The Root Cause: Links Between Insulin Resistance & Disease ft. Dr. Benjamin Bikman || #96


(light electronic music) – And that was when
the whole thing started to kind of crumble. And I had to realize
that my own opposition to saturated fat was
because of the findings from artificial models, where we were explicitly infusing or directly treating saturated
fat into these situations. And that is not the same as
a human eating saturated fat. Those two, that is not analogous, that is not a fair comparison. So I had to not only realize
that flaw in my own findings, but I also had to then be open minded to what was happening from the whole human physiological perspective. – [Geoff] Hey, friends,
this is Geoffrey Woo here. Thanks for tuning in to this
week’s episode of HVMN podcast. One topic that’s come up often in 100 plus episodes of the podcast is insulin resistance. A growing body of data
suggests that insulin is an important metabolic driver behind diseases like diabetes, neurological conditions like Alzheimer’s, and even some forms of cancer. Today, I speak with Dr. Benjamin Bikman. He’s a professor at BYU, who’s an expert in insulin and ketosis. He also personally practices
a low-carb lifestyle, and we nerd out about
different dietary, fasting, and exercise routines. Ben and I discuss the role
of social media for science, what true physiological
insulin resistance means, nuances of ketosis, and how
ketones are metabolized, and some of the debate between
the calories in calories out, versus the carbohydrate
insulin model for obesity. – [Brianna] Hey there, listeners. Dr. Brianna Stubbs here. By visiting www.hvmn.com/pod, you can get 15% off our HVMN
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and sharing the show with your friends are just as appreciated. Without further ado,
enjoy this week’s episode of the HVMN podcast. – Professor Ben Bikman, great to have you on the program. – Hey, Geoffrey, thanks so
much for the invitation. I’m delighted. – I think there’s a lot
of ways we could go on about the conversation here. Obviously, you’re well-known researcher in the field of ketosis, ketones, all things
low-carb, and all of that. And I think, there’s a
lot of different ways to slice it here, but I think one of the ways that I want to just start
off the conversation is that, I see is one of the most
prolific communicators on Twitter posting science papers, and communicating to sort
of the average population. And perhaps, the way I start it off is, what do you think the role of social media is in this new role of academic research? And why have you adopted that channel as a communication platform? – That’s a great question. And it’s relevant because I
was increasingly frustrated, especially as a scientist
who was studying something that people cared about. It is relevant that it’s my great fortune to study something that people care about. I’m in a hallway at BYU of scientists who study really neat stuff, but not a lot of people care. You know about much of
what life scientists study. And through just a series of
fortunate accidents in a way, my research interests
focused more and more on insulin and insulin resistance. And mind you, it’s kind of funny the way you mentioned that I’m, sort of, a ketone scientist. Even that is because I still I’m really at my heart an insulin guy, and that the two are so connected that it was just a logical progression for me and my research interests to
get into that realm of ketones. But again, the foundation was and always has been my interest in insulin, and its relevance in disease, in the origins of most chronic
non-infectious diseases. But specifically to your question, with regards to social media, my good fortune to study something that most people care about, and yet within academia, so much of what we publish
stays in the small little, very insular world. I’ll publish a paper, the only one who ever sees it
is these 10 other scientists, and I’m the only one who
ever sees their stuff. – [Geoff] Right. – And we go to an academic
meeting and give a talk, and it’s generally the same
people just nodding along to the same kind of information we already generally know about. And I thought, the more I would go and give a talk somewhere, whether it was a grand
rounds talk at a clinic, or hospital, or whether
it was to a public, like a Rotary Club, within a nearby city, or something, people cared about this. And I thought, how can I share this outside of the conventional methods, outside of my own classroom, or outside of my own manuscripts? So social media, of course, was the low hanging fruit. And my aim there became not
to promote my own ideas, I hope, but to objectively
share the most relevant research in real time as a paper
would get published if it seemed to be relevant
in this metabolic insulin, ketone context, that so
many people care about, and that I care about as a scientist, I thought this is an easy way to share it. So sharing a little, kind of, snapshot of the abstract, often with some sort of one
or two sentence description of the study to make it
very palatable for the user or the person who would see it, that became something I was interested in, and have continued to do. So really, it was just
a method to disseminate the latest most relevant research, just so people can stay informed, frankly, and not feel like they have to devote time on PubMed or Google Scholar every day, and finding these things on their own. – I think one of the most
important pillars of academics is, how do you communicate this in a way that’s practical for normal people? Because a lot of the funding
bodies are government funded, or military funded, or nonprofit funded, and that requires buy in and
momentum from everyday people. Otherwise, we don’t want
to be in a world academics are just some scholars in an ivory tower that are not doing some real stuff. And I think that’s kind
of the critique from folks that don’t quite understand
what valuable work researchers are working on. But I also see on Twitter, and you’ve probably have
seen this on ancillary to the low-carb ketogenic
diet versus, the carb diet. I guess it’s a calories
in calories out folks, versus the metabolic
advantage of ketosis folks. It’s also that dark side of social media, where there’s almost a
holy religious war of, is keto the best thing ever, is keto the worst thing ever? I’m curious to get your take
on the polarization side of social media, and how that’s impacted, or does that impact how you think about science communication? – It is relevant to note that they’re, even within this few
minutes of conversation we talked about, there is that lurking
kind of war in a way, hopefully, it’s not a war, but certainly a war of words in a way. But they’re the sentiment that the metabolic plagues of society, obesity being the obvious aspect of that, is it purely a function of
calories in calories out? This kind of perfect thermodynamic model. And then there’s others who would say, “Well, no, it’s an endocrine,
it’s a hormone-driven model.” And mind you the ketone, I would summit the ketone
aspect falls under that. To me, my very first step
into a non-academic meeting was speaking at Low Carb
Breckenridge two years ago. And it was to touch on that very topic, which is that, my sentiment is that the endocrine model of
obesity actually incorporates the thermodynamic model
of obesity in so far as, especially relevant with
David Ludwig’s paper, just published a couple weeks ago, when you put a human into a
condition where insulin is low, which would also mean ketones are high, that’s going to be
consequence of low insulin, you are increasing metabolic rate, and that’s what David
Ludwig’s papers showed. And Kevin Hall’s paper showed that too oddly a couple years ago, that the humans in ketosis had significantly higher metabolic rate. And my labs research
over the past two years, we’ve just been waiting to publish this until we had more human data, but we have data from adipose cells, we have data from rodents, and now from humans, where we’re taking abdominal subcutaneous fat biopsies of humans in and out ketosis. The ketones are stimulating
the metabolic rate in fat tissue. So the fact there is, when we try to balance how
can the endocrine theory, I mean, how can I be justified in saying the endocrine theory of obesity is that hormones control fuel used and thus have a strong handle, basically, control the
levers levels of obesity, that encompasses the caloric, or thermodynamic model, because we introduce a new
aspect of calorie expenditure. In fact, when you’re in ketosis, I would submit, you
introduced two new aspects of caloric expenditure, in that if ketones are elevated, you are one, increasing metabolic rate by enhancing what’s called
mitochondrial uncoupling in the adipose cells. And that’s fascinating. We can talk about that if you’d like, and you understand it. But you increase uncoupling, which means that the cell is basically wasting energy as heat, which sounds bad, but it’s favorable when it
comes to body weight control. But then you also have the literal wasting of energy in the form
of ketone derivatives that are exhaled, or urinated, or even eliminated through
sweat in the form of acetone. – [Geoff] Acetone, right. – Yeah. You have this explicit elimination, and someone would say, “Well, so what if you’re breathing out, “or urinating, or sweating out acetone.” Well, the so what is, where did that acetone come from? It came from fat. We’re literally cleaving the fat molecule into little pieces through
the process of beta-oxidation. In fact, it’s happening so
much when insulin is low. Fat oxidation or fat
burning is so high that we almost are burning
more fat than we need. If you think about energy, we should only be breaking down molecules. Our catabolism should only be matched energetically speaking
with how much ATP we need. How much energy does the cell
need to get the job done? All right, we need this much energy, so let’s break down that
much nutrient to get it. But in the case of low insulin, we just keep burning through the fat, and yet we’ve reached our ATP target, and so you could, I submit the extra is the body saying, Well, we’re burning more fat than we need, so we’re going to turn the access into ketones because we
have a way to get rid of it. And so we’re literally breathing out these little pieces of a fat molecule. And mind you, that doesn’t
account for a lot of energy, but it’s still energy
that must be considered, if the caloric proponents are so staunchly not giving any ground. That’s fine. Let’s just say, okay, the middle ground then is that, we need to account for these two other methods of energy
loss when hormones are, what I would say, in a state favorable to fat loss which is low insulin essentially. The increased metabolic rate
from mitochondrial uncoupling, and adipocytes, and the acetone loss, which those are carbons that we’re losing, that could have been used as energy. We’re not talking like carbon dioxide, which is the spent sign
of energy if you will. But they had the potential to be energy because they could have gone to acetone, or could have gone to
beta-hydroxybutyrate. And then all it would have been if it was beta-hydroxybutyrate, one step back to the pseudo acetate, now you’ve got energy
again that you can burn. So, anyway, for me, it’s not me trying to be diplomatic, it’s me reconciling my own findings as a PhD in bio energetics, which is the study of
energy and neo organism. And then this growing appreciation
for the human evidence, especially, that finds that
if you’re controlling insulin, you really do seem to have
this flexibility with calories, where it doesn’t have to be, where you can have someone
whose put on a diet, and this is, multiple papers show this. They split the people up, you’re on a calorie
restricted low-fat diet, you’re on a calorie
unrestricted low-carb diet, and these people still lose more weight, despite eating potentially 200
or 300 more calories a day. And that matters. – We touched on a lot of
different topics there. I want to talk about
the metabolic advantage. I want to talk about mitochondrial uncoupling and acetone loss. And I think when people
think about those subjects, I think they talk about it in this context of metabolic advantage. I want to unpack that a little bit, because I think from a weight
management perspective, mitochondrial uncoupling, seems we’ve favorable. But I think on performance perspective, do you want to be lose energy? – [Benjamin] Yes, exactly. – And I think that’s an
interesting discussion to talking about. – That’s exactly right. Yeah, I love that Because people always want to talk about, “Hey, take this product, “then it helps your
mitochondria be more efficient.” You literally will hear
that in the advertisement. And I’m thinking, well, if you want weight loss, that’s the last thing you want. You actually don’t want your
mitochondria to be efficient, because if your mitochondria
in your fat cells, let’s say, are perfectly efficient, they will go back to that idea. They will only use as
much energy as they need. So they’re never going be use any more. But if you have your adipocytes, your fat cells are inefficient, like I’m proposing happens in the evidence supports the ketones are inducing, well then you’re burning
through energy like gangbusters, and you’re just wasting it as heat, which is fine, that means
increased metabolic rate. But to your question, our data shows that the uncoupling that ketones induce in adipocytes, it does not happen in
myocytes and muscle tissue. And we have this from isolated muscle cell cultures and rodents. In fact, we published
this earlier this year, we found that there was no change. In fact, if anything, the ATP production for
every unit of oxygen used went up this P to O ratio, that production of ATP
per unit oxygen consumed went up as the muscle cell was fueled with beta-hydroxybutyrate. And when we insulted the
muscle cells with molecules, just to induce some kind
of muscle cell damage, they were actually more
resistant to damage, and survived better in the
midst of this noxious stimulus. So what appears to happen, at least energetically at the adipocyte, does not happen in the muscle cell. And in the muscle cell, you in fact do have greater efficiency, whereas in contrast, in the adipocyte you
have this inefficiency. So metabolically speaking
and performance wise, it’s a perfect situation. – Yeah. I think that’s a level that I think a lot of people don’t get the nuance. I think you explained it quite well there. Then when I think about
metabolic advantage, I oftentimes think about, if you remember, I believe the Veech paper, and I think ’96 showing that
you increase the electron span between site one and site three of the electron transport chain, burning PHP versus glucose. And there was, so they increased
delta G of burning ATP, as more the more primal ways of how you could talk
about metabolic advantage. So I’m curious, when people bandy about that term. What notions do you think about? What do you think are the
dominant characteristics here? I mean, I think it was
instant result that you said that you see mitochondrial uncoupling in adipose tissues but in myocyte, which is kind of cool explanation of why you see enhanced performance, and also enhance a weight loss, where is that, oh, you’re just burning energy, or wasting energy, but that which could be
used for a performance case. – For me, I use the term
of metabolic advantage to someone being in ketosis, what you just mentioned. Specifically the idea that, to me, it’s an advantage, that you have more wiggle-room,
calorically speaking, where you don’t have to ensure, all right, I eat 1600 calories today. And as long as I expend more than 1600, and I’m going to be losing weight. What a horrible way to live. I don’t know anyone who
keeps that up long term. Calorie counting is tedious
to the point of insanity. So, for me, the metabolic advantage, when I use that term, I state that in the
sense that I mentioned, and you’ve mentioned, which is, you don’t have to
be counting every calorie you’re getting in because
you have this wiggle room. You have this ability to
be a little more liberal into truly just eat until you’re full as has been done in
human clinical studies. I’m not making that up. They just tell them eat
as much as you want, just restrict your carbohydrates. That’s what they’ve been told. I can think of three manuscripts
at the top of my head, where that was the explicit instructions. And the low-carb ad
libitum eaters outperformed metabolically the calorie
restricted low-fat eaters. That to me, is a metabolic advantage. – I feel like when you actually
dive into the literature of someone like Kevin Hall at NIH pub, who I would say is more in the school of calories in calories out. I feel there is some
middle ground that people, all could agree on. But I feel on the Twittersphere
it is very polarized, can we still man the calorie
in and calorie out arguments? I think you mentioned Kevin
Hall’s paper a couple years ago. I think he saw a modest
increase in metabolic rate. But for some reason, he kind of hand wave that away, as saying, “Oh, it’s not significant, “and therefore calories are dominant. “And this keto stories
is not super compelling.” – Yeah, and I would be okay. I actually don’t mind that he or anyone came to the conclusion. But can we still man that argument. In a way, I think we can say, I’m comfortable saying calories matter, insofar as, this is energy
that must be accounted for, and there’s no getting away from it. And my simple position is that, in hormones, it would be adding this. And hormones drive caloric use. In other words, hormones dictate
how the body uses energy, is it storing it, or is it expending it? And if it’s expending it, are we considering all of
the ways that it’s expended? The uncoupling which would mind you be, that would be encompassed in someone measuring metabolic rate, and I would contend that any study that has shown increased metabolic rate and low insulin states, it’s probably through this
adipocytes uncoupling. And then also making sure we
account for the wasted acetone, which again is breath, urine and sweat. But this goes beyond David
Ludwig’s and Kevin Hall’s papers. My initial interest in
pursuing this hypothesis of insulin versus ketones
in all three metabolic rate through brown fat, was actually based on research
from Jocelyn and Benedict. And so, we’re talking 100 years ago. These extensive studies
in the type one diabetics, they would see metabolic
rate would be remarkably high in type one diabetics that were untreated, and what happens when
insulin therapy was used. And this is in type one diabetics and in type two diabetics more recently, metabolic rate goes down. – [Geoff] Crushes, yeah. – And so, to me– – [Geoff] Interesting. It makes sense. – It really fits, exactly. I would see these papers, and I would think, could it be the ketones? And then I’d seen, I think it was one of Veeche’s
manuscripts in rodents, finding this enhancing coupling, and I thought, well, let’s just
kind of run with this idea, and see how deep it goes. And sure enough, we have
it in all three levels, isolated cells, rodent adipose, and human adipose, increased
expression of uncoupling, and mitochondrial
biogenesis related genes, likely due to this reduced insulin. That’s part of it. And of course, powerfully
the increased ketones. But you can’t eliminate
the insulin from this. We want to say, well, it’s
just the increase ketones. And until someone does a study
whether increasing insulin, and giving them a ketone, like a ketone ester, we can’t say that it’s just a ketone, because whether– – But you can’t unpack yet? – [Benjamin] You can, yeah. – It’s deflated, right? It’s ketogenic, it’s like
your eating ketogenic diet. So it’s just like, okay, basically, you’re
forcing high ketones low insulin at the same time. But can we play it the opposite, or can we play it both at the same time? – That may be a question
to ask with the kind of birth of this widespread
use of exogenous ketones, that may allow us to
tease that apart and say, well, are the effects of ketones just because of the ketones themselves, or does this have to happen
in the state of load insulin? And frankly, I bet it’s
somewhere in between, I bet without a doubt, insulin will inhibit those same genes that ketones are explicitly activating. And so, I think there was going to be some kind of moderate
middle ground in that context. – That in the sense I want people ask me, can you replace a ketogenic
diet with the ketone ester? I was like, “There’s going to
be overlap on the indications “that they can both treat.” But there’s also different effects, right, with a ketogenic diet. The carb restriction is probably even something that exogenous ketone, like a ketone ester is not doing, and vice versa. – Yeah, in fact, I would submit that I bet the most relevant, at least obvious
application of that is going to be neurological disorders, where we have certain
neurological disorders that are linked to a
glucose hypometabolism, whether that’s a result of
insulin resistance or not, and to a degree probably is. But the neurons, as you know, and listeners entirely know too, there are two fuel sources, it’s glucose or ketones. – Well, that’s smart. And you can also lactate
in some other things. – [Benjamin] Yes, that’s true. Yes, that’s true. – But, yes, I agree. The two dominant ones
are glucose and ketones. – When someone in a low carb state, or they’re taking ketones, let’s say, they’re not low-carb, but they’re suddenly
introducing this other fuel, well, now the brain actually
can use a fuel that maybe, if they aren’t able to restrict
their diet to that degree, to put themselves into
ketosis through ketogenesis, that’s an obvious application
even if they aren’t low carb to the point of ketosis. I would submit the most obvious relevance of an exogenous ketone is
the neurological benefit. And who knows what else? – Yeah. And that’s something we hope to explore. I want to get back to the diet debates. I think it is just an
interesting and applicable to almost everyone. And I feel like perhaps
one reason why some of the folks on the calorie in
and calorie out side is that, if you’re eating just 5000
calories of fat a day, you’re probably not going
to lose weight, right? So I think on the side of the keto crowd, or low-carb crowd, I think everyone reasonable
would realize that, yeah, calories matter at some point. If you’re just eating, 10,000 calories of fat a day, you’re not going to lose weight because you’ve so much calorie intake. But I don’t think anyone
serious in the low-carb keto space would be arguing, you can eat ad infinitum of fat, and still lose weight, right? – I certainly wouldn’t think that. Yeah, I don’t know, any
of the people that I know, they even have kind of most
staunch endocrine theory of obesity individuals. I don’t know. There are probably are some
who would say, you wouldn’t. But man, that’d be hard
for me to reconcile. But a part of me, there’s this kind of itch my brain, wondering whether someone’s
looked at that already, and tried to force feed higher lipid. I don’t know. I’m wondering whether
there’s similar University of Minnesota studies that did that. For some reason, it
seems like someone did. But, nevertheless, yeah,
my hope is that both sides are reasonable enough in a way. When you actually sit them down, and remove the kind of
polarizing binary environment of Twitter, and you sit
them down around a table, I think there’s probably
more common ground than not. I’d like to think. – It feels that way, when you read the literature. It feels like they incorporate both. And perhaps the differences of
how they weight the factors. They think calories matter more. They think the endocrine system matters. And I guess that’s where
the edge of science says, okay, let’s tease out exactly
weighting of these factors. – What I’d like to say is that, what I hope is that there’s
this teeter-totter of theories, and no one is ever trying
to force the one side down all the way. I myself lean more in favor
of the endocrine theory, simply because I believe the endocrine theory encompasses the
caloric thermodynamic theory. But that does mean I give credence to the thermodynamic model. I just think if we ignore the endocrine, then we’re not considering
a necessary aspect. – I think you put it really nicely there. I’d love to get that idea and notion out there because I think there is, just both aspects make a lot of sense, and how we can reconcile this. Right, its kind of quantum
mechanics and relativity, how do we have this standard
model of everything, perhaps of dietary nutrition? One thing that I’ve seen
you post a lot about, and I think this will be interesting for a lot of our listeners who
follow a ketogenic diet, or have been following carnivore diets, which has been a recent fad trend, we had a lot of most popular carnivores on our podcast recently is, does too much protein
kick you out of ketosis? – [Benjamin] Yeah. – And I think that’s when, something that I think a lot of the folks in the community just debate about. Too much protein, you get gluconeogenesis, that raises sugar, You’re going to get kicked out of ketosis. What is your opinion? What is your thought? What does the data tell us there? – So, in fact, I thought
so much about that. That, that was the subject of one of the only other few talks I’ve ever
given outside of academia. Because when I first
started taking my steps into low-carbs and in
ketones specifically, I was struck at how many people, I considered were eating
in a very bizarre way. And I joke, but it was
based on real people I knew. Or they were basically in a day eating almost nothing but MCT oil, because they were so
determined to stay in ketosis. And I thought, what a
bizarre way of eating, when people are just drinking oil. And I thought that’s not healthy, and it’s someone who’s chasing ketones. And they were doing that
because of their fear of protein in this idea, that protein will kick
them out of ketosis. It is so important to just appreciate the very basic biochemistry
which I believe is rational in a way. That it’s quite pretty easy
for people to not along too. But gluconeogenesis, or the process of the liver taking carbons
and turning them into glucose, that’s not demand-driven. If it were, you could
have someone who’s taking a whey protein shake, and they would become
dangerously hyperglycemic, and have this potential of a
hyper osmotic glucose to urea, where the glucose is so high for so much, 220 milligrams per deciliter
and above for so long. Then now it’s fully– – So you mean supply-driven? So when you take way does– – Supply-driven. I’m sorry. That’s right, yes. Yeah, you can push the gluconeogenesis into this hyperglycemic range. So, that’s one aspect of this. My contention that there’s
no need to fear protein. And in addition to that, if someone is activating gluconeogenesis, you can’t afford to have a
substantial increase in insulin, because insulin inhibits gluconeogenesis. And so, the two ideas are in
opposition to one another. If someone’s taking protein, you can say, well, it’s either going to increase the insulin, or it’s going to increase
the gluconeogenesis. And they may say, well, wait those are the same. No they’re not. If you’re increasing insulin, you’re inhibiting gluconeogenesis, the liver will potently
smash down gluconeogenesis because it doesn’t want to be creating– – Right, because insulin
sucks down sugar, right? – Yeah. It doesn’t want to create glucose and releasing it in the blood. It wants to tell the liver, and the muscle, and other
tissues to pull the glucose in. It wants to lower blood glucose
not increase blood glucose. So the way we reconcile all of this, and, indeed, the data supported, I encourage anyone to look at old papers from Roger Unger and Dennis McGarry, to look at this, especially Roger Unger. If the person is taking a
fairly large bolus of protein, like one gram per kilogram protein, if they’re in a low-carb or fasted state, there’s no significant
increase in insulin, none. The insulin just hums along like normal. And that’s because if they’re
in a low-carb or fasted state, they can’t afford to stop gluconeogenesis. And so, even if the protein and some of it is used to
create glucose, that’s fine. Who cares? We need it. We do need glucose, not because the brain needs it, I’m not going to say that. But we know there are
cells like erythrocytes, red blood cells, that rely on glucose to, they have a non oxidative
metabolism entirely. And so, regardless of what
cells may or may not need it, we have some that do need glucose. And still, thank heavens, that can happen. In fact, we need it. That if you’re not eating it, good thing we can make it. And if there was a
substantial bumping insulin for meeting protein, it would stop that process
when the person faints, or goes unconscious from, through genuine clinical hypoglycemia. So my response to that is, there is no need to fear protein. Someone should continue to eat real food, including meat, which is
high in protein, of course. And they don’t need to
fear they might going to get kicked out of ketosis. And I think the carnivores, the keto carnivores are a good example. A lot of them post their pictures before and after with ketones, although many of them get to the point of not caring about that. But I’ve seen enough do it, they don’t get kicked out of
ketosis when they eat a steak. They’re still very much in ketosis. In that much steak, Shaun Baker should be dying
from hypoglycemia in amber. They should be dying from hypoglycemia. They’re eating so much
protein from their meat, and they’re not only healthy, I would argue that they’re quite remarkably healthy, frankly. – [Geoff] Yeah, I mean– – So there’s the answer. Someone has to consider
what insulin is going to do to gluconeogenesis. And you can’t afford to
have this insulin spike if you are truly carbohydrate
restricted in your diet, because you can’t stop gluconeogenesis. And that means if insulin doesn’t go up, because it doesn’t want to
inhibit gluconeogenesis, it also isn’t able to inhibit ketogenesis, which is why if someone’s on
a ketogenic, low carb diet, the protein will not
kick them out of ketosis. – What do you think that mean came from? I guess perhaps when people are eating a mixed diet with some carb– – [Benjamin] Definitely. – And some protein, then
maybe you’re accumulating– – [Benjamin] Then you get– – A little of the carbon
and protein load together just to keep you out of ketosis. – [Benjamin] Yeah. And that is– – But we’re talking about
just protein and fat. – That’s right, yeah. It’s forgivable for people
to make that conclusion that, oh, proteins are always going to spike insulin inhibit ketogenesis. Because when you add protein
to a carbohydrate meal, you do enhance, you do get
that additive insulin spike. And so, I can see why we came
to that conclusion in general. But we came to that conclusion, despite the evidence that
existed from decades ago, refuted that idea, that if you’re in fact– – But that makes sense. That makes a lot of sense to me. Because I think when I’ve been wearing a continuous glucose monitor, I’ve just been thinking, I’ll see mild sugar spikes
when I’m eating meat, but I’m also realizing that I’m oftentimes when I’m doing that, eating some salad, I might have some little
bit of carbs in there. So it’s not a perfect
experiment, just on a personal, and equals one, right? – Yeah, that’s right. And even still, though. I wonder, did you ever measure
ketones before and after, and see substantial change? – When I was going on a
carnivore diet I didn’t go that deep into measuring
blood ketones for some day. – Yeah, usually people
step away from it, yeah. – I did a six-week block
of doing twice a day, finger sticks, for six
weeks on ketogenic diet. And I never went full
carnivore on that same block. I was thinking about doing that again. But it just ends up being annoying, when you’re traveling, and doing business. It’s hard to just pull out
needles and stabbing yourself when you’re on a business
dinner or something. – [Benjamin] Oh, yeah. – So what do you think of carnivore? I think that’s been interesting in terms of a fad diet that has definitely cuts, the attention of some mainstream media, where people have been conflating it from a Silicon Valley Bro
diet to something tied with the alt right? – [Benjamin] Yeah, yeah. – We have Mikhaila
Peterson on the podcast. And I know that her and her father, Jordan Peterson, have been big carnivores. And I think some people have tied Jordan Peterson to alt right, and made this whole weird shenanigan. – I’m fascinated by it. And when I learned that
Jordan Peterson did it, so, Jordan Peterson, not to change the topic too wildly. I’m also from Alberta just like he is. He’s from northern Alberta, I’m from southern Alberta, but same kind of small little town. So much of what he says, it’s so funny for me to people
lump him into alt right, because to me, it’s almost sort of a tough love of parenting. Everything he’s ever said, I think that’s what my dad told. And I was raised by a dad, and my mom died when we
were all quite young. So it was very kind of dad
heavy parental environment. And very loving wonderful father, but also just pragmatic to the point that everything Jordan Peterson has said, that to me, is just so
intuitive, frankly, his lessons. But nevertheless, the
fact that Jordan Peterson not only speaks such nuggets of wisdom, but is a carnivore, makes me think, hey, maybe there’s something to it. Because Jordan Peterson he’s no dope. And I suspect his daughter is neither. Anyway, to your question, explicitly, I’m fascinated by this
rise of the carnivore diet. I’m fascinated by it. And what I appreciate
about it is the simplicity. A part of me kind of envies just the true simplicity of such a diet, where you can just tell yourself, I’m going to eat these
things and nothing else. And I look at that and I
think, that really does. I mean, if you can commit
to that simple idea, it is in a way, just easier in a way than even a low carb-diet, because you’re always, with low-carb, you’re always kind of flirting
with the carbohydrates. You’re flirting with them. And how much– – A couple of knack carbs here, kinda squeeze by. – [Benjamin] Yeah, yeah, exactly. – Yeah, it is. – Exactly. That’s exactly it. That’s for me, the main appeal is that. Not that I am an anti
vegetable kind of guy, but I’ve really appreciated some of the sentiments
that have been revealed and expressed in social media around that, and the relevance of vegetables. But I appreciate the simplicity of it, where there’s just, no question. This is what I’m eating. And so you’ll eat it. It fascinates me. – How about the fiber story, the vital nutrients story. Obviously, when you talk to carnivores, it’s like, oh, maybe you
don’t need that much fiber. Maybe you’d actually don’t
want these vital nutrients. Maybe these are stimulated
immune response actually. – To me, a lot of the discussion of fiber and even polyphenols are
relevant to gut bacteria. That to me, is the obvious application, because not only do the polyphenols, they’re used by gut
bacteria, and the fiber. I think it’s nonsense
to think dietary fiber is necessary for bowel movements. I think that is laughably silly. To me, I think it’s as
a fuel for bacteria. And even then, you’d
say, well, then, so what? What do we need them for? To me, much of the benefit of bacteria, and now I’m not a gut bacteria guy. To me, it’s just a big black box. And too many people speak with
too much confidence about it. I get very skeptical because I don’t think we really know too much. – I agree. I think people make too
broad claims on it, yeah. – What I will say is this, much of the benefit to me, and gut bacteria is the production of short chain fatty acids, that we have the butyrate in the propionate, for example, that we just really don’t get in any other way except
the gut bacteria making it. And then that gets moved
into the bloodstream. And we know these short-chain fatty acids are very beneficial signaling molecules for mitochondrial biogenesis, and mind you, even
uncoupling in fat cells. And so, to me, the
polyphenols and the fiber, despite any other claims anyone makes, I like to think of it as those could be potential sources
of short-chain fatty acids from the bacteria. But then even then, do we need those short-chain fatty acids? No, you do not need them. And could someone get the
short-chain fatty acids in other ways? I actually deliberately drink a little bit of apple cider vinegar in water, because I like that acetate. And that’s a short-chain fatty acid. Mind you, exogenous ketones
are doing the same thing. In a way a pseudo acetate is basically a short-chain fatty acid. Mind you, it’s slightly altered structure, but even exogenous ketones
kind of check the same box, that to me, apple cider vinegar checks, and then it’s the source of
these short chain carbons that are going to basically
activate these same processes. But in someone who’s eating a conventional standard American diet, I would be vehemently say, eat fiber. To me, there’s little
question that’s going to help. But if you’re going carnivore, then maybe you just don’t need it as much. – [Geoff] You can get away with it. – Maybe, I don’t know. And I’m going to say maybe, just because I only want
to talk about science that I know is published. I hate making a claim, and I don’t think there’s any study on that – I agree, I think let’s
be proper scientist. I think we can speculate, and give some hypothesis. But, yeah, I think it. Just on a charted territory, I think a lot of people are curious about. Again, I think hearing from you, how you speculate about
some of these more untapped areas is interesting to hear. – [Benjamin] Yeah. – Another constant, I think this is more of an open area of debate and discussion
is constant ketosis or cyclical ketosis. Is there trade off benefits
for one or the other? I think there’s been some studies coming out of the Buck Institute, looking at cyclical ketogenic diets, have shown just as much improve longevity as constant ketosis. What are your thoughts there? Do you have a specific preference? I imagined this trade offs and benefit for both types of protocols. – I agree, I bet there are. I suspect whether there’s a true benefit, probably depends on the context. In other words, what is
the person going for? If this is a person who needs to control a neurological disorder, like seizures, or even migraines? In fact, I think the
very first publication looking at ketosis and
migraines was published in 1910. But to remarkable effect where, the study in fact is quite fascinating, not to go off from a tangent, but the physician noted, I think like 12 patients, and noted what happened from the moment they went into ketosis. And he actually adds
this little note based with each subject. And it’s fascinating to see
it would be something like, “Had frequent migraines three
times weekly for 10 years, “experienced an immediate
resolution upon entering ketosis, “and has not had another since.” This little blurb. And that’s powerful
stuff that you just don’t really get in publications nowadays. And another one he said, “Had two migraines daily for 15 years, “and has experienced three
in the following six months, “and has not had another one since.” Something like that. I mean it’s pretty powerful stuff. Nevertheless, back to my point, if someone’s trying to control a neurological disorder like seizures, or say migraines, then I think I’d say, don’t mess around. You just stay in ketosis because you’re probably going to trigger an event the moment you get out. And that does seem to be the case, at least, for some. If someone’s an athlete,
then I don’t know. I’ve kind of wavered on whether, like Zach Bitter, this really
kind of paradigm athlete, should he be stepping
in and out of ketosis? I guess the fact of the matter is, I think he does train
with some carbohydrate, and does exceptionally well. So I’d say for him and these
maybe endurance athletes, maybe that helps, if someone is trying to really lose a lot of weight, I would argue, all that’s going to happen and really bump up their
insulin is they’re going to stop fatty acid oxidation
for some period of time, because that’s what insulin does. However, I would say if someone is going to go in and take
a glucose tolerance test in a clinic, they will
probably be well-served by doing a bit of cyclical
ketosis with some carbs just to make sure they
stay glucose tolerant. And having disclosed that, I worry that some people would say, well, wait a minute, that means they’re also insulin resistant. Because so often, if you
are glucose intolerant, that means you’re insulin resistant. But I don’t think that is the case in someone who’s on a
low-carb ketogenic diet. I think they do start to become
somewhat less carb tolerant, at least for a period of time. But that’s not the same as
being insulin resistant. What I haven’t seen, or if I have I’ve forgotten, put someone into ketosis
through ketogenic diet, give them glucose. So often we just track the glucose, and yet it might take them longer to clear the glucose because they’ve kind of become glucose intolerant. But I bet their insulin
doesn’t go up nearly as high as the other person. And so it’s the seaming kind of disconnect and uncoupling from insulin sensitivity and glucose tolerance where
you can be insulin sensitive, and yet have induced this
glucose intolerance state simply because of such a
prolonged shift in fuel use. The person has been in such a
fat burning mode for so long. – All the enzymes shut
down for glycolysis, and it’s optimized for fat burning, yeah? – There’s almost this method of saying, well, I’m not using this pathway, I’m using this pathway. And so, wait a minute, now we got to use this one. Not only are we using it, but you just drink up 50
freaking grams of pure glucose. I mean, that’s more than a
little bit of pure glucose coming right into the system. I would suspect that’s enough, I hate to use these kind of terms, but you can forgive me for it, enough of a metabolic shock, that there is this glucose intolerance. And I would argue that’s not bad. If the person’s not eating glucose, they’ve just clearly switched
their body to fat oxidation. Why mark around with maintaining anti-glycolytic processes when
you’re simply not using them? I submit that is not the
same as insulin resistance. So when people want to
say the ketogenic diet is causing insulin
resistance, no, it’s not. It’s causing glucose intolerance. That’s what the research shows. Those are not the same thing. And so, I think if someone
actually has to go in, and they need to play the game of reaching typical clinical cut offs, you probably ought to start
cycling in some glucose, maybe a week or two before, just to make sure you pass that test so your doctor doesn’t freak out. – [Geoff] Yeah, interesting. – Or you just say, to
hell with the doctor, and you say, I know what I’m doing. But I’m not an insulin physician, so that’s not medically advice. I’m a scientist for heaven sakes. No one can listen to what I say in it. But I’m not a doctor, I’m not a physician. – We’re touching upon
a lot nuanced aspects of ketogenic diet fasting, ketones, insulin, glucose, and I think there’s one thing that I don’t think a lot people are articulated, is that, when you’re on a ketogenic diet or fasting for a long time, I’ve never heard this
articulate in your way of where it’s glucose intolerance
versus insulin resistance. But people will say that cycling glucose after a long period of a
ketogenic diet or fasting, there will be sort of
insulin resistance because you’re less good at pulling down sugar, because your enzymes and processor focus so highly on ketosis and fat oxidation. So your argument is that, it’s not appropriate to necessarily call
that insulin resistance has increased, it’s mainly
a glucose intolerance, and you’re going to have
some adjustment period where glucose is going to be
processed and broken down. – So when people say this is a physiological insulin
resistance, in a way, I kind of resist that. I mean, I can see what they’re saying, and I’m diplomatic enough to
kind of nod along with that. But even still, a part of me as an insulin resistance scientist, who looks at insulin
resistance as overwhelmingly a pathological event, I don’t like to say
carbohydrate restriction causes physiological insulin resistance. I would rather say it causes physiological glucose tolerance. And that may be semantics, but I would argue that’s
a better definition. But because there are actual
states of physiological insulin resistance such as pregnancy and puberty, those are the two known identified states of physiological insulin resistance, where it’s not pathological in origin. It’s not a result of someone
changing to an unhealthy diet. And it is, in fact, serving
a genuine physiologic need, where with pregnancy and puberty, these are the two exaggerated
states of human growth. This is growth at a level, at a stage, you just don’t
see at any other time of life, really, when a woman is actively growing the placenta and the fetus. That elevated level of insulin
helps promote the growth. I mean, it’s stimulating, not only lipid accumulation on the mom, so that she can have this energy reserved to be prepared to breastfeed, but also growing the
tissue of the placenta, and physically providing this
slightly hyperinsulinemic environment for the fetus
to stimulate growth. And the same thing goes with puberty, where we’re just stimulating this growth because insulin is a growth molecule, and it’s assisting in the growth. So that to me, is true physiological insulin resistance when,
if we’re physiological, that means it’s serving a good purpose. At least, that’s what we should mean in the case of saying ketogenic diet is physiological insulin resistance. I don’t like that, I
don’t think it applies. I don’t think it’s the same thing. I would prefer that we
all come to a consensus that I’m right. And that it should be called physiological glucose intolerance. (laughing) – This a good argument for that, right? Because with true insulin resistance, it’s much harder to re-shift out of that state versus
a temporary period of glucose intolerance. – That why I think that. I mean, it seems right. I mean, we’re two rational guys, and we agree, so this must be right. (laughing) – Of course, we know everything. This is Geoff jumping in here to share a really nice HVMN customer
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your own testimonial, just send us a link to
your audio testimony to [email protected] Hope to have the chance
to shout you out soon. Now back to the podcast. It’s kind of full circle here
around insulin resistance, your core initial area of research. And it seems to be that
idea that insulin resistance is such a core piece of so many diseases. You can make that argument
that insulin resistance, it has huge implications in diabetes, neurological implications, we talked a little bit about
glucose uptake disfunction, and case of Alzheimer’s, for example, obesity, maybe some cancers have some relationship to insulin resistance. And then you look at the historical case, where we, you know we’ve had
Gary Taft on the program, and you hear that whole story of around, okay, you see sugar
spike intake in society, and then you see all the
modern diseases spike. Again, that’s not necessarily
a causation argument. But there’s some smoke around there. And I’ve known, some
friends in Silicon Valley are saying that, “Insulin resistance is
basically the root of all evil.” Just curious to get your thought of it. – Yeah. So, oh, man, I’m just
tickled you brought that up. So let me just provide
some fun little context. So, here I am, during the course of my PhD with a wonderful PhD advisor at ECU, East Carolina, name Linus Dome, an insulin resistance guy. Then I kept seeing his
manuscripts getting published, and was so delighted to join his lab, and study the changes in insulin resistance pre
and post gastric bypass. And even then, I moved into my postdoctoral fellowship at Duke, this collaborative Duke Medical School, actually in Singapore of all places. So I move my little family to Singapore, and I study with another
incredible scientist named Scott Summers. Again, in the realm of insulin resistance, and in particularly, the biochemical causes. In this whole time, I’m thinking, really, the only relevance of insulin resistance is type two diabetes. And then obesity, my thought was, obesity is causing insulin resistance, which is causing type two diabetes. That was the paradigm. And I never even imagined there was any other directions and arrows here. And mind you, I’ve come to actually kind of flip those around a bit. But nevertheless, that’s
what I’m thinking. And then I get hired as a brand new assistant professor at BYU. So we leave Singapore, move back up into the mountains of Utah, which is great for skiing, mind you. And then, all of a sudden,
I’m teaching a class. The task that my department
of physiology department asks me to teach a class
called, pathophysiology. And I’m thinking, what on
earth is pathophysiology. I had a lot of physiology
background in the course of, my PhD was a lot of physiology, and biochemistry, but
almost all the context of metabolic diseases. But, nevertheless, I’m very
familiar with physiology. And so pathophysiology is the study of the physiological processes when they go wrong basically in the explanation and
identification of diseases. And so the class is about 100
nursing and pre-med students. So here I’m about to teach a class, and they give me a semester to prepare. And I’m thinking, I don’t know what causes fatty liver disease. I don’t know what causes heart disease. I know insulin resistance. And so, in an effort, as I was structuring the class, and I would go through
neurological disorders. I would go through
hepatic liver disorders, musculoskeletal disorders, all this kind of through the body, breaking down the most common diseases, and their physiological origins, or when things are going
wrong, so pathophysiology. And I’m so desperate to try to speak as an authority on this, because at the time, I’m one lecture ahead of these kids. I barely know what they do. And that’s the kind of
unspoken truth in academia, at least when you start generally, you barely know more than your
students at the beginning. And I’m so desperate to
come across as an authority, that I would think, as I was
preparing that first semester, I thought, I’m preparing the neurological disorders
lecture, for example. And I’m remembering some conference where someone talked about the link, how type two diabetics had significantly greater risk of dementia. And I thought, maybe I can
talk a little bit about that. And so, I would look in some
research there and be amazed. Wow, there’s a huge connection between insulin resistance
and Alzheimer’s disease. And then I’m looking at heart disease. And mind you, that connection is just overwhelmingly as strong. And same thing with fatty liver disease, same thing with musculoskeletal disorders, like osteoarthritis, and sarcopenia, or muscle wasting. Same thing with infertility, whether it’s ovaries or testes. There’s a profound link between altered fertility
functions and it’s resistance. And it just kind of kept going. And I was amazed and delighted, mind you, because at the end of each one
of these different sections, I could do my liver section, and talk about liver diseases. And then get to the end, and talk about the most
common liver disease, which is fatty liver disease, and say, “Hey, you know what, “let’s talk about some
of the actual ideology, “or the processes that cause this, “and look at how relevant insulin is.” And I found that I could kind of basically wrap up almost
every one of these topics, do the kind of genuine pathophysiology textbook version of it. And then have it kind of wrap up my way, which is, say, hey, insulin
resistance is highly relevant. And isn’t that great news? Because we can do something
about insulin resistance. It is so modifiable, so rapidly through lifestyle changes. And that started to really
shape the way I appreciated what I once considered
some very narrow disorder or insulin resistance that
was only relevant to diabetes. And then suddenly finding that you can take the most common cancers, breast and prostate cancer, yet strong connection
to insulin resistance, numerous neurological disorders, hepatic disorders, muscle, bone disorders, and seeing that most chronic
diseases can be linked, at least, explicitly to insulin resistance or insulin resistance is
exacerbating the condition, which is what I would
usually say, with cancers, insulin resistance is not
causing the prostate cancer, but it’s probably making it worse. It’s not causing the breast tumor. But when you think of
the average breast tumor has seven times more insulin receptors than the normal breast tissue, that’s pretty relevant. And so not only is it more sensitive to the anabolic signaling of the insulin, but hey, in the same situation, you’re also often hyperglycemic, and what’s fueled is cancer cells prefer the most, well, glucose. So you’re stimulating the growth, and you’re fueling the growth. Anyway, cancer is a
pretty hot button item, we don’t need to get stuck on that. But you can look at virtually
every chronic disease, some aspect of it will be exacerbated, if it wasn’t explicitly
caused by insulin resistance. And again, the good news of
that is when you can take any of these seemingly separate disorders, someone is taking a
hypertension medication, they’re taking a hypoglycemic medication, they’re taking migraine
medication, whatever. When they just wonder, could all of this have a
common metabolic origin with insulin resistance? I’m going to change my lifestyle to address my insulin resistance. I have seen this happen
so often in people, friends and acquaintances, where they get off every
one of their medications. I mean, four or five medications simply because they
addressed the one root cause. That’s good news for people. And that’s one of the
reasons I’m so interested to talk about it whenever I can. It’s because I want people to know, you don’t have to be
looking at all these things as different diseases, they’re not different trees, they’re just branches off the same trunk. – That’s super exciting. And I know that there’s
interesting discussion around the role of statins, are they reasonable
given if it’s metabolic origin for cardiovascular disease? Is a lipid hypothesis for, again, with the statin treats, is that the right approach? And sometimes I catch myself thinking, are we just too in Kool-Aid? Is the answers so simple, or if that you have one route ideology for all these conditions? I kind of want to pinch myself, be like, okay, what is a
skeptical response here? Are we being too neat and too cute here by answering all the disease? – Right. In fact, It is so necessary to say that. I try to be honest enough with myself to ask myself the same question. And in fact, heart disease
is a very relevant example. And mind you, there are people who could speak much more
lucidly intelligently on that domain, like Ivor Cummins, has devoted much more time to that specific topic than I have. But even then, so, I would say insulin is in each of these
disorders we’ve talked about, it is always relevant. But is it the only relevant disorder? No. Absolutely not. And some of them it is. If we take Polycystic Ovarian Syndrome, the most common form
of female infertility, yeah, if you get rid of the insulin, as far as I’ve seen in the data, you are resolving the problem. – [Geoff] Right. – You have absolutely
corrected the imbalance, and androgens, and
estrogens being produced from the ovaries when
you’ve lowered the insulin. Now, with heart disease,
or Atherosclerosis, is it purely insulin? No. I don’t think anyone’s going to say that. But I think a lot of us would say, if you’re ignoring the insulin, you are ignoring what could
be the most relevant variable, and if not the most, one of the most. – When I took on this journey of going through the literature that’s, it had got me personally
excited about a ketogenic diet and all of that, because you’re like, oh, wow, I gotta change my lifestyle. Otherwise, I’m just going to
die of all these diseases. But I want to still man
the role of carbohydrate. It doesn’t mean we should
all use sugars all the time. But what do you think are the appropriate use cases of carbohydrates? So I know for a lot of our customers, and a lot of our listeners actually are also professional athletes or athletes trying to improve, and break PRs, and all
of that, and glucose, unnecessary anaerobic fuel, a very potent readily available fuel. So given the context of longevity, and health, versus performance, is there just like a trade off there? And I think that might be
part of the conversation. Are we optimizing for performance so he can win the Olympics, or you’re trying to optimize
for longevity and health span? I think there’s one dimension there. And then there’s a dimension around is the way they cycle these things, or you use carb strategically, and then you use a
kitchen at strategically, or using exogenous ketones strategically to maximize some objective
function that matters for you specifically as an individual. – I agree with what you said. We really do need to just
ask what is the goal? And I think we can agree
that these modern day endurance events are really artificial. We can say that, hopefully
it’s not insulting. Frankly, I don’t mean to insult anyone. I have nothing but massive respect for the people who do these. But they are very fake situations. I can say the same
thing about my workouts. I’m not really much endurance guy, I’m much more of a calisthenic. I mean, why do I need to do muscle ups? That’s pretty fake. But I would say maybe it’s less fake. At least if I’m stuck in a pit, at least I have to do a muscle up to get over a fence or whatever. But even still– – How many muscle ups
are you doing in a set? – Oh, man, those are so hard. – They’re fun. – If I do them in the afternoon when I’m genuinely warmed up, I can do four with just
a little bit of kipping. If I kip, I can add a couple more. – [Geoff] Respect, nice. – Man, that’s pretty humiliating though, because I always considered
myself really good at pull ups. And then when I turned
40 a couple of years ago, I decided to stop weight
lifting for awhile, and just do calisthenics, because I’d always wanted to do a freestanding handstand pushup, always, my whole life. And I thought, I’m 40-years old. It’s time to freaking do this thing. And I’m still trying. I can’t keep the balance. But a part of that was also
adopting other aspects, like trying to do a planche, trying to do muscle ups, a back, a front lever, anyway, anyway. So– – Yeah. I distracted you there. I guess I was curious, because I like doing muscles by itself. I think it’s a great exercise, yeah. But I think, yeah, we were talking about the
role of carbohydrates, and how do we incorporate all
this stuff and performance, and all of that. – Yeah, in endurance events, where we have people just
running incredible races, and incredible events, I would say you probably do
need some kind of carbohydrate. Then I think even the most
Ketogenic of these athletes, like let’s take Zack Bitter, for example, who just
broke the world record for the 100 mile run. He’s taking carbohydrate during his event, and he’s even taking some
of it while he’s training. And he’s very, very
honest about what he takes and what he does. But he’s also decidedly a low carbohydrate ketogenic kinda guy. And so in those situations, I think and again, I would argue, those are very artificial situations where you’re creating a
need that might not be real. You know what I mean? Does that make sense? And so, if we’re talking about these remarkable feats
of human performance, yet we probably have created
a need for carbohydrate, because we’ve have a created– – [Geoff] I see your argument, yeah. – A situation. In the context of, does someone need
carbohydrate for longevity? I would absolutely say no. And that’s because as I
often do with my class, when I first start to present this idea, mind you, I actually tried to be diplomatic with my students. And I when I introduced
insulin resistance, I say what can we do? Change the diet to lower insulin. You can do that through a low-fat waves. Mind you, it’s just you have to step away from any processed foods, and you can kind of
get to that same point. But nevertheless, when I start to first introduce the low-carb aspect, that can be shocking to some. And that just kind of present
the situation I asked them, can you think of essential amino acids? Are there amino acids that human must eat? Yep, and all 100 of my
students are nodding along, “Yep, of course.” – [Geoff] Yep. – Are there such thing
as essential fatty acids? You can already see where
I’m going with this. And they’re nodding along, 100 nods. And they can begin to see where I’m going with this when I say, Are there essential carbohydrates? No. And people want to say fiber’s essential. No, it’s not. Not at all. Again, that’s a very
polarizing type of sentiment, but my hope is, anyone listening to this, before they want to start
throwing potatoes at me, this is a way of getting
carbohydrates in my diet, mind you I eat carbohydrates anyway. I’m a dad of young kids, it’s pretty hard not to. I’m not saying someone
shouldn’t eat carbohydrate. That’s not what I’m saying. But I am saying I don’t think it has any real role in human health, or human longevity. And I think we need look
no further than the fact that it is not essential. You can truly eliminate that entirely from a human diet as we
have seen done in people, as have been done, even in clinical studies
with Vilhjalmur Stefansson, for example, and not only all of the rise of all these numerous anecdotes from these keto carnivores today, and other human cultures
in existence still. We do not need carbohydrates, at least as far as I know. And I’m willing to be proved wrong. But the fact that there
is nothing essential to a dietary carbohydrate, that to me settles it. – But is that optimal? I think a natural extension is that now is that optimal? – I don’t think so. But that’s speculation simply because until we have a human
study that can truly, which is impossible, right? Track a ketogenic adherence
throughout their whole life, and track the low-fat, semi-vegetarian people
throughout their whole life, who’s gonna live longer, we just don’t have those kinds of death. – And control that. Put them in the same
kind of family structure, same environment, same everything. – Yeah, exactly. And someone wants to cite any of the kind of Seventh-Day Adventist’s
supported studies, looking at well, the vegetarians, are they living longer, versus omnivores? Not when we had studies that controlled for healthy user bias, they don’t. And moreover, the evidence
admittedly correlational that suggests in humans that
after the age of like 60 or 65, that LDL cholesterol is protective, that the people with higher levels of LDL have better health, and better mortality, longer living when LDL goes up. I would suggest that, mind you that’s not
going to prove any point, but as someone’s getting
further and further away from the essential parts of the diet, which is protein and fat, we can all agree on that. Those are essential. Anyone has to even
reluctantly admit that those are going to help LDL stay high, and helps the older person stay– – Which would shock the
standard cardiologists out there who are like, “You want to tell people “that increase LDL who are under 65? “You’re crazy.” – And I’m not necessarily
telling someone to do that. But the fact is, the correlational
evidence supports that. Numerous studies find that correlation. But could there be other factors involved? Absolutely. And it may not just be the LDL, but the correlation is pretty strong. – I think that’s almost its own episode talking about the LDL hypothesis, and how that relates to
cardiovascular disease. And is inflammation,
or instant resistance, is that more of a core driver. And I know that you
mentioned Ivor Cummins, and some of the other folks
have written a lot about that. – Yeah, Ivor and Dave, Dave Feldman. I wouldn’t be the one to
have that conversation. There are other guys who
are much more steeped in that than me. And frankly, you know what? These guys aren’t PhDs or MDs. These are what I call the PubMed warriors. – They’re software engineers, yeah. – The wonderful thing about that is just how egalitarian
science has become, that it is so accessible. All the stuff that we’re
kind of kicking around, I think it is so important
for someone to know that I did not step lightly
into this realm of low-carb. It was a very deliberate and kind of uncomfortable journey for me. I was as much an advocate
of the pure caloric theory, and saturated fat being
the devil as anyone. In fact, maybe even more, because in my studies, when we were infusing
palmitate into rodents, when we were treating muscle cells with palmitate that kind of
prototypical saturated fat, man, we saw some massive
insulin resistance start. And so I was as much an advocate of this traditional way
of thinking as anyone. And then it’s simply, as I began to appreciate
the relevance of insulin in disease more and more, and how insulin was
driving insulin resistance, elevated insulin driving
insulin resistance, and then driving disease, that started me looking
into human clinical studies that were separating
patients based on diet. And that was when the whole thing started to kind of crumble. And I had to realize
that my own opposition to saturated fat was
because of the findings from artificial models where
we were explicitly infusing, or directly treating saturated
fat into these situations. And that is not the same as
a human eating saturated fat. That is not analogous. That is not a fair comparison. So I had to not only realize
that flaw in my own findings, but I also had to then be open minded to what was happening from the whole human
physiological perspective, which shame on me, as a physiologist, I really hadn’t been appreciating. So, my point in saying all of this is, I went through my own journey of saying, okay, I’m not believing any more dogma. Whatever I have considered as fact, I’m putting away, and I’m only gonna look
at what has been published in human clinical
studies and nothing else. And that’s what took me to
the conclusion I’ve come to, which is hormones matter, and controlling carbohydrates to improve the overall metabolic or endocrine milieu elicits a
greater metabolic improvement, than strictly trying to control calories. That was basically my
conclusion in a sentence. And I’m okay if people disagree, especially if they have data, because they can show me a
study well, and I can say, you know what, that’s a good study. Here are my studies. And then we can kind of say, you know what, yep, maybe there isn’t a consensus in the fact that you’re
tipping more on this side, I’m tipping more on this side, let’s shake hands across
this subtle divide. But what I have no tolerance for, and this is especially
relevant as a professor, when I have my students that will say, “Dr. Rick I wanna disagree with you.” And I say, oh, isn’t that just so cute, that you think your opinion matters, when I’m talking about fact. So you can’t disagree with the study. You can try to find data to refute it, and until you do so, you
darling little undergraduate, and as I pat you on the head, and mind you I love my students, but I just have no tolerance
for that kind of sentiment. Don’t bring opinion into this. You can’t say I disagree with you. You can find a study
that refutes the study that I’ve shown you. Because I know this is
such a sensitive topic, I only ever show my students data. And again, I show the data
on both sides of this. I really do. I try to be even handed. But to me the some tips in favor of carbohydrate restriction, at least in the context of
improving insulin resistance as a vehicle for improving
metabolic health. So, I hope anyone listening to this, mind you, people who are listening to this are probably already generally on that side of the fence, if you will. Well, let’s not say fence, that’s too divisive, on that
side of the teeter-totter. But this is something people can find. And again, Ivor Cummins and Dave Feldman are such
wonderful examples of this. And Tucker Goodrich, and other guy who was very
active on social media, these are guys who don’t
have the credentials that people classically want to look at. And Geoff, I mean, you’re
a good example of this. These are people who’ve
become deeply familiar with the research, not because their degree
made them familiar, but because they just had such a drive and a curiosity to find that out. I submit that’s a better way to do it, because when you have to learn something because of your degree, you have to, to get through
your comprehensive exam, or your dissertation defense, you’re going to learn it, but with that little bit of reluctance, that means you’re going to
forget it soon after perhaps. When you have learned it
because it’s a passion, and you just learn to
navigate the resources, like Google Scholar, and PubMed, you can learn it all. And so, no one needs to ever just take me or you at our word. They should challenge this, and they should want
to know for themselves because then whenever
they find their conviction of how viable and real it is, it will be so much more. – I think there’s a kind sentiment. I think that is exactly
the scientific method, is not about degrees or credentials. It’s about talking about data. And if you have data that
proves me wrong then, then we’ll follow the data. That sounds like just coming
from how you speak about it. I don’t think we’re dogmatic, at least I know that it doesn’t
sound like you’re dogmatic about any one specific point. But there’s like a moving body of data that suggests something very different. Then there’s no reason why I would focus on the ketogenic diet or ketones, if there’s new data showing
that that’s going to kill me. – [Benjamin] Yeah. – I’m not trying to be suicidal, and I don’t think you are either. – [Benjamin] That’s right. (laughing) – And then, how has this informed
your day to day lifestyle? Are you constantly in Ketosis? Are you constantly low-carb? Has Your research informed
your day-to-day life? – Absolutely. And you know what, when it doesn’t, when a scientist hasn’t been influenced by their own findings, if it does have physiological
relevance to them, then they don’t really
believe what they found. To me, that really is just
sort of a truism of life. That if you have this conviction, this kind of testimony, that what you know is real and true, it ought to have altered your behavior. And I use this example with my students. When I was a PhD student, a lot of my classes, and all of my research was
that the medical school. (clearing throat) And I would have to bike
to the medical school and hospital on the other
side of the road because that hospital medical
school sidewalk was covered with all the nurses and doctors who were on their smoke break. They would have to leave
hospital grounds to smoke. And do you know if that doctor was going to go back into a medical
employment with a patient, and the patient had hypertension, and they see the patients
smoking one pack a day, the first thing they’d say is, “Well, you need to really
cut back on smoking.” And yet the hypocrisy as
the stench of their own cigarette is wafting
into the room with them. No, that’s a person who doesn’t
truly have this conviction, or maybe you could say, “Well, that’s balanced with
some addiction perhaps.” For me, the evidence in my own findings with insulin and now with ketones more recently are so clear, and have such a relevance
in human physiology, that I would not be doing myself justice if I weren’t adhering to some of this. So to your question, I am always low-carb. That does not mean I’m
always in Ketosis of course, and I appreciate that you
separated those two things. I’m often in ketosis as
frequently as I may check, which isn’t that often anymore. It was more often than I
first was experimenting. But a part of this is
just the practical aspect of me being a dad with young kids. Mind you, my whole family
is fairly low-carb. Breakfast this morning, for example, was bacon
and eggs, and nothing. But with my kids, mind you, they reluctantly ate the scrambled eggs, but they gobbled up the bacon. So bacon’s like breakfast
dessert for my kids. So, yeah, very rarely will there be a loaf of bread in my home, very rarely is their chips and crackers. And it’s just more real food as much as my wife and I try to do that, which again, with little kids
it’s easier said than done. You know what I mean? – [Geoff] Right. – And in a part of this
is me also being practical as a father in that, if we’re having family movie night, I’m going to eat popcorn with my kids. Actually, to be honest, not to let anyone indulge too much, I find that popcorn actually
doesn’t take me out of ketosis. I can eat a lot that night, and movie night, for family movie night, and I’m well into
ketosis the next morning. Nevertheless– – Metabolically flexible. – Yeah, exactly. That is a perk of, mind you, controlling carbohydrates. But when my daughter made
dinner for the family, and wanted to make
grilled cheese sandwiches, I always use this example. I’m not going to pick the cheese
off my daughter’s sandwich. “So, daddy?” “Yes, sweetheart. “Daddy can’t eat the bread, sweetheart. “So I’m just going to get the cheese.” No, that’s crazy. I’m going to eat my daughter’s
grilled cheese sandwich, and I’m going to smack my lips, and give her a hug and kiss for making it. So I would say I’m a very
practical low-carb guy, where when I can adhere
to a low-carb diet, and it won’t, especially in any way kind of affect my family dynamic, I’m going to do it. And then that means
breakfast and lunch for me are always low-carb, always. There’s never an excuse
for me to not be low carb at breakfast and lunch. It’s just so easy. Even if my kids have this
very rare indulgence, sometimes make this buckwheat rice mix, and they can eat it
with milk and cinnamon. I won’t eat that. I either I’m fasting that breakfast, or I’m eating something else. But breakfast and lunch
are always low-carb. And then dinner is often low-carb, but it kind of just depends
on what the family’s doing. I don’t want it to adversely
impact the family dynamic, where my whole family’s eating something, and I’m just sitting
there watching them eat. – You mentioned fasting. I’m curious to get your thoughts
on some of Satchin Panda’s work with circadian rhythms and fasting. Do you incorporate that as well
into your personal routine? So, to give you a sense
of my general protocol, I’ll cycle in and out of
strict ketogenic diet, and then I’ll usually have a
pretty tight eating window, and I do run a 24, or 36-hour weekly fast. So I’ll do a blend of fasting, low-carb diet, and then cycling in and out of a strict ketogenic diet. – [Benjamin] Yeah, that’s– – That’s kind of my, dependent on if that kind of
works well for my lifestyle. – I do the exact same thing, exact same, as often, I’ll do a 24-hour fast weekly. And that’s typically on a Monday, frankly, where I find the weekend, just having that outside
of my normal routine, and being around the family a little more. I do tend to indulge a little more. Although I hate to say it like that, the Monday, because it
almost is sort of reminiscent of the kind of eating disorder, where it’s like this binge and purge. But I don’t think that’s what it is. Well, if it is, I at least I’m justifying it, which is maybe terrible. – I’ve heard that comparison
with some reporters. They think it’s like an eating disorder. But I think my snippy
comment back is that, everyone being obese and over
eating is eating disorder. – Oh, no kidding, no kidding. – Right. So just, I think it’s
like we’re just trying to be sensible here, in terms of just, if we’re going to be repleting with plenty of glucose over the weekend, if we drink beers, or all of that, it is called sensible to deplete some of that glucose
that’s stored glycogen. I would just reopen the conversations. I would argue against
that eating disorder kind of poke at this, because this is, I think a
more sensible enlightened way of consuming. – Yeah, I agree. I guess I’m disclosing
that is a possibility because I can see how
it’s low hanging fruit, where someone just says, oh, well you’re doing, well, just what I basically just said. So I can see how some, mind you, I’d actually never heard
anyone else say that. So in a way, it is kind of validating that someone else would
have that perspective, even if they’re using it as
fuel against the low-carb diet. You’re right though. It’s obviously a lot better than what other people are doing, but I do it for the exact
reason you just said. I have to a degree loaded my
liver backup with glycogen. I just want to empty that back out, and to help my body get back
into a lipid fat oxidation mode as quickly as possible. And I find I also just appreciate
the simplicity of a fast, where I just tell myself I don’t have to make decisions about
food for the next 24 hours. It is in fact, I’ve heard a lot of people describe they actually do multi-day fast, which is something I’ve
never really embraced. In fact, well, I haven’t at all. But I can at least intellectually embrace other people doing it. I really appreciate the simplicity, where it just eliminates
some of the decision making for the day, where it
is I’m drinking water. And typically for me, when I am doing a 24-hour
fast therapeutically, now I also do it for
religious reason once a month, as a member of my church, but that’s different, when it is for this metabolic benefit. I will drink water, and I’m often just
spiking in a little hint of apple cider vinegar. And that’s not as much
for metabolic boost as, although the although the
apple cider vinegar may in fact do that. But I do it because I
just like the flavor. It just helps me keep drinking water. I’ve really come to appreciate
that little bit of tart. So typically on a Monday, it’s not uncommon
depending on the weekend. And just kind of depending
on how I’m feeling, I may or may not do a fast through Monday. But even then, it really is just to seek
this metabolic advantage of getting myself back into
lower-level of liver glycogen, and all the perks that come with that, which is ketosis and lipid oxidation. – Yeah. That makes a lot of sense. And I feel like I got
to get you to experiment with a longer fast. The longest fast I’d ever
done was a seven-day fast. – [Benjamin] Oh, man, no. I kind of– – Which is kind of a religious
experience in and of itself. But I mean, I think we could go on for another hour if we have the time. So I wanna wrap up with one last question. – Geoff, but before, one of the reasons I’ve been reluctant for multi-day fast is, I look at myself and think, right, I’m a middle aged man whose
main physical priority, as oddly as this sounds
with three little kids, I got a long game in mind. And my priority is I want
to be a healthy grandpa. And so I’m thinking, what’s going to help my health span? And that’s going to be maintaining as much lean mass as I can. And so with that kind of as a priority, maintain lean mass. I just can’t get around, now I have huge respect
for Dr. Fung, Jason Fung. And he really does
insist that there really isn’t this loss of muscle mass. And again, I really
respect what he’s saying, but yet, the academic in me thinks, well that’s impossible. How can there not be some muscle mass? And I bet if he ever listened to this, he’d be already thinking
of numerous mechanisms. And people want to invoke
growth hormone being up. But yet, I still think
at the end of the day, if you were in genuine
choleric restriction, how can the body not be burning some, expending some lean mass to fuel the body? I mean, it happens. And so, my reluctance in a multi-day fast, is simply because I just really shutter at the thought of losing lean mass, and I’m working so darn hard to keep it. (laughing) – No, I agree. And I think likewise, when I was doing some of
these longer fast experiments, part of it is in terms of, yeah, I want to maintain my
lean muscle tissue, obviously. And I think, I was about to just reference Jason Fung. And he sort of convinced
me around the notion of, on these longer day fast, the nitrogen that you excrete out of your urine actually
falls precipitously. – [Benjamin] Right. You start conserving. – So from that respect, you can serve your protein mass, and then you referenced
the growth hormone spike. He actually has working
with some athletes, that he’s trying to time
the growth hormone spike with heavier workouts. – [Benjamin] It’s clever. – So his kind of story is that, to gain muscle or to
maintain muscle you work out. And so when I was doing these longer fast, I was working out fasted. So I was like lifting heavy, which I actually maintain decent amount of strength doing lifts, but I just felt like I couldn’t run. My aerobic friends felt
really, really bad. And then this is not super scientific, but I was doing a DEXA scan, before and after a seven-day fast, and weekly, 36-hour fasts, for about a two month period. And, again, there’s a lot of data, and a lot of time span there, but I actually saw increased
lean muscle tissue, and reduce body fat composition. So I had a very similar concern as you, where I don’t want to
be melting lean tissue, it takes all this effort
to lift all these weights, all these calisthenics,
all these muscle ups. They build up some muscle, I don’t want to just be burning that away. – And you can see it, and frankly, Jason is a smart enough guy. And I mean that it doesn’t surprise me that he would have some justification and evidence to support that. It doesn’t surprise me. I guess even hearing it, a part of me just sort
of revolts to the idea. – I don’t do it that often. I mean, that last time I
did it was about almost two years ago now. I’m not necessarily trying
to do this all the time. It’s more of a just an
equals one experiment, just to get a sense of
how it kind of feels like. And then, of course, it was like sort of the longevity story, in terms of, kind of, vulture along those research around, can you recycle your immune system, and all of that stuff. – I think it’s worth
mentioning that when people invoke a lot of the benefits
of calorie restriction, and Mr. Valter Longo, perhaps protein restriction
more specifically, I think it’s not fair of them to try, with all due respect, and
I really do mean that, that’s not just lip service, with all due respect, and as scientists, part of me, can’t help but wonder, well, what happens when you continue to fuel the body with sufficient calories, and yet you’ve simply lowered insulin? That to me is the low hanging fruit that some people have
addressed in rodent studies. And then human studies, people aren’t quite as
willing to acknowledge that, Hey, you know what? Maybe it’s not so much
protein restriction. It’s magic. It could just be that we’re
restricting insulin activation. And that, to me, one of the strong, as we’ve already been
kind of talking about, I don’t do a ketogenic diet because I care as much about the ketones. Although over time, as I continue to do
experiments with ketones, I can appreciate them more and more as viable beneficial
molecules for the body. But my main motivation is keeping insulin in control for every
reason, including longevity. Because so many of the longevity studies are kind of skirting around this issue of, it’s just simply lowering the insulin. And so to me, I’ve not seen a
good evidence to refute that, that may in fact be the
mechanism of longevity. It’s not the protein restriction. – I actually agree with you a lot. I’m glad you brought that point up. I think a lot of the caloric
restriction benefits. I agree with you. I think it’s basically
lowering of insulin story, and the caloric restrictions, kind of this mechanism
of lowering insulin. But what if you could
just do that directly without being caloric restrictive with a ketogenic diet or something, right? – Yeah. That’s the magic. – And apparently in the primate
studies that showed that, they were comparing caloric
restriction, and a healthy diet, versus a calorie restriction, and an artificial high sugar diet. And the one results showed that there was no change of life span, for with a calorie
restricted healthy diet, versus a healthy diet for these primates, and the caloric restricted
unhealthy diet versus had improved lifespan, versus un-calorie
restricted unhealthy diet, which I think hearkens back to the point that you were talking about, that perhaps it’s really the
insulin as the driver here, not the calorie story. – I would say before we leave that topic, could there be a separate immune function or immune aspect of fasting? And I would say there could be, and I bet that is actually
through altered gut bacteria. When you’ve done, basically, we know that the gut bacteria, the whole microbiome, I say we know, and I think we know, I believe that basically kind of turns over every three days. And so, when you’ve gone
beyond a three-day fast, you’ve basically– – That’s interesting, totally. I’ve never heard of that before. – You basically starved
all of your gut bacteria, and now you have given
the growing appreciation of gut bacteria, and immune health, let alone gut bacteria
in your logical health. There could be something to fasting and specifically immune changes that go beyond insulin control, and has to do more with what have we done to the gut bacteria in
this prolonged fast, where if they aren’t getting
that roughage or something, and I don’t just mean referred from fiber, because even carnivores have gut bacteria, but you have maybe changed
the whole microbiome, maybe literally changed all of it, because they’re starting from scratch, because you’ve killed
off all the other stuff that had been in there, because they literally couldn’t
eat for however many days. So some of the immune benefit
may be partly a function of this genuine shift in microbiome that is because of the fasting itself. But then any of the
other longevity benefits, I think the big elephant in the room, the confounding variable is, well, what happened to insulin? – That is a primary driver. If I had to put a percentage on it, I think it’s probably through
the dominant factor there. – [Benjamin] Yeah. – So I want to the wrap
up with a final question. What areas of research are
you most excited about? I think you’re looking around ketones, looking out on insulin? What can we expect in 2019
coming out of your group? What do you think are the most
promising areas of research? – So, I’ve already mentioned, the obvious one that I think
will have the biggest impact, well, at least my own thinking is the one I mentioned earlier, which is the evidence that we’re finding, and hopefully will get
published this next year of ketones providing this
boost in metabolic rate, via increased adipocytes
mitochondrial uncoupling. So, basically, turning the white
fat of subcutaneous tissue, making it more so called brown fat, and then they’re more mitochondria and they’re more uncoupled. However, I’ve already mentioned that one, perhaps some other kind of most exciting area is what we’re finding
with neuroplasticity, which is kind of biochemical corollary or surrogate I should say, of learning and the ability to learn and create new thoughts, learning new skills, retaining new information. What we do in this model, is we take the rat brain
and make these slices, and I’m doing this as a collaboration with my colleague Jeff Edwards, who’s the brain guy. It actually started with
this idea of me saying, “Can we keep brain tissue viable “when we eliminate all the glucose?” Because there’s always this question that you can never answer
in an in vivo situation, which is, does the brain
actually need glucose, or is it just using it because it’s there? We know that with long fasting, than even I would say a ketogenic diet– – There’s always some glucose. – We always have glucose, so the brain is always pulling in some. But it shifts to majority
of beta-hydroxybutyrate as its fuel, and so there’s this predominant shift to Ketones. But then the question still lingers, but does the brain need the glucose, or is it just using it because it’s there? So that was part of the
original thought here. Can we keep the brain tissue viable in the absence of glucose, maintaining all the osmotic gradients, and just using ketones as a fuel? And the short answer so
far is yes, actually. – [Geoff] That’s cool. – But independent of that, we’re measuring this neuroplasticity, which is one of Jeff’s, kind of, one of his bread
and butter techniques, where we are, normally,
the classic kind of bath, when we put these brain
slices in this solution to try to mimic an in vivo setting. It is a very high glucose setting. Which is very standard
for almost any ex vivo or in vitro conditions. It’s always high glucose. And so, what we’re doing here now is just cutting down the glucose, and increasing the ketones to a situation that you would see in fasting, kind of this kind of three to
one or four to one type ratio. And what we see is that the
neuroplasticity is enhanced. We’re seeing a significant improvement in these outcomes
suggesting that the brain, at least with these assays, measuring neuroplasticity, is working better when
it’s fueled with ketones. And this certainly fits with the idea of people with cognitive decline, thriving when ketones are up. We’ve seen this in humans. There’s very little debate on that. It’s quite obvious evidence. This is providing a bit
of a molecular mechanism. So it’s pretty exciting. But because I’m not the brain guy, and Jeff is, that’s my
second most exciting. I liked the adipose mitochondrial
story a little more. But they’re both pretty provocative. – Well, when they’re out, I mean, that’s going to
shake up some of the scenes. I think those are pretty
astonishing results. That’s really cool. – [Benjamin] Yeah, it’s fun. – I think there’s a lot of
interest with the neurological, can you improve cognition
from a therapeutic side and also from an enhancement side? It was also very interesting to a lot of our listeners out here. – And, Geoff, you know what, I’ll say that is the beauty
of being a scientist. It is the glory of just
getting paid to ask questions. I mean, think how cool that is, I get paid to just ask questions. So if I’m not teaching my
class in any given day, I can just sit back in my office and ask myself a question
for eight straight hours, and try to find an answer. Then come to the conclusion, okay, no one’s answered this, let’s answer it if we can. And mind you, mind you, there’s not a lot of
money in being curious, so scientists don’t get paid too much. But it’s a glorious thing. What we lack in salary will make up for just true intellectual freedom, to just get paid to ask questions. And these two questions, are the result of just
me and some students shrugging our shoulders and saying, “Has anyone asked you this yet? “No one has. “Let’s do it.” – [Geoff] This conversation
is going to generate a lot of questions from our audience here. – [Benjamin] Good. – [Geoff] So, I mean, I definitely have to bring you back on the program
to answer those questions. Thanks so much. This is actually a really
fun discursive conversation. I mean, clearly a lot of
shared interests here. And I appreciate your depth and nuance in exploring these topics with us today. – It was my pleasure. Geoff, thanks for the opportunity to talk. I really enjoyed it. And like you said, having this common intellectual ground, always makes for a very fun conversation, especially when it’s grounded
with some justified evidence. – [Geoff] All right. Thanks, professor. – Thanks so much, Geoff. – [Geoff] Thanks for tuning
in this week everyone. Remember to check out www.hvmn.com/pod for this month’s special podcast offer. For December 2018, that offer is 15% off our entire HVMN performance supplements line. This is the perfect holiday
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