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Practice English Speaking&Listening with: Dr. Benjamin Bikman - 'Insulin vs. Glucagon: The relevance of dietary protein'

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Thanks, Eric,

thanks for the introduction. Yeah,

Im 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. Its fun

to be here now and see friendly faces as opposed to

strangers,

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, Ive 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

following conversations in the community with regards to the role of

protein. And its been somewhat,

sometimes concerning when I hear the fear

in peoples voices when they talk about protein and so Ive made

sort of an academic pursuit,

and decided to share with you some of my conclusions.

Before I get going, heres my disclosure. I have two,

Im 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. Im not going to talk about

that today, as you could tell from the title, so collective

disappointment, Im 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.

Thats 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 Ill be able to tell the

full story. So, if Jeff and Ron havent had

enough of me, then Ill see you next year. Same time,

same place.

Okay, now lets get into the story then. So, heres 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, whats interesting is

that theyre produced right beside each other in these little pockets

of cells within the pancreas, and theyre enemies, in a way,

and theyre 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, its 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, lets zoom-in

on what theyre 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, lets look at these three very metabolically

relevant tissues. Now, you cant necessarily tell what Im 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 cant 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 dont 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 livers 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 isnt 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

glucagon.

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 Im not sure thats justified, and Im 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 its 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 weve put these arrows

the way the textbooks have, and thats how Ive done it,

it really depends on underlying glycemic

status and its 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, lets 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, thats 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, youll see the only difference between

these two instances is that on the left-hand side

they infused glucose and youll see right along the very top

it mentions a glucose infusion. So, theyre 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, its 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 thewhy 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 its 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.

Thats all interesting.

What happens, then to the insulin and the glucagon?

On this left-hand side, what we see in the state where

there theres an underlying elevated glucose level,

we see that insulin goes up massively:130

microunits per mil. Thats 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 didnt change a bit.

And glucagon doubled.

Isnt 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 cant

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 cant afford

to inhibit gluconeogenesis, we need to keep that process going,

because thats the only way the animals are maintaining

normal glycaemia. Because of that,

insulin was maintained, and glucagon was

elevated. And well come back to this in a bit with some human data.

So, with this somewhat revised

system in place, we will look at, we, Im 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 lets 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 isnt to say that you can have muscle growth and not actually

pay the price. You know, you cant just take a drink and say Im 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 cant ignore, catabolic effect,

where, where insulins 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 well 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 whos sort of winning. In other words,

if its 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 thats

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, theres some

justification. I sometimes

worry a little bit about it.

People jumping on a little too quickly,

and maybe not fully informed of

whats 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. Youre maintaining this fuel

intake that allows

the body to continue to function well

and, of course, it can function well with fasting

too. But youre 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. Lets 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 lets 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, its 0.8.

That is a true sort of,

I say, fasted. Im not talking 12

hours, this is like a 24 or plus

hours sort of fast.

Around point eight. This is in humans.

Weve 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 Im saying that ketogenesis

is catabolic. Someone would argue, well, its

anabolic.

Its catabolic but, even still weve made

a nutrient from it. So, I could

appreciate the counter, but it's a catabolic.

Its 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.

Were inhibiting autophagy

and were inhibiting ketogenesis.

We know thats 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

were seeing generally the same

processes activated at around

1.3. And Im 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, lets look:

In the fasted state, if someone

is doing this long-term issue

fast, hopefully theyre being smart about

it. Hopefully theyre 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.

Thats not surprising. Thats exactly what

we saw with the dogs. Do you remember? How

the insulin didnt 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 its 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

its 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

(loughs)

There is in fact no change. And, technically

speaking theres 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

cant afford to have insulin spiking

too high. Because, if it did, it would

clamp down on gluconeogenesis,

and the person would become hypoglycemic.

Now, lets 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 ...

Im 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 Im saying that and yet even as

Im we need the glucose,

as a scientist, I

only know of one cell

that actually needs glucose.

And we know theres 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? Im putting

this out there ... (public - "the beta cell")

The beta cell, cant use, cant use any

other fuel? Neither ketone o lipid or

anything else? It can, it

can. I think so. But

its erythrocytes. (Public - "Oh, Yeah, yeah")

We know erythrocytes. We know for a fact,

thats my little erythrocyte there. We know

for a fact, erythrocytes,

that lack any sort of mitochondrial presence,

absolutely must use glucose

for fuel. Theres 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 couldnt test this in a living mammal,

because they would die from the lack of glucose.

But theres no study that I have

ever seen that proves the brain

needs glucose. Can you see where Im

going? Ive never seen

that being proved. But thats 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?

Ketogenesis.

Yeah, this beloved process,

or feared, or much

maligned, whoever were 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 toinhibits

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 theyre chasing

their ketones so doggedly

that they worry: wolf its gonna kick me out of ketosis.

I cant 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, Im not, I dont

think thats the best way to do it.

Even if there is some alteration

in ketosis. Nevertheless,

lets 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 youll see along the y-axis

theyre measuring this relative change in

beta-hydroxy butyrate in these animals.

And along the bottom its a somewhat confusing

axis, in a way. So, Im 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, lets 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,

youd think if there is no insulin,

which theres none in those animals

that were talking about, an untreated

one diabetic here, you would say theyre

dying from ketoacidosis. There should be massive

amounts of, of ket,

ket, of ketones here. They should be

well into ketoacidosis. And yet, theres

just a very subtle increase.

That we would say that there may be in ketosis

in this state. Thats because theres 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 keprotein

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. Thats 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, Im simply wanting us to

appreciate theres 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 weve 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 its

this wonderful mix of stuff?

Well, its 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, heres 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 its a version that is somewhat

more appreciative of protein, on the right

its 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 thats, thats 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 its 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 theyre 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 Im not your physician Im gonna give you some

advice. (Public laughs)

And I have no fear of

litigation.

Because this is purely academic.

Heres mine, heres

heres one way you might do this.

And this is my sort of cheeky

attempt at making it

memorable and,

and, of course Im 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, lets 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 its

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 persons

getting that range of protein,

one to two grams per kilogram body weight.

And, please, throughout

this talk Ive had references

in corners. If I ever feared there was something

deeply controversial,

please, look into this, and make your own conclusions.

Just like Ive 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 were getting in that range.

And I think our love of

fat sometimes prevents us

from getting that. And thats 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, theyre, our

need for dietary protein goes up

as we age. So, as were getting

older, we need to make sure were on the higher

end. Dr. Stuart Phillips has found that

and hes 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 were

sometimes not getting it.

And then, third, as I mentioned, we fill all

the remaining calories, whether thats 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 weve 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 weve

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. Were giving the body what it

needs, by making sure that theres

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

The Description of Dr. Benjamin Bikman - 'Insulin vs. Glucagon: The relevance of dietary protein'