Dr. Benjamin Bikman – ‘Insulin vs. Glucagon: The relevance of dietary protein’

Thanks, Eric,
thanks for the introduction. Yeah,
I’m an insulin-mitochondria guy so what am I if half of this
conversation in insulin yes, I can talk about glucagon
will be the new character here. Before I get going though,
Jeff and Rod, thank you
so much for the invitation. I am
delighted to be here again. It’s fun
to be here now and see friendly faces as opposed to
like it was last year. But last year was my first time and when Jeff and Rod
reached out invited me that was my first step into the
low-carb community. And it has just
been delightful. I have
appreciated making new acquaintances
and some genuine friendships, and in fact,
as a scientist, I’ve really appreciated some
actual collaborations that are coming from me
getting into this space, so I am genuinely grateful.
Thank you. So today, insulin
versus glucagon. I have been
conversations in the community with regards to the role of
protein. And it’s been somewhat,
sometimes concerning when I hear the fear
in people’s voices when they talk about protein and so I’ve made
sort of an academic pursuit,
and decided to share with you some of my conclusions.
Before I get going, here’s my disclosure. I have two,
I’m a part of two groups:
insulin IQ, where we are
trying to make people more mindful of
the relevance of insulin in health, and the best my
most favorite audiences
are the Grand Rounds talks that I get to do to physicians,
and then best facts is just our efforts to
contribute to this blossoming
low carb high fat supplements space.
So, last year of my first step
into the low carb community, I spoke about the relevance
of insulin and ketones, and the effects that they have
on the contrasting effects on
adipocyte mitocondrial uncoupling. In other words,
white fat or brown fat. I’m not going to talk about
that today, as you could tell from the title, so collective
disappointment, I’m sure. (laughs)
Um, but let me give you an update. So, this was the paper we just
published a few months ago.
My students and I published this paper in a good journal,
biochemical journal, where we found that insulin was basically,
as I talked about a year ago, and we finished all the evidence here, or
put all the evidence in this paper. Insulin
was, um, slamming on the brakes of mitochondrial
uncoupling, forcing the mitocondria in the fat tissue
to be more tightly coupled. In other words, only
use energy when you need it.
That’s was insulin was doing.
I Will give the final update next year.
We will have all the rest of the human data
with regards to the ketones and I’ll be able to tell the
full story. So, if Jeff and Ron haven’t had
enough of me, then I’ll see you next year. Same time,
same place.
Okay, now let’s get into the story then. So, here’s the pancreas. In fact,
I had to pick this image for fear of using an image that
looked a little dirty. But I
hopefully, this is the pancreas, tucked underneath the stomach.
And of all the myriad cells the pancreas has,
that are cells involved in endocrine functions,
cells that are involved in digestive
or exocrine functions, we want to zoom-in on the beta
and the alpha cells. And these are famous
because they produce insulin and glucagon, respectively.
And then, insulin and glucagon, in addition, what’s interesting is
that they’re produced right beside each other in these little pockets
of cells within the pancreas, and they’re enemies, in a way,
and they’re each antagonizing the other in almost
every posible biochemical event. If insulin is trying
to do something, glucagon is trying to stop it. If
glucagon is trying to do something, insulin is trying to stop it.
So, it’s pretty much like my kids. (Laughs)
Nevertheless, we see insulin, to quote
Mike and Mary Dan Eades, needs because, they said it, well
insulin is the hormone of feeding and storing, and
glucagon is the hormone of fasting and burning and what that
means then in a bigger biochemical sense, is
that insulin is a hormone of anabolism, or building things up,
taking simple molecules and making them into
something bigger and keeping it, and then glucagon wants to
take the complex molecule and break it down.
Usually breaking it down into an energy source that the body
can then use, so it is catabolic, it is
one of those fundamental or prototypical
catabolic hormones, whereas insulin
is the prototypical anabolic.
Now, when we look at these hormones, let’s zoom-in
on what they’re doing, because now, mind you, insulin
and glucagon are affecting
most of the tissues of the body. Then, insulin affects
every cell of the body, insofar as every cell has an
insulin receptor, and glucagon affects most. But
nevertheless, let’s look at these three very metabolically
relevant tissues. Now, you can’t necessarily tell what I’m talking about
here based on my pictures, so we have
muscle on the left, adipose tissue in the middle and
then the liver on the far right.
When we look through each of these three tissues,
these hormones have varying effects. In particular,
insulin is completely anabolic at the muscle,
promoting muscle synthesis and promoting glycogenesis
or the storage of glucose in the muscle to be used
later. And glucagon has no effect.
This is one of those instances
where there are no receptors for glucagon on muscle, so
glucagon has no catabolic
actions. It can’t tell the muscle to do anything.
In contrast, adipocytes have
both receptors and so, now, we begin to see this
antagonistic yin and yang between
these two hormones. Insulin wants to promote the growth
of the adipocyte by storing lipids through lipogenesis,
glucagon wants to oppose that, and induce
the shrinking of the adipocyte through lipolysis
or the breakdown of the stored lipid. And then, the antagonistic
theme continues in the liver, where insulin
is telling the liver to make lipid and make glycogen or
storing fat and storing, um, glucose.
Glucagon is antagonizing that. We want to break down lipid,
we want to break down glucose,
we want to make glucose,
we also want to make ketones, an alternative fuel,
if we can use that word, or just
another fuel for the body.
Now, they, these hormones don’t have
comparable effects across these tissues.
So, muscle is then completely driven by insulin, in
the case of just insulin and glucagon, and then, adipocytes
appear to be more sensitive to insulin than they do
to glucagon. So, if you had a
one-to-one ratio of insulin to glucagon,
theoretically, the insulin is going to win that tug-of-war.
Insulin has the chokehold on the adipocyte.
In a similar way, glucagon is the primary
driver of whatever the liver is doing. So,
if the liver’s seen both glucagon and insulin,
ususally glucagon is going to be setting the tone.
It can beat insulin there, as opposed to
the adipocyte, where insulin tends to win that race.
So, just like these two hormones, insulin and glucagon
dictate the biochemical actions in these three
metabolically relevant tissues, and we could have listed more,
we need to explore how do
then, the macronutrients dictate
the levels of insulin and glucagon.
And this isn’t as clear as we usually think,
and this is, this was, the matter of my pursuing
this topic. It was to get to this issue.
When we look at carbohydrates, we see this
opposing effect. Where carbohydrates will,
in any situation, increase insulin and reduce
The textbook version is this complementary
effect of protein, where protein is both increasing insulin
and glucagon, making it somewhat of a
macronutrient that people in low-carb community fear.
And, and I’m not sure that’s justified, and I’m making the case that
perhaps we need to revise the way we think about it. And in fact,
and each of these are just when it’s consumed in its pure form.
If you take a spoon of carb, a spoon of protein,
or a spoon of fat, fat will not increase insulin, it
will only increase glucagon. And that makes it very friendly
to those of us who appreciate, or respect, the relevance
of insulin and the pathogenicity of insulin. Aknowledge that
it has a hand in virtually every chronic disease.
Now, however,
one of these depends on context
that when we’ve put these arrows
the way the textbooks have, and that’s how I’ve done it,
it really depends on underlying glycemic
status and it’s insulin,
the insulin effect, the insulinogenic effect of protein
is heavily influenced by the underlying glycemic
status. And other, what, well, get into it. In fact, let’s get into one
study right here. Now, by way of disclosure, this
was a study done in canines, and but before you start thinking
oh, well, that’s not relevant to humans,
you actually will be hard-pressed to find a mammalian
digestive system that is as similar to humans
as canines, even to the point of bacteria,
where canines have similar mouth and
digestive bacteria as humans do.
So, it is more relevant than you might think.
Nevertheless, challenge it as you will. So, in this
study, on the left-hand side, you’ll see the only difference between
these two instances is that on the left-hand side
they infused glucose and you’ll see right along the very top
it mentions a glucose infusion. So, they’re providing these animals
an underlying hyperglycemic state.
And in the condition on the left it was there no
infusion, and the animals were just simply in a fasted state.
And then, they had those two repeated boluses of
alanine infusions. Now, alanine is
relevant, yes, it’s an amino acid, remind you, of course,
once we ingest the protein, it all gets
broken down to amino acids. So, we always say,
well, in protein spike my insulin we technically
should say amino acids right, but nevertheless,
alanine is the … why is it so relevant? Alanine is
is the prototypical gluconeogenic
amino acid. When we teach this concept,
how certain amino acids are glucogenic, we
use alanine as the textbook example. Because it’s so good
at bumping up glucose, and you see that there, you see that green
line takes a little skip up, whenever they infuse
the alanine.
That’s all interesting.
What happens, then to the insulin and the glucagon?
On this left-hand side, what we see in the state where
there there’s an underlying elevated glucose level,
we see that insulin goes up massively:130
microunits per mil. That’s an incredible bump
over where it was already elevated because
of the hyperglycemia. It went beyond that,
130 more microunits.
So, insulin responded remarkably to
this amino acid infusion. In contrast,
glucagon plummeted by almost half.
Now, when we compare this to the
fasted animals, look at that orange line:
insulin didn’t change a bit.
And glucagon doubled.
Isn’t that a remarkable difference? And the only difference is
in one state there was elevated glucose,
in the other state there was not. And the
reason to explain this or how we explain this is we can’t
afford to inhibit gluconeogenesis.
Because those animals were fasted, if we had
had a substantial insulin effect, what would
that have done to their fasting glucose levels?
And the animals would have lost consciousness. So, we can’t afford
to inhibit gluconeogenesis, we need to keep that process going,
because that’s the only way the animals are maintaining
normal glycaemia. Because of that,
insulin was maintained, and glucagon was
elevated. And we’ll come back to this in a bit with some human data.
So, with this somewhat revised
system in place, we will look at, we, I’m now showing
what might be happening then with insulin and glucagon
in the case of a low-carb environment, where
there is not this consistent steady source or stream
of carbohydrates spilling into the blood as glucose.
And then let’s come back to these same three tissues. So, then,
in these instances now, of the low carb
individual consuming carbohydrate we still have the same effect,
of course. In this case, carbohydrate
and protein are both anabolic at muscle and
then fat would have no overt effect in this
instance of the low-carb individual.
Now, mind you, I say that carbon protein is anabolic.
That isn’t to say that you can have muscle growth and not actually
pay the price. You know, you can’t just take a drink and say I’m getting big.
You got it, you got to still earn it.
And then, with the adipocyte, carbohydrate once again is
anabolic, like it is everywhere. In fact, these two are
similar. Because the adipocyte and the liver,
both contain insulin receptors and glucagon receptors,
we have this contrasting effect,
especially in the case of protein. Where
there is going to be some degree of anabolic, but also, in the
case of a low carb individual,
a pronounced, that we can’t ignore, catabolic effect,
where, where insulin’s trying to increase the storage
and activate anabolic pathways, glucagon
is there to counter that, especially in the low-carb state.
And then, to make this relevant, or
to give it sort of a palatable easy takeaway, I submit
that one helpful way of looking at the relevance of
all this is to consider the insulin to glucagon ratio
and this is particularly relevant in the liver,
as we’ll get into that in just a bit. But the insulin-to-glucagon ratio
provides this underlying metabolic tone.
In other words, it tells the body, or the tissues,
the cells of the body, what is the prevailing metabolic
pathway I need you to be
undergoing or I need activated.
Insulin-to-glucagon ratio provides us some
understanding of who’s sort of winning. In other words,
if it’s a high insulin to glucagon ratio, we
know that anabolic pathways are predominating.
If, in contrast, it is a low insulin
to glucagon ratio, then we know that the catabolic
pathways are predominating. And, you know,
in this constant tug-of-war and all of this
is happening, we have this constant check and balance.
But in these instances, high insulin
to glucagon ratio represents
an anabolic state, low insulin to
glucagon ratio represents a catabolic
state. Now, one thing that’s
noteworthy is almost sort of a pit stop,
before I go too much further:
having a low insulin
to glucagon ratio is relevant because
that is what, I submit,
actually matters in a fasted state.
Fasting has become
very popular.
And ,perhaps, there’s some
justification. I sometimes
worry a little bit about it.
People jumping on a little too quickly,
and maybe not fully informed of
what’s happening, that there are some metabolic benefits,
but also some deleterious
consequences, but nevertheless,
there are benefits, and I submit that most
of the benefits occur due to this
favorably low insulin
to glucagon ratio. Because these,
this ratio induces these
sorts of benefits, where we see improvements in
insulin sensitivity, we see the activation
of autophagy, which is heavily
driven by hormones, insulin
absolutely clamps down on autophagy,
whereas glucagon activates it.
And we could say the same thing of this
sort of subprocess of autophagy
known as mitophagy,
where we are recycling old
mitochondria, keeping them healthy
and viable, and producing fewer
reactive oxygen species. Then we have
lipolysis predominating and then, of course,
what I talked about last year,
we have the activation of brown adipose tissue.
All of these things are happening
in this low insulin to
glucagon ratio state that predominates in a
fasted state. Yet, the benefit
of a low-carb diet in maintaining
an, a low insulin to glucagon ratio
is that you get the benefits
of this fasted state, without
actually starving
the body. You’re maintaining this fuel
intake that allows
the body to continue to function well
and, of course, it can function well with fasting
too. But you’re getting the benefits of fasting
insofar as hormones
are dictating most of the metabolic pathways
we care about. Alright, with
that is the pitstop. You can
hopefully appreciate the benefits of a low insulin
to glucagon ratio. Let’s look at
what happens to insulin and glucagon
when a person consumes three
general dietary states:
The one is the standard american diet,
next would be just fasting,
in a fasting state, and then,
the low-carb diet.
And let’s look at each of the insulin to glucagon
ratio in each of these three states.
So, in a fasted state, the insulin to
glucagon ratio, not surprinsing,
is pretty low, it’s 0.8.
That is a true sort of,
I say, fasted. I’m not talking 12
hours, this is like a 24 or plus
hours sort of fast.
Around point eight. This is in humans.
We’ve left canines behind.
So, all the doubters, skeptics,
come back.
This is, absolutely,
unarguably, a catabolic
ratio of insulin to glucagon. We
have these catabolic processes activated,
and I’m saying that ketogenesis
is catabolic. Someone would argue, well, it’s
It’s catabolic but, even still we’ve made
a nutrient from it. So, I could
appreciate the counter, but it’s a catabolic.
It’s evidence of catabolism. Nevertheless,
we can all agree this
insulin to glucagon ratio of point eight
must be catabolic
these are the catabolic processes
that are active. Now, in the case of
someone consuming the standard american diet,
the insulin to glucagon ratio is quite
high, relatively at around
four. This, we know,
is an anabolic state, and
we have the activation of anabolic processes,
like the storage of lipids, the storage of glycogen,
and we have the inhibition of processes
that a lot of us care about.
We’re inhibiting autophagy
and we’re inhibiting ketogenesis.
We know that’s happening in
this fed state of the standard american
diet, with this insulin to glucagon
ratio of around four.
Now, lastly, our beloved low-carb diet.
Here we have an insulin to glucagon
ratio of around one point three.
A little higher
than the fasted state, but
substantially lower than the standard american
diet fed state. And, once again,
we know in a low-carb
diet, where carbohydrate consumption is
low, or very low, that
is catabolic. We have the same
biochemical processes occurring
in this low-carb
fed state, as we do in the fasted state.
So, we can say that just what we were seeing with
the insulin to glucagon ratio of 0.8
we’re seeing generally the same
processes activated at around
1.3. And I’m going to come back
to this in the relevance of this
number when we talk about the ingestion
of protein. But that brings me to that point:
what happens, then, when we
add protein to the diet, to these
ratios. We are a
community that appreciates and respects
insulin to what degree do we need
to worry about the insulinogenic
of the amino acids, as a
part of the proteins that we ingest. Well, let’s look:
In the fasted state, if someone
is doing this long-term issue
fast, hopefully they’re being smart about
it. Hopefully they’re avoiding refeeding syndrome.
When they eat protein,
we see a change in the insulin
to glucagon ratio going from 0.8
down to 0.5.
And so, we see this
relative increase in glucagon,
over whatever relative change is
happening with insulin.
That’s not surprising. That’s exactly what
we saw with the dogs. Do you remember? How
the insulin didn’t change? Yet
the glucagon changed substantially? It
lowered the insulin to glucagon ratio. So,
putting this person, at least maintaining
them them in this very catabolic
state. Now, with the standard
american diet, are you ready?
When this person eats
protein, we see that their ratio
goes up to 70.
So, about a 20-time increase.
And so, this kind of gets to the heart.
This gets to the heart of our
collective appreciation of the insulinogenic
effects of the proteins we eat.
Because it’s justified,
but we have to put it in the right
context. For those of us who
are controlling carbohydrates and have a healthy respect
for insulin, thus,
this is us here. Now, what do you think
it’s going to happen? You ready? When a
person eats protein on the low-carb diet,
it changes from this
relatively low level and goes up
to …
There is in fact no change. And, technically
speaking there’s a 6% change,
which means that it stays at 1.3.
… There’s a 6%
change, as opposed to this 20-
times change that we saw
in the standard American diet.
So, if we put these two head-to-head,
and we feed them the diets,
the standard American diet and the low-carb
diet, as was done years ago,
and we give them one gram per
kilogram of protein,
and this is sort of recapping
what we just talked about,
and we look at the insulin to glucagon effects,
we see that there is this dramatic
increase in the insulin to glucagon
ratio on the standard American
diet fed side. And yet no such
phenomenon occurring. We have the maint…,
the maintenance of the relatively
low insulin to glucagon ratio that we see with
the standard american diet. Ando so, the numbers
changed accordingly, like we saw
earlier. The substantial effect,
and the standard American diet fed people,
who have glucose coming in quite
readily, the …, an insulin climbing
and the protein simply
adds to that. It compounds the insulin
effect of the carbohydrate. Where
oral carbohydrate consumption is quite
limited, we see no such
effect. Why
might this be? As a repeat, in fact, let me
quote one of my heroes, Dr.
Roger Unger, he mentions, without exception,
that the insulin to glucagon
ratio is dictated by the need for
gluconeogenesis. And because,
in those low-carb fed bodies,
gluconeogenesis is important,
it is important, we
can’t afford to have insulin spiking
too high. Because, if it did, it would
clamp down on gluconeogenesis,
and the person would become hypoglycemic.
Now, let’s look at the liver, and look at
this particular process, in just a little
more detail. In the
standard american diet and the low-carb diet, I’m …
I’m submitting to you, that the reason
we have these differences in the insulin to glucagon
ratio is because of the need
for gluconeogenesis. In the
standard american diet state there is
no need for gluconeogenesis.
In the low-carb fed state,
we need gluconeogenesis.
And I’m saying that and yet even as
I’m we need the glucose,
as a scientist, I
only know of one cell
that actually needs glucose.
And we know there’s no exception.
Do you wanna, do you wanna do you know
what it is?
Some people are saying brain, and yet, I’ve
never seen a study that proves …
Has anyone? I’m putting
this out there … (public – “the beta cell”)
The beta cell, can’t use, can’t use any
other fuel? Neither ketone o lipid or
anything else? It can, it
can. I think so. But
it’s erythrocytes. (Public – “Oh, Yeah, yeah”)
We know erythrocytes. We know for a fact,
that’s my little erythrocyte there. We know
for a fact, erythrocytes,
that lack any sort of mitochondrial presence,
absolutely must use glucose
for fuel. There’s no alternative. We always say
that brain needs glucose and yet,
well, the brain readily
uses ketones. In fact, I would submit the brain
prefers ketones because, as ketones become
available, the brain begins using it more,
and displaces the glucose. But,
I appreciate this is purely academic,
because you couldn’t test this in a living mammal,
because they would die from the lack of glucose.
But there’s no study that I have
ever seen that proves the brain
needs glucose. Can you see where I’m
going? I’ve never seen
that being proved. But that’s way off topic.
… But maybe
someone will talk about that later. Anyway,
if you know, if anyone knows of a study that proves that,
I genuinely would love to know. Okay.
So, we have gluconeogenesis,
we have these respective insulin to glucagon
ratios, high insulin to glucagon
ratio and the sad, low insulin
to glucagon ratio in the low
carb, and in each instance, we
have this very expected
regulation of gluconeogenesis,
where we have the inhibition of gluconeogenesis
in the high ratio state,
and the activation of gluconeogenesis
in the low insulin to glucagon
ratio state. Now,
in addition to main regulating
gluconeogenesis, what else
do insulin and glucagon regulate at
the liver? What do you think?
Yeah, this beloved process,
or feared, or much
maligned, whoever we’re talking with.
But nevertheless, they both regulate
ketogenesis, just like they regulate
gluconeogenesis. And here,
the standard American diet, and its
roughly insulin to glucagon ratio
of 4, very potently
inhibits the insulin to … inhibits
ketogenesis, sorry. And then,
the low insulin to glucagon ratio of
the low-carb diet activates ketogenesis.
Now, then,
what is the relevance of protein
in this process, and this why many people
fear protein, because they’re chasing
their ketones so doggedly
that they worry: wolf it’s gonna kick me out of ketosis.
I can’t eat it. And I,
I submit, and the reason I wanted to talk
about this is that I think that
leads to somewhat bizarre eating,
in a way. Where we,
we end up issuing real food
because it has protein in it.
and we end up just adding oil to everything.
And I, I’m not, I don’t
think that’s the best way to do it.
Even if there is some alteration
in ketosis. Nevertheless,
let’s briefly just look at l
the biochemical process of how ketogenesis
occurs. Yes,
indeed, low insulin
is in fact, a part, in fact a necessary part
of ketogenesis.
But the other part of this is that we must
have elevated glucagon.
And this was highlighted in the study published
just last year by some very good friends of
mine. And you’ll see along the y-axis
they’re measuring this relative change in
beta-hydroxy butyrate in these animals.
And along the bottom it’s a somewhat confusing
axis, in a way. So, I’m going to
clarify it. They had animals with functioning
beta cells producing insulin,
and animals that were not producing insulin.
Then they had, within that,
those groups, subgroups
with animals with functioning glucagon receptors
at the liver, and animals without
functioning glucagon receptors.
In other words, no glucagon signaling.
And then, let’s look first
then, at the no glucagon states between
insulin and no insulin.
Within that group we see that in the absolute
absence of insulin, we see
ketones go up from the left side
to the right side, by about four or so
times. A small little
bump, right, and if you think about insulin being
the absolute driver of ketogenesis,
you’d think if there is no insulin,
which there’s none in those animals
that we’re talking about, an untreated
one diabetic here, you would say they’re
dying from ketoacidosis. There should be massive
amounts of, of ket,
ket, of ketones here. They should be
well into ketoacidosis. And yet, there’s
just a very subtle increase.
That we would say that there may be in ketosis
in this state. That’s because there’s no,
there are no functioning glucagon receptors.
When we, then, look at
the differences between insulin deficiency
or surplus, and
functioning glucagon signaling, we
signaling, we see that once we add glucagon signaling
into the mix, we have this almost
50 times increase in
ketone production. And this is just
simply indicative of the need
for functioning glucagon,
in the process of ketogenesis.
And the fact that ke … protein
increases glucagon,
then is another reason to appreciate
the protein. And indeed, even the proteins
ketogenic effect. And this was highlighted
by one of my other academic heroes,
Denis McGarry, where he mentions
that glucagon is the primary
driver of ketogenesis in the
liver. But, despite
me emphasizing insulin and glucagon,
before I finished this little bit,
let me mention that there is one other
player that needs to be discussed.
And that is carnitine.
And this fact this was mentioned
earlier. I think Rob Wolfe mentioned this
yesterday. Carnitine is
this escort, basically. No in
the bad way. It is escorting,
it is escorting the lipid
into the mitochondria,
allowing the lipid to be oxidized.
And, just as a reminder,
we must have a lipid be oxidized
for it to then be
ketogenic. We have to get down
cleaving off those pieces, those two
little pieces of carbons at a time,
and then that turns into acetyl-CoA,
and then gets turned into
the ketone that we know and love.
So, we have to have sufficient
carnitine to escort the lipid
into the mitochondria, and induce the oxidation,
and then we have the magic of ketogenesis.
So, all of these
are relevant. This was a
study by Denis McGarry in animals, in
rodents, where he took the livers
out of animals that were
fed, and fasted. And you see
that when the animals were fasted,
the level of ketones was about three
times higher. That’s that
upper level. And in the fed animals, he
simply took and fed their normal standard
chow, and then supplemented
carnitine. Now, mind you, we all
make carnitine. But there
are, in fact, known instances
of carnitine deficiencies,
where the human is
unable to create sufficient carnitine
for functional mitochondrial
processes. So, in this state
they added carnitine to these animals diets,
and look at what happened to ketogenesis.
So, I’m simply wanting us to
appreciate there’s this extra player here,
where we need sufficient carnitine
for ketogenesis. Well, indeed
we need it for just lipid oxidation
in any general sense.
So, these are the three characters
then, or part, the parts
or components of the formula,
where we look, we need a low insulin
level, and elevated glucagon level,
and at least sufficient carnitine,
and then we’ve created, we have the
formula for ketones. Now, this is
a pretty academic way of looking
at it, me saying low
insulin, increased glucagon,
and perhaps the more practical side
is to simply add in the relevant macronutrients.
And I submit, when w’ere
eating a real diet,
and nevertheless, appreciating the relevance
of carbohydrates and keeping them
controlled, it ends up being a mix
that would look something like this. Where we have protein
combined with fat, combined
with carnitine, providing
the recipe for ketogenesis. And you
might look at this and say, where could we get
such a magical
food, that contains it’s
this wonderful mix of stuff?
Well, it’s not very hard
to find it:
red meat is the perfect source
of these three components of ketogenesis.
Now, I appreciate, as I,
as I have been offering
this version of a low-carb
diet that is not assuring protein
to the degree that some people do,
I appreciate that I may be
inadvertently upsetting people.
And so, here’s my diplomatic
conclusion here. There are
multiple ways, of course,
to do what, to adhere to a low-carb
diet, I kind of have two
versions of that presented here.
On the left it’s a version that is somewhat
more appreciative of protein, on the right
it’s a version that is
wary of protein. But, what do they
have in common? They
both are controlling carbohydrates.
And that really is the
common strength between these
two. And that’s, that’s the foundation
that they share. And then,
what might be relevant in
determining which of these two versions
of the low-carb diet is best?
I submit, perhaps it’s helpful
to consider the underlying
glycemic status of the individual.
In other words, if someone is
starting from this metabolically unhealthy
state of hyperglycemia and
hyperinsulinemia, in other words,
prediabetes up to type-2 diabetes,
most of, most of the
adults in the civilized world,
or industrial and not even industrialized,
we have this very common,
it may be justification
to be a little wary of protein at
first. Perhaps, depending on
what the person would prefer to eat.
Nevertheless, I submit the unifying
sort version of these two
or hypothesis, or union
of these two versions of the low-carb diet,
could be that the person is starting
in this version on the right, where it is
relatively low in protein,
and then they’re progressing as the
insulin and glycemia is improving,
towards this state that is
still controlling carbohydrates, yet
acknowledging the relevance of protein.
Now, then,
what might this look like?
Because I’m not your physician I’m gonna give you some
advice. (Public laughs)
And I have no fear of
Because this is purely academic.
Here’s mine, here’s
here’s one way you might do this.
And this is my sort of cheeky
attempt at making it
memorable and,
and, of course I’m using alliteration
quite heavily. So, firstly I submit
to maintain a low
insulin to glucagon ratio, a person,
one must control carbohydrates.
To a person then,
I submit, would be well-served
by then prioritizing protein.
Ensuring sufficient protein
intake to maintain lean body
mass and healthy function. And then,
third, all the remaining calories
are filled with fat. And so, let’s talk about
each of these. But, just a moment,
in more detail, very briefly.
By controlling carbohydrates, I do mean this very
widely accepted range
of around 50 grams or so per
day. And this depends, of course, on the person.
And that would have to be optimized. A little
lower or a little higher, whether the person can
fudge it up a little bit. But, nevertheless,
whatever range they come to,
to have a healthy range for that person,
they do need to scrutinize the
quality of the carbohydrate, and this is no
surprise, of course.
I exclusively define a carbohydrate as good or bad,
based on the degree to which it’s
going to spike insulin. And so, this would
be just some very simplistic version
of that.
Next one, prioritize protein.
By this I mean that when a person is
ensuring, um, sufficiently
controlled carbohydrate consumption,
there is then, I submit, a
benefit to ensuring the person’s
getting that range of protein,
one to two grams per kilogram body weight.
And, please, throughout
this talk I’ve had references
in corners. If I ever feared there was something
deeply controversial,
please, look into this, and make your own conclusions.
Just like I’ve done by just
pursuing data and coming to a
conclusion. But I submit to you
to maintain healthy lean body mass.
We need to make sure we’re getting in that range.
And I think our love of
fat sometimes prevents us
from getting that. And that’s why I
wanted to mention this. Now, mind you,
as I just turned 40 very recently
a mindful of my getting older and my
kids are getting older, they’re, our
need for dietary protein goes up
as we age. So, as we’re getting
older, we need to make sure we’re on the higher
end. Dr. Stuart Phillips has found that
and he’s really one of the legends in this
area, that the older we get, the less
capable our body is at converting
ingested protein into muscle
protein. So, we do indeed need
a little more, and I worry that we’re
sometimes not getting it.
And then, third, as I mentioned, we fill all
the remaining calories, whether that’s 1500
or 2000 calories, that is
fat. All of our remaining
caloric needs come from fat.
And, once again,
as our, we know this very
well, and Nina spoke about this very well yesterday,
we need to scrutinize the quality.
And, in essence, I basically say,
we just stick with the fats we’ve been eating as a species
since time immemorial.
It was either from the animal, or make
a lever big enough to compress the fruit and get
the oil from the fruit. It was simple we’ve
been doing it. So, animal and fruit fats,
I submit, are better than any industrial
seed oils, as we all
now. And so, in sum,
I submit that this overtly
simplistic paradigm
of three steps of a
healthy diet, it is, I consider
healthy because it maintains what
I consider a smart,
metabolically prudent insulin
to glucagon ratio, keeping it low,
keeping it in control, allowing the
the benefits of the fasted state,
yet without the need for caloric restriction.
And then, it also
ensures that we are properly nourishing
the body. We’re giving the body what it
needs, by making sure that there’s
some focus on protein or,
to maintain the alliteration, a priority
on protein.
With that, I thank you for listening, and I look forward to any questions during the Q&A.
Thank you. (applause) Thank you

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