit the LD50.
Meanwhile, it's got caffeine in it, so you're dead.
Good luck.
Or if it was capsules, can you imagine taking 43,000 capsules at one time?
I mean, you'd probably like rip your inside apart.
Be like something out of saw at three.
Yeah.
On the other side of all this, what's one food that most people think is healthy, but you think
it's overrated or counterproductive?
What are people sort of hung up on where you're like, ah, give it up.
Who cares?
What's overhyped right now is like bone broth.
How about that?
Sure.
Yeah.
By the way, I love bone broth.
I get it from this Korean place that makes this amazing soup and I can eat it every day.
But yeah, people are obsessed with it.
You're right.
Yeah.
Hey, if you like the way.
it tastes and you like to have it, totally fine. Yeah, there's some vitamins and minerals in it,
but it's not like this panacea of stuff. And yeah, there's some collagen in there, but I already
talked about collagen a little bit. But hey, if you like the way it tastes, by all means,
I don't think it's necessarily bad for you or anything. And this is the problem that a lot of people
just, the society we live in now, it's so hard to have these conversations because everything
is so polarizing and so politicized right now. I just put out a video today talking about,
Hey, here's the data on a Cidaminophen and why I think it's very unlikely that has any contribution to autism.
Shut up, Lib Tard.
Yeah, right?
Yeah, yeah, exactly.
Me, I get accused of being a liberal.
And I'm like, me, who comes from Indiana, a red state, whose entire family is conservatives.
But yeah, if I don't agree with every single thing that the conservative party says now, it's you're a libtard.
Right.
You're rooting against your own team.
That's the problem is it's become teamified or gamified,
and now you're on the wrong team
because you're not to towing the line
when it comes to Tylenol or whatever.
I didn't even catch that.
It's the Tylenol thing.
My wife had to tell me about it.
Yeah, and I'm like, listen,
bullshit is bullshit.
I don't care who's shoveling it.
When people on the other side aisle say dumb stuff,
nutritionally, I'm going to call it out.
And I do call it out.
When it comes to these arguments,
if I say something like, hey, bone broth,
I think it's overrated.
People say, you're saying it's bad for you.
No, never said that.
Didn't say that.
Or if I say, like, for example, diet soda is a healthy substitute compared to sugar, sweetened beverages.
And people go, you're saying diet soda is healthy, I said in place of.
Okay?
Now, I could make a strong argument that it is healthy, but I won't do that.
People say, you're defending or encouraging diet soda.
I'm like, that's not what I said.
Why don't you go back and just actually listen to what I said instead of having a two-year-old emotional temper tantrum about something that doesn't align with your personal belief system?
I think that's well said.
And it's very tough to get people to take an information that comes from a source they don't like.
That's really tough.
I try to manage that on this podcast.
It's very tough, though.
I mean, because now any information that people don't like, you're automatically off the team.
That's a bigger problem.
And it's probably a different episode of the show, honestly.
But I want to stay on food and nutrition because we're on fire here.
I'm curious about autophagy and fasting.
A lot of people are like, look, man, there's no magic to fasting.
It's fancy calorie reduction.
And other people are like, no, there is magic.
weak cells dying that would normally cause cancer. Can you shed some light on this? Because I honestly,
I don't know what's true. I know what sounds true, but that doesn't mean anything.
So again, whenever we are approaching a question, we always have to ask, compared to what?
So does fasting increase autophagy? Yes. But compared to what? First of all, we have to back up,
because the way people like Mindy Peltz and some of these people who talk about this stuff,
which, by the way, she has no scientific training whatsoever.
Just going to throw that out there.
They'll say, insert number of hours, the autophagy switch flips on, and this happens.
So the body doesn't actually work like that.
These processes are always happening.
These things are always going on.
Now, the relative rates can change, but there is no switch where you hit a certain point.
A body doesn't work like that.
It doesn't make sense they would ever work like that.
Now, if you fast over time autophagy, which is lysosomal protein,
degradation, you have in
yourselves these organelles called lysosomes.
They can engulf
different cellular components
and then they have a bunch of proteases
and enzymes inside of them to chew
them up. They take whole proteins
and turn them into
individual amino acids, which can then
be recycled and used for different stuff.
So elements of what they are saying is
true. Atophagy can go up
and also autophagy
is involved in
remodeling and breaking down
old or misfolded cellular components.
That is true. By the way,
autophagy is not always a good thing.
Otophagy is elevated in various cancers.
It's how various cancers are able to feed themselves.
Atophagies elevated in wasting diseases.
So it's not always a good thing.
If I could impress anything upon people,
it would be to stop trying to get things to fit into black and white boxes.
There are very few things are either
are blankedly good or blanketly bad.
And in the human body, I want you to consider a lot of these things that you consider bad or
unhealthy, if they were bad for us, why would we evolve to have those systems?
If they were going to kill us faster, why in the hell would they be passed down from generation
to generation and conserved?
Because if they killed the organism faster, they would be bred out of it.
of the population. That is just plain all natural selection. Because nothing is good or bad in the human
body. Any system, if it's dysregulated, can have a negative effect. But those systems all exist for a
reason. Like cortisol, everybody thinks cortisol is bad for you. Take cortisol completely away.
And that's called Addison's disease. And it's not good. A lot of problems with that.
Yeah, one of my friends kids has that, actually. He's got to take hormones, I believe, because he doesn't
prednisone most likely. Yeah. He's a chill kid, and I don't ask too many questions, but I know he
doesn't have cortisol. And my friend's like, he's so chill, he doesn't have cortisol, but it's actually
not that cool. There's a lot of medication involved, basically. Yeah, because your body evolved to have
these systems. So back to autophagy, not always a good thing. But it exists for a reason,
and it does serve a purpose, some of which may have benefits. Now, what happens when you are not
eating. Well, you are in a negative energy balance. Now, if you're not eating for, say, 16 hours,
18 hours, you're in a negative energy balance. But what happens in the last six or eight hours?
Because a lot of these fasting people, they go, well, it's not about weight loss. Has nothing to do
with weight loss. Okay. So let's take two people, right? One person's eating 3,000 calories a day,
and let's say that's their maintenance. They don't fast. They just kind of eat throughout the day.
The other person fasts for, let's just say they eat one meal a day.
3,000 calories at one meal, right?
Because they want to get maximal autophagy.
When they are fasting, are there rates of autophagy greater than the people who are continuously feeding?
Probably.
But guess what happens when they have that massive meal?
Otophagy is going to go way down.
It is going to very much suppress autophagy and protein breakdown.
And if we look at the area under the curve, the question is, is the area under the curve different?
Over a 24-hour period or over a week, do we see differences?
I usually don't put a ton of weight in single studies, but this was a well-done study.
So they looked at autophagy.
They looked at other things, too, including weight loss, fat loss, lean mass, with alternate day fasting.
And the way they did this was they had one group, so they ate at 75% of their normal maintenance calories.
So they were in a 25% calorie deficit doing alternate day fasting,
which means that one day they did zero, the next day they did 150.
So 150% above their maintenance on another day.
And they alternated those days.
Another group that just did 75% calorie restriction each day.
And then they had another group that did alternate day fasting,
but they did at maintenance overall.
So they did 200% one day, zero percent the next day,
so that overall of the course of the week they're at maintenance.
what they found was that autophagy was not different between any of the groups.
I feel very confident in saying that the atophagy effect is a calorie effect.
If you eat less calories, you have higher rates of autophagy.
And if we look at the research data on longevity, on risk of cancer, all those sorts of things.
Again, here's the issue with design limitations.
You can't conduct a human randomized control trial looking at longevity.
Because you're going to go to one group of people.
we're going to control this until you die.
Second off, if you're in the trial, aren't you going to go,
so which group do you think is going to live longer to the researchers?
You know what I mean?
You can't ethically do that, right?
But they have done it in rodents and probably the best studies we have are in eresis monkeys,
which are closer in proximity to humans and human physiology.
And some of the headlines years ago, calorie restriction improves longevity.
I'm sure you've heard this research as well.
I've read this research, and I am very well familiar with animal study design because my research was in animals.
So when they say calorie restriction in animals, what they're actually referring to is typically you let animals just eat however much they want.
We call that ad libitum.
And then if you want to do restriction, you pull back whatever they normally eat by a certain percentage.
So in these studies, they pull 30% out of their normal diets.
And they call it calorie restriction.
calorie restricted over the course of their life.
But they weren't calorie restricted over the course of their life
because if they were, they would just keep losing weight indefinitely until they starve to death.
In most of these studies, there's no weight change or a small period of weight loss
followed by weight stabilization.
Guess what animals do in captivity?
They overeat because they're bored.
So what you're actually doing is just preventing them from becoming overweight or obese,
from having too much body fat.
So in my opinion, a lot of this data is basically explained by,
hey, if you maintain a normal healthy body fat level,
you're getting the benefits of longevity.
Animals in captivity, overeating because they're bored.
It just sounds like me in the pandemic.
During the pandemic, it was like, yeah, all right.
That was the beginning of my weight loss journey because I was like, I'm getting fatter.
It's really obvious.
There's one way to handle this.
Speaking of which a lot of people said, no, it's just because you're older and your metabolism slowed down.
So this is maybe a dumb question.
But is it true that people's metabolism slows down as they age, or are we just moving less than we did as kids because we're sitting at a freaking desk all day?
Everybody's going to hate the answer to this question.
So, first of all, probably one of the best studies we have on this is a study from Duke University from Herman Ponsor's lab, who's one of the foremost experts on energy metabolism, looking at total daily energy expenditure, which we have to define our terms.
When people say metabolism or metabolic rate, that is your resting energy expenditure or your BMR, which is basically how much does it cost just to run your body's basic energy systems?
It's not exercise, it's not activity, it's none of that.
It's what is the cost of if you just laid down and breathed for 24 hours,
how many calories would that take?
Now, what Herman looked at was total daily energy expenditure,
which is what is everything, right?
Your resting energy expenditure,
the cost of extracting energy from the food you eat called thermic effective food,
your physical activity, exercise, your spontaneous movement
called non-exercise activity thermogenesis or neat.
what are all these things sum up to?
Like your calorie burn, your calorie expenditure, the whole thing on a daily basis.
And he showed that it rises, obviously, in childhood, up to adulthood.
Then from about age 20 till about age 60 is completely stable in this large cohort of people.
And then after age 60, it starts to slowly decline.
But it's less than 1% decline per year.
And it's also, by the way, completely explained by the fact that people just become less active
and have less lean mass as they get older.
When you normalize for lean mass,
most of this stuff goes away.
And if we looked at BMR specifically,
so just the basal metabolic rate
literally does not change.
Leave into elderly like 70, 80.
Now, your absolute resting energy expenditure,
absolute metabolic rate does decline
because you lose lean mass.
But if we normalize your metabolic rate
to your lean mass,
we don't see any differences.
And that goes for people with PCOS, people with type 2 diabetes.
Actually, people with type 2 diabetes, believe it or not, have a slightly higher metabolic rates, if anything.
Even when standardized for lean mass, people who are overweight or obese.
When you standardize for lean mass, no difference in energy expenditure or metabolic rate.
So we want to keep working out, basically.
That's the lesson here, is keep working out so you keep your lean mass.
probably the biggest proof of this, the most effective obesity treatments in the history of mankind.
GLP1 memetics like Ozympic, like Chesapeotide, they do not increase energy expenditure.
They do not.
They have no effect on energy expenditure.
What they are is powerful appetite suppressants.
People who are like, my metabolism, it's just my metabolism.
I need to use Ozypic.
I hate to tell you this, if it's your metabolism, Ozympic isn't going to do anything for you.
And the reality is that people don't want to admit that they eat too much for their given level of
energy expenditure because that feels like somebody saying it's your fault. And I could go into a lot
more detail about why it's more complicated than the fault of the individual when it comes to obesity.
Obese people are more likely to have, especially obese women, more likely to have sexual
trauma in their past, assault trauma in their past. People who are obese have a greater
reward from food. They have less sensitivity to satiety signals. There's differences. People will go,
you're fat shaming. And honestly, one thing that I think I've just changed my mind or maybe just learned
is a better term for it in the last five or ten years is I really think there's just a difference
because when I had to go on a diet for 10 months, I was like, okay, and I went on a diet for 10 months,
and I ate Chipotle for lunch or similar, and then I had turkey breast for dinner every day
for 10 months, and I had a protein shake for breakfast, and I just did that for 10 months,
and it didn't bother me that much, but it's not like, oh, I'm so good, I have such good
willpower. I just don't get that much of a dopamine hit from, like, eating, it don't care as much.
I feel full when I'm full.
and other people, they don't have that.
Not that they don't have willpower.
It's a completely different pull for them to eat something
and then get a reward from it than it is for me.
And we can't compare that ever.
There's no way to compare that.
So I can never put myself in the brain of somebody else
who's 100 pounds overweight and be like,
dude, just eat less, man.
It's so easy.
He will never understand how not hard it is
for me to just eat turkey breast for 10 straight months
out of a package because that's a completely alien thing.
I don't want to excuse everything,
but I really do think there's like a different,
level of people feeling the pull and people feeling full, like you said.
People have difficulty holding what they feel are two seemingly opposing things in each hand
at the same time, which is obesity is likely not completely the fault of the individual,
but also there is a personal accountability and responsibility aspect to fixing the problem.
It may not be your fault that it happened, but it will be your responsibility to try to change
things. And so I think people try to equate responsibility and fairness. And the reality is, no,
everybody has, in one way or another, some things are unfair or happen to them. But regardless of
what happens, you have to take the responsibility to try and to change it for the better.
And so I think people have trouble reconciling those things.
You know what I love about Lane? He doesn't just believe in science. He lives it, which is kind of
my vibe, too, whether it's nutrition, psychology, or picking podcast sponsors that don't make me
lose brain cells when I read the copy. We'll be right back.
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Now, for the rest of my conversation with Lane Norton.
We see this even in criminal law.
Like, you see these people who come from terrible backgrounds.
We still put them in prison because they're dangerous for society, but we don't
rehabilitate them, right?
We blame them for having a moral fault for being born into a gang life with no parents, right?
And it's, I don't know how effective that's going to be.
But again, like you said, not your fault, but also your responsibility, right?
That's why we love stories of redemption.
Anyway, it's a completely different podcast.
I think I should probably switch gears here.
What's one thing you used to eat regularly that you completely avoid now based on either
new or new-ish science, and don't room Cheetos for me or we're done.
I don't think there's anything that I completely avoid.
I eat less saturated fat now.
It's so funny now because I'm known as a pro-seed oil guy now, which is not my position.
That's one of my questions, too.
Like, are these bad for you?
I came from a low-carb lab.
The lab I was in for graduate school was known as being lower carb.
And my belief in graduate school was saturated fat intake, it's got a bad rap, doesn't matter,
LDL cholesterol doesn't matter.
And over time, seeing enough data, I changed my mind because I think it does matter.
But I don't just say, oh, I never eat saturated fat.
I still have bacon sometimes and I'll still have a fatty steak here and there and I don't
like completely avoid it.
I try to limit it as much as I reasonably can.
I just don't get that scared about stuff.
Doseage makes the poison.
And so I just think it's funny that these crazy anti-seed oil people, that they somehow think
that I'm in the pocket of like big plant oil.
When in reality, like my research, who funded my research?
Who's actually given me money?
The National Dairy Council, the Egg Nutrition Board,
and the National Catalan's Beef Association.
If anyone has a bias towards saturated fat, it's me, okay?
Yeah, not a plant insight.
So is there any true to the claim that seed oils cause cancer,
hormonal issues, whatever it was, or is that just internet noise?
All right, so I'm going to take the arguments as I understand them
from the anticidal people and point out where the evidence actually says.
So the arguments that exist are something like the following.
There's the very mechanistic argument that people like Paul Solino make that it's
linoleic acid, this polyunsaturated fat, can be oxidized more easily.
And that oxidation is going to cause damage to your blood vessels.
It's going to cause inflammation.
And that inflammation is going to cause heart disease and cancer.
Okay, all right.
Keep that in mind.
Put it to the side.
I'm going to come back to it.
Then there's the people that go,
the processing of these oils is what's causing it.
They're heated, and it caused them to oxidize, and they're rancid.
The processing is processed with hexane, industrial solvent,
and it's processed with sodium hydroxide,
and they scare you with all that stuff.
I could make anything that sounds scary if I wanted to tell you how it was processed.
Then the last one is, if you look at the rise in obesity,
and the issues would make it.
metabolic health, it associates with the increase in seed oil consumption. And it does. But we have to
ask ourselves, okay, is that a calorie effect? People just adding oil to stuff or oils being present
and ultra-processed foods? So let's go top level. If we tell people, eat more polyunsaturated fats,
mostly from seed oils, things like sunflower oil, sapphire oil, canola oil, soybean oil,
If we tell them in a one-to-one ratio,
we want you to sub-in polyunsaturated fats from these seed oils
versus saturated fats, what happens?
And the worst case scenario is a neutral effect on metabolic health.
Most studies, or I'll say it depends on the metric,
but for sure, polyunsaturated fats, lower LDL cholesterol
compared to saturated fat.
Now, the anticidal people will deny that LDL cholesterol makes the difference, and I'll explain why they're wrong.
But also, if you overfeed polyunsaturated fats from, I think it was sunflower oil versus saturated fat from, say, I forget the source.
But they overfed both of these things.
Both increased the levels of liver fat, which liver fat is a strong predictor of overall metabolic health and insulin sensitivity.
Saturated fat increased liver fat 70% more.
The liver fat in these people went up by 86%
from saturated fat overfeeding.
If you look at insulin sensitivity,
either a neutral or positive effect
from subbing in polyunsaturated fats
in place of saturated fat.
You will not find a study that I'm aware of
showing improvements in actual insulin sensitivity
by subbing in saturated fat for polyunsaturated fat.
You won't find the reverse.
Inflammation, either neutral or positive effect
by subbing in polyunsaturated fats.
Entethelial function, either neutral or positive effects.
Okay, so those are the human randomized control trials.
So, okay, where is this effect of inflammation that you're talking about?
It's not happening.
This metabolic health effect that you're talking about.
It's not happening.
We're not seeing that.
In fact, we're actually seeing the opposite
from what your hypothesis would suggest.
Now let's take the processing argument.
So hexane is used as a solvent to remove impurities
from seed oils. The reason it is used is because it is a non-polar solvent. And seed oils, oil,
is non-polar. And so if you want to pull impurities out, you have to use another non-polar solvent.
Now, the reason they use hexane is because it has a very low boiling point, 69 degrees Celsius.
So once they put it through the solvent, they boil off the hexane. The amount of hexane that is left
in almost half of seed oil products
is not even detectable via the methods we have to detect hexane.
It's so low you can't even detect it.
The ones that have detectable levels of hexane,
it's in the parts per million
and far below the threshold
of what would cause any kind of negative effects.
And now people go,
if it's bad in a high dose, it's bad to low dose.
Okay, well, then you've got to make the same thing for water.
Yeah, or apple seeds, cyan, and everything else
that we just talked about.
Yeah, exactly.
That's so interesting.
They don't like to have logic symmetrically applied.
They only like to apply it asymmetrically.
What you see this with Paul Soledino.
He'll say, all epidemiology is garbage.
And then they'll get on the Joe Rogan podcast and cite multiple epidemiological studies that fit with his narrative.
He literally has a video that says all epidemiology is garbage.
If you are saying it is garbage, then you have to throw it out.
You cannot use it when it benefits you and then disregard it when it doesn't.
You can't pick and choose that way.
You have to be symmetrical in how you apply that logic.
So hexane, and I looked for studies for hexane toxicity.
I couldn't find them in humans.
They basically, like, they got negative side effects.
I really couldn't find any, like, I think there was one person.
They said that might have died from drinking, like, a ton, like, literally taking hexane and drinking.
Interesting choice.
He ran out of diet soda.
Now, sodium hydroxide, again, the processing of these compounds through the processing
turns into sodium and water and then they just get rid of it. There's no sodium hydroxide that's left
over in the product, or the amount is so small, it's not going to cause you any issues. Then the
heating portion of it, heating oils, frying with oils, can be a problem, especially if you're frying
in a very low amount of oil. The amount of time it takes to oxidize oil and say like, I believe it was like
looking at a centimeter of oil versus four centimeters, it's like a five X. You need like five times
longer to actually see oxidation of the oil when you have a bigger amount that you're frying it.
Which oils are safe to use then, which ones should we avoid for cooking?
Well, the reality is that you can oxidize any oil if you have a small amount of it and
you heat it long enough, okay? And you repeat it like, frying stuff,
repeatedly in oil over time. Yeah, you're going to have some oxidize in products, but I would argue
like, okay, the bigger problem is that you're eating a lot of fried food. Right. That's the bigger problem,
okay? But spraying canoil oil on your pan and heating it for a few minutes while you like saute
something, not nearly long enough to cause any significant amount of oxidation. The processing,
they show that like soybean oil, which I think is moderate in its ability to be oxidized,
soybean oil, you have to heat it at like over 450 degrees for like more than two or three hours
for you to start to see any kind of significant amount of oxidation above 1% of the oil
or any kind of negative byproducts begin accumulating.
So the processing actually of these oils removes impurities and removes oxidized components.
That's part of what the processing does.
You actually have less oxidized components because of the processing.
And then people do the whole scaring.
They used it as motor oil.
Yeah, well, they use beef tallow as industrial lubricant too.
So if you want to use that line of logic, fine.
But I can scare you.
That's true.
Used to be in the lights.
They used to put it in the lights.
Oh, you're eating lamp fluid.
Yeah, okay.
It's attached to a steak.
It's delicious.
Yeah, it's all sort of fear-mongering.
It's important to note, like some of the names you're mentioning,
a lot of these people, they make a lot of money selling supplements
that don't have this thing in it that they say is demonized.
They're selling seminars on how to live.
this way or they have a special diet that you have to follow and a book that goes with it,
all that stuff.
Well, I don't sell seed oils.
So there's that.
Yeah, you don't sell seed oils.
I don't make any money on seed oils.
Not yet.
Not yet.
I'm going to email you, but our seed oil side hustle after this podcast.
Exactly.
People like, how much is big pharma paying you?
I'm like, not nearly enough.
How much is big seed oil paying you?
I'm like, oh, man, I wish.
I wish.
Yeah.
Are they listening?
Geez.
The final component of that is the mechanistic component.
Linoleic acid, which is one of the most common fatty acids,
for a lot of these oils, more prone to oxidation, and that's going to cause inflammation.
Linoleic acid causes inflammation.
If you look at linoleic acid consumption in the U.S. or in Western societies, it's gone up by like 75-fold
over the last 150 years, and they go, see, it's got to be the linoleic acid.
Okay, two things.
What happens in populations where they consume more linoleic acid versus less?
And if we feed people linoleic acid, what happens?
Okay, so there's large cohorts of millions of people showing that basically there's a linear association between dietary linoleic acid consumption and the risk of heart disease.
There's a linear reduction in heart disease the more linoleic acid people eat.
And the anticidal crowd will say, well, that's dietary meat call logs.
You can't rely on those.
Okay.
They've also done tissue sampling because the fatty acid composition of your diet will be reflected in the fatty acid composition of your adipose and your plasma.
they've done those tissue samples
and shown that people with more linoleic acid in their tissues and plasma
have lower rates of heart disease.
So just on that alone, your entire hypothesis is debunked.
We don't even need to go any further into it.
But let's do it.
So one of the things Paul Salino says,
it's not about the LDL cholesterol,
it's about the oxidized LDL cholesterol.
That's what you have to worry about
because oxidized aldeal cholesterol is way worse for you.
And, on a mechanistic level,
he is correct. Oxidized LDL is more easily taken up by the endothelium.
What is that? Indothelium. What is that?
That's the lining, that's like the cells that line your blood vessels.
That's true, but I'm going to get back to why you don't have to worry about that.
And he'll say linoleic acid or polyunsaturated fats in LDL are easier to oxidize.
Also true. Now, let me explain why it doesn't matter.
So I dug into this very deeply. First of all, regular LDLLLL is,
LDL can penetrate the endothelium.
And once LDL penetrates
the endothelium, and it's
concentration driven, so people with higher LDL levels
get more LDL going into the
endothelium. Once it is
in the endothelium, all
LDL particles
contain a lipoprotein called
apolyproproteen B.
Each LDL particle has one.
That APOB
gets enzymatically modified
once it's inside the endothelium, and it
causes that LDL molecule to be retained.
because of the modification.
And once in the endothelium,
that LDL starts to be oxidized.
Okay?
That oxidation
recruits macrophages and inflammation
to the site because it's an injury.
And that causes over time
foam cells to form
and eventually leads to plaque and blockage.
Hang on, Lane, you just said
linoleic acid can be more easily oxidized.
Here's the rub.
If you consume more linoleic acid, your LDL concentrations go down.
So you're getting less LDL penetrating the endothelium that can even be oxidized at all.
But what about oxidized LDL in the bloodstream?
Because that's a big argument that Paul makes.
Well, it's the oxidized LDL in the blood.
Oxidized LDL in the blood is present, but it is actually reflective, and they have shown this in studies.
It's reflective of spillover from the tissues.
oxidized LDL that has been already oxidized in the endothelium,
and there's so much of it that it's starting to spill over into the bloodstream.
It's not oxidized hardly at all in the bloodstream because your bloodstream has
antioxidants in it that prevent the oxidation of this.
And they have shown this in vitro, in animal studies, they have shown it over and over.
The amount of LDL that gets oxidized in the bloodstream is,
infinitely small compared to what gets oxidized inside the endothelium. So if you want to prevent
LDL oxidation, you are better off trying to drop your overall LDL levels so that you're not getting
so much going into the endothelium, because in the indithelium, they're not exactly sure where,
but in the microenvironment there, they believe at some point you have less of these antioxidants
around, and that is when those polyunsaturated fats and the LDL particle can begin becoming
oxidized. And again, they're looking at it as oxidized LDL is causing these problems.
Yeah, oxidized LDL in the plasma is a problem, but it's not coming from the plasma to any appreciable
degree. It's coming because you've already oxidized so much LDL inside the endothelium
that it's beginning to trickle out in the bloodstream. By that time, you're looking at oxidized
LDL is like saying, yes, it's atherogenic, but no more atherogenic than regular LDL.
And it's kind of like being like fire extinguishers are causing the fire, because when there's
a fire, there's a fire extinguisher.
It's more reflective of the downstream rather than the upstream.
So again, linoleic acid reduces this risk because consuming polyunsaturated fats like
linoleic acid reduces your overall LDL levels, which means less is going to get into the endothelium
and get oxidized in the first place.
And there's one more kind of mechanism they use, which is linoleic acid is a precursor to
arachidonic acid.
Arachidotic acid is a precursor to prostaglandins, which are pro-inflammatory compounds.
And so they could have a equals B, B equals C, C, equals D.
They've already shown that increasing linoleic acid consumption does not increase arachidonic acid
formation, and it does not increase prostaglandin formation.
So we can just, again, at every single level of their argument, it has been debunked.
I love this. This is a very thorough explanation. Are food labels essentially lying to us?
Not like a conspiracy, but how accurate is the 400 calorie energy bar label? Is there a tolerance here? And we just kind of have to deal with that? Or is it like they're just guessing and nobody's going to know?
So there's a few different answers to this question. First off, you are allowed a 20% error either direction on a food label. Now, that doesn't mean that they take it. And the reason they do that is because, geez, chicken in San Francisco.
maybe slightly different than the tissue of chicken in, I don't know, Arkansas.
Or a chocolate bar just has a little bit more poured onto it from one machine than the other.
I don't know.
So they allow a tolerance.
Now, what I'll tell people is people make a big deal.
Counting calories is stupid because these food labels.
Okay, but maybe there's a little bit off.
But if you're always tracking something the same way, it's like measuring body fat.
People don't realize, like, they get a dexter.
And they're like, oh, that's my body fat exactly.
No, Dex is still relies on assumptions, algorithms, equations,
but if you're getting Dexed the same way every time,
if your body fat goes down, you can be relatively confident it goes down.
Now, are you 15% really, or are you 13.5% really?
You don't know.
The only way to know exactly what your body fat is to die and have your adipose tissue excised and weighed.
That's the only way to know, okay?
So nobody's signing up for that.
And same thing with Calipers.
We don't know exactly we're making assumptions and equations.
Same thing for food.
Maybe you don't know exactly how many calories you're consuming,
but if you're tracking everything the same way over time,
if you're not losing weight and you want to,
then you need to eat less calories,
regardless of what you think it is versus what it actually is.
So I find this hand-wringing argument is kind of an excuse
as to why people, well, that's why I don't track calories,
because it doesn't matter.
And then, now that being said,
there are standard values in the USDA database.
If I create a food product tomorrow,
I don't have to throw it in a bomb kilometer.
I don't have to do that.
I don't have to go get my own Keldahl analysis done.
Now, I can, especially if I want to show something,
but I can take, if it's a multi-ingredient food,
I can just take the weights of each ingredient and say,
okay, here's what the calories, carbohydrates, and fats and protein should be.
You can do that.
That's accepted.
And there are companies who have misrepresented things.
I remember, I know Lenny and Larry's cookies got looked at
and they had way more calories in the,
and they were claimed on the label.
There was this company, which wasn't available in stores,
they were selling them through their business,
and these high-protein brownies,
high-protein, low-carb, low-fat,
claimed to have 17 grams of protein,
12 grams of carbohydrate, 3 grams of fat.
Had a client that couldn't lose weight,
team-biling client couldn't lose weight,
and we found out she was eating like several of these brownies per day,
had them analyzed in a food lab.
You know what the actual macros were?
Three grams of protein, 50 grams of carbohydrate,
and like 17 grams of fat, I want to say.
It was basically just a regular brownie at that point.
Just a regular old brownie, right?
And I put out that video and the company threatened to sue me.
Yeah, I bet they did.
Yeah, which I didn't do any more follow-up videos, but I didn't take it down.
I don't want to get a lawsuit either, but I'm kind of like, if you want to sue me,
then you go right ahead if you think this is going somewhere.
Yeah, yeah.
You know what discovery is, right?
It's where they have to prove that they are not lying, and that's not going to work if they
know that they're lying, right?
That's called a bluff.
Right, exactly.
It's too bad that some people decide to lie.
Not saying that they did.
Some people have decided to lie.
Some brownie companies.
Yeah, maybe they just accidentally dump sticks of butter in there.
Who knows?
But what I'll tell people is like, if you're having trouble losing weight
and you're consuming some of these like lower calorie non-single ingredient foods,
it's probably more likely that some of them may be underestimating the calories
that are on the label versus you violating the laws of thermodynamics.
Yes.
And a lot of people do things like they don't count sauces and they're putting 50 grams of mayonnaise
on sandwiches throughout the day.
I'm curious if you can do one last thing, which is name some quick ways that my listeners can spot science-washed supplement marketing here in 2025.
What are some of the common, like, oh, this says this, and you're like, that's meaningless or that's just hype?
Typically, the veracity of evidence is inversely proportional to the number of exclamation points used in the marketing.
The more extreme to claim, the more likely it is that it's bullshit.
I tend to use what's called Hitchens Razor, which is from Christopher Hitchens, where he said,
extraordinary claims require extraordinary evidence.
So the amount of evidence you should need to support whatever it is your claiming should be
proportional to how big your claim is.
And that which can be asserted without evidence can be dismissed without evidence.
So many times people will say, well, you can't prove that it doesn't do this.
I'm like, uh, yeah, I also can't prove there's not a teacup orbiting Saturn for sure.
But I feel a high degree of confidence that no teacup is orbiting Saturn.
And just as a primer for people, a quick 60 second on how to spot bullshit, listen to less of what people say and more of the way they say it.
Which, if you listen to how I was talking in this interview, very few things were black and white.
I was giving you a lot of context, a lot of nuance.
I was even giving you the devil's advocate argument in several of these cases.
but then I gave you the reasons as to why I thought my argument was better or superior.
And so that's how experts talk.
Experts don't use the following words very often.
Always never best, worst.
And it just don't talk like that.
They just don't talk with like fear, to invoke fear,
which is exact opposite how most social media people do things
because the best way, the absolute best way,
to get what you want from somebody,
is an emotional response
because people do not buy based on logic.
They buy based on emotion.
That is how you get somebody invested.
This happens in politics.
People appeal to emotion.
It happens with the regular media.
They do stories that make you angry,
that scare you because they know,
even if you say you hate them,
that you will watch.
Because I think a lot of people are addicted
to being pissed off these days
or being scared or worried or what.
whatever it is. It's why horror movies are so popular, right? Like, people want to get that big
cortisol rush. They want to get, like, anxious. And I say this all the time. The news cycle.
People complain about all they do is show of negative news. That's because you want negative news.
I'm sorry. If everybody in the planet stood up tomorrow and so we're not taking this shit anymore,
we're not going to watch unless you actually put on some positive stuff. I promise you,
in a couple of months, the entire news cycle would flip. But it's not going to happen because I
I think human beings are inherently attracted to things that emotionally ramp them up.
And if somebody who's really an expert, is not going to try and get you emotionally charged up.
They are going to present the data and then let you make sure.
Even when they're like saturated fat, which I said, I changed my mind on.
I didn't say, don't consume any saturated fat is going to kill you.
It's toxic.
I didn't say any of that because I don't think that.
I do try to limit it.
But that's how I talk.
That is a measured way that a real expert talks.
I think one of the hard parts for people to understand is real experts actually sound unsure.
Whereas there's a quote from Bertrand Russell that is one of my favorite quotes.
And he said, the whole problem with this world is only fools and zealots are sure of themselves and wise people are filled with doubts.
So look for people who sound unsure of themselves and who give you a lot of context when they're answering a question.
That's right.
Yes.
And you've done that on this episode. Thank you very much. I really appreciate your time, man.
Thanks, Jordan. Appreciate it, man.
What a master of the art of communication. Charles Duhigg, author of Super Communicators,
reveals key strategies for enhancing your connections and conversations and this enlightening podcast episode.
Why do some people manage to connect with everyone else so effortlessly? And then there's times when I talk to my wife and like,
we cannot connect with each other. And it turns out it's just a set of skills, right? Like it's just literally a set of skills that super communicators
know and that any of us can learn and become super communicators ourselves.
Looping for understanding.
It has three steps.
The first is ask a question, preferably a deep question.
Secondly, repeat back what you just heard the person say in your own words.
And thirdly, and this is the one everyone always forgets, ask if you got it right.
And the reason why this is so powerful is because it proves that I'm listening to you.
It's really easy to stop thinking about how we're communicating.
It's really easy to stop thinking about what's going.
on until we get in the habit of it.
Communication isn't something that happens just one to one.
Sometimes it's one to many, but the same principles still hold up.
You're still having practical or emotional or social conversations.
Laughter is actually one of the non-linguistic ways that we connect with other people.
There's been studies that show that in about 80% of the time when we laugh, it is not in response
to something funny.
It's because we're basically in a conversation and we're saying to someone, I want to connect
with you. Nobody is born a super communicator. That's what feels tiring is when you feel like you want to
connect and you can't. Right. This isn't a behavior. This isn't a personality type. This is a tool that
once we learn we can use when we want to use it. Learn how to categorize conversations,
improve active listening and overcome communication barriers to build stronger relationships.
Tune in and transform your interactions into meaningful connections on episode 963 of the Jordan
Harbinger Show.
That was Dr. Lane Norton, and man, this one is going to stick with me next time I stared on a menu pretending to eat clean.
Big thanks to Dr. Lane for bringing the receipts and not just the reps.
I love how he takes the emotion out of nutrition without taking the humanity out of it,
because it's one thing to read studies and another to actually live this stuff day in and day out.
We covered a lot.
Protein myths, diet soda, panic, fasting fads, the fine line between science-based and science washed.
And if you're listening to this while pounding your fifth scoop of weight protein,
maybe take a walk and let your kidneys know you love them.
All things Lane Norton will be in the show notes on the website,
advertisers, deals, discount codes, ways to support the show,
all at Jordan Harbinger.com slash deals.
Please consider supporting those who support the show.
Also, our newsletter, We Bit Wiser.
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Jordan Harbinger.com slash news is where you can find it.
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In the meantime, I hope you apply what you hear on the show so you can live what you learn.
And we'll see you next time.
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