Diet Doctor Podcast #23 — Dr. Jason Fung, MD

Diet Doctor Podcast #23 — Dr. Jason Fung, MD

August 1, 2019 86 By William Morgan


#1Welcome to the Diet Doctor podcast.
Today it is my pleasure to be joined
by Dr. Jason Fung, from the IDM program.
Now Jason has been revolutionary
in his use of intermittent fasting
to treat obesity and to treat diabetes
and in this discussion we cover a lot of that
but we take it a little bit further
and you get to hear Jason’s perspective
about how other diseases such as cancer,
polycystic ovary syndrome
and even little hints at longevity,
how they can all be related to a similar
process of too much insulin.
And we talk about where the levels
of evidence exist for this
and how we can kind of approach patients
both with and without the evidence.
I hope there’s a lot of take home messages
that you can take away from this interview
to see how you can implement them
in your lives,
if you’re suffering
from any of these issues,
but also sort of how to refrain
this issue of insulin,
its impact on our lives and our health
and how we can implement fasting
as a way to approach that.
Now, to be fair, fasting means
a lot of different things to different people
so we talk about the definitions and we talk
about ways to make sure it’s done safely,
because that’s very important.
Just because something’s good,
doesn’t mean more of it is better,
and I think that’s an important take home
with fasting as well,
doing it under supervision, doing it safely,
can have a positive impact
and that’s part of what Jason has devoted
a big portion of his career to.
Now, he’s still a practicing nephrologist
and that’s sort of where all this started,
but now with the IDM program
he is reaching so many more people
and spreading the word more
about the benefits of intermittent fasting.
So, enjoy this interview with Dr. Jason Fung,
and if you want to learn more
you can get the transcripts and you can see
all our prior episodes on dietdoctor.com.
Dr. Jason Fung, thank you so much
for joining me on the Diet doctor podcast.
#2Great to be here, finally.
#1It’s great to have you.
So, we already had Megan Ramos,
who worked with you at the IDM program
and talked about the amazing work that you
and she and your whole team are doing,
implementing fasting as a tool for metabolic
health and reversing diabetes and weight loss,
but it’s not without its controversy is it?
#2No, I mean I think it’s because of…
it’s really not been standard
sort of for the last 20 to 30 years.
Prior to that,
people didn’t care much right,
but you know in the last 30 years,
everybody thought we had to eat,
had to eat, had to eat– to lose weight,
you know and all this other stuff,
so it has been controversial
mostly because it goes against the grain.
I mean, when I first thought about fasting,
I thought it was a bad idea too.
And then you hear so much,
like it’s going to burn muscle,
it’s going to wreck your metabolism
and don’t skip breakfast,
and all these sort of things that make it
sound really scary,
until you realize that people have been
doing it for thousands of years.
#1Right and when you talk about fasting,
I think the definition is really important
because some people get in their minds
that 10 day, 15 day prolonged fasts.
It’s mostly shorter fast that you’re using
in your program, isn’t that right?
#2Yeah, exactly.
So, in the 60s for example when people
were doing all these studies,
they would be doing
like 30 to 60 days of fasting
and you’ve got to remember
these are not like obese people.
These are people that had, you know,
very low body fats
because there just wasn’t that much obesity
and they’re going on 60 days of fasting,
it’s like that’s not a very good idea,
and that’s where people got into trouble
like they shouldn’t have been fasting,
but they did it for some study.
I mean I look at some
of these studies they did
and they’re incredible, like one of them
for example, they had like–
I think they had nine people
or something like that
and they fasted them for like 30 or 60 days,
then they gave them a big whack of insulin.
It’s like, I’m thinking why did they do that?
And the answer was,
“Just to see what would happen.”
So, they dropped the sugars
to very low I think
and it was like 1 point something
in the Canadian unit
so it’s probably like 30 or something
like that, it’s ridiculously low.
And everyone was complaining
they were asymptomatic,
so you know these are the kinds of studies
that no one would ever do,
you don’t do that kind of thing,
it’s you know you don’t have
to take those kinds of risks.
So that’s where people go more towards
the shorter fast
and there’s no reason not to do them.
And you’ve got to understand
that fasting is a part of the normal life,
like that’s where the word
breakfast comes in,
you’re supposed to feast
then you’re supposed to fast.
Well what’s wrong with that?
And you have a word that is actually part
of your daily schedule,
and now fasting for 12 hours is like insane,
it’s like everybody in the 70s did it
like without even thinking about it.
So it’s sort of come all the way around that,
you shouldn’t even go like more
than two hours without eating,
it’s like okay well, what about
the normal nightly fast, right?
#1Yeah, and that’s what makes interpreting
the science of fasting sort of difficult,
because depending on how you define it,
it’s going to depend
on how you interpret the science.
So, you and the folks at your program
recently just published three case studies
of some remarkable benefits with fasting,
with people getting off their insulin
and reversing their diabetes
within days, with fasting,
but it was an alternate-days fasting
with never more than a 24 hour fast
in those three patients.
#2It’s stunning.
So, all three people, middle aged, they had
between 20 to 25 years of type 2 diabetes,
most of them 5 plus years on insulin
and big doses, 60 units sort of thing,
and it took a maximum of 18 days
to get them off all their insulin.
#1So, a maximum of 18 days,
that’s incredible.
#2It was ridiculous how quickly
they got better
and the schedule we used,
because we had to protocolize it somewhat,
is 24 hours, three times a week.
So, this is the thing
that within less than a month
they had significantly reversed
their type 2 diabetes,
even a year later, I think
two of them are off all meds
and non-diabetic by the classifications,
you know by A1c
and I think one of them
was on some metformin still,
but came off all the insulin and three
out of the four medications or something,
so doing ridiculously well for an intervention
that is actually free, available to anybody
and has been used for thousands of years.
So, it’s sort of ridiculous how quickly some
people can get better
and you know as I was saying this is
something that really needs–
people need to understand because
it causes so much disease, type 2 diabetes,
because I mean 20 years of diabetes,
and we had just proved
it was all completely unnecessary.
Like do you know the amount of damage
they did to their bodies
with 20 years of type 2 diabetes
to their hearts and to their kidneys,
and to their eyes?
#1It was all completely preventable.
#2Exactly, like in a month they could
have taken care of the whole thing.
#1Now in the case series
they were following a low-carb diet
in addition to the intermittent fasting.
So, do you find the success varies
with low-carb and without low-carb
when you’re instituting intermittent fasting?
#2Yeah, for sure we recommend
low-carbohydrate diets
for all of the type 2 diabetics,
and it’s really along the same lines.
I think type 2 diabetes is largely a disease
of hyperinsulinemia,
so therefore both low carbohydrate diets
and intermittent fasting,
the goal is to lower insulin, as you lower
insulin in a disease of too much insulin
and you’re going to get better,
just like PCOS,
if it’s too much insulin
you’ve got to lower it.
With type 1 diabetes, if you don’t have
insulin, you got to give it,
that’s how you’re going to get better.
So, it’s not like the insulin is evil
or anything like that, it’s juts all context,
like if it’s too high
you’ve got to bring it down,
if it’s too low you’ve got to bring it up,
and that’s how you’re going to get better.
#1Yeah, a very simple perspective,
but it can get a lot more confusing
for a lot of people,
they just need to realize
the perspective there.
So, the concerns about fasting
are the safety of it.
So, one being your resting metabolic rate,
is it going to go down with fasting
and again time frame matters, doesn’t it?
#2Yeah, for sure and you know if you’re
looking at some of the studies now
so that nobody does these 60 day fasts
sort of and studies it,
but there have been studies
of alternate day fasting
and a lot of these are not true fasts
so you have to extrapolate somewhat.
They are the ones that do measure
resting metabolic rate,
don’t show any significant difference
from chronic calorie restriction.
In fact most of the studies and there is
a number of them,
so you have to kind of pick
which one you choose,
but most of them show that there’s less
of this drop in metabolic rate
with alternate daily fasting
and studies for example…
one study where they did
four straight days of fasting,
their metabolic rate was actually 10%
higher at the end of the four days
compared to the day zero.
And again it all comes down to physiology
because I don’t know why,
people get so bent out of shape.
So if you don’t eat, insulin drops,
we know that, that for sure happens
and when insulin drops, the counter
regulatory hormones go up, we know that,
that’s why they are called
counter regulatory hormones,
they go counter of insulin,
and one of the big ones is sympathetic tone,
like that’s not for debate, right.
#1So, sympathetic tone,
you mean adrenaline, noradrenaline.
#2Yeah adrenaline– so basically
it’s the fight or flight response.
So if you see a lye and your sympathetic
tone goes way up
and you’re either prepared to fight or run,
really, really fast,
your body actually increases growth of
hormones, sympathetic tone or adrenaline,
to actually bring glucose into the blood,
it floods the body with glucose
you can use to run away.
That’s medical school physiology,
okay so if you think– and cortisol too,
so cortisol is one
of the counter regulatory hormones.
So, if you think about it, okay so
if sympathetic tone is going up,
you know you’re activating your body,
that’s what sympathetic is,
parasympathetic, you’re toning it down,
but you’re activating the body,
what do you think
that’s going to do to your energy?
It’s going to raise your energy,
it’s going to increase your metabolic rate.
It’s like come on, this is medical school
stuff, like why is this a debate.
And all the studies show
that there’s probably less effect
on the basal metabolic rate from real world
studies on alternate day fasting and stuff.
Most of them allow calories and so on,
so you have to interpret them a bit.
It’s like why do we worry about this?
Where does this notion even come from?
Because if you fast you’re going
to decrease you metabolic rate,
that actually runs counter to what
we all learned in medical school,
of what happens when you don’t eat.
#1With a one to three day fast, at least
we can say that with pretty certainty.
#2Yeah, if you’re going
30 days and 60 days,
yeah you’re talking about something totally
different and almost nobody does that,
like we generally
don’t recommend that either,
I mean for us, we’re like why take the risk.
So, if you’re doing 30 days,
if you want to, it’s great,
but if you look at it,
it’s more powerful but there’s more risk,
so why don’t you just do
more shorter fasts?
And that’s the sort of trend
towards where we’ve gone.
So, in the 60s everybody’s like,
oh fasting is like a month right
and it’s like okay,
fasting nowadays 16 hours is controvert.
#1Yeah, it’s amazing how times change,
and so the other big concern is
lean body mass loss, muscle loss,
nitrogen wasting and depending
on how you measure it,
it seems like you can come up
with different conclusions.
#2Yeah, so again you can definitely measure
nitrogen waste
and then you have to say,
is it muscle or is it not muscle?
Not all protein is muscle, right?
#1So, I should actually clarify
nitrogen waste,
meaning sort of measuring the nitrogen
in the urine that you urinate out
and then the question is where did
that nitrogen come from in the body?
#2Right, right, and I think it depends
a little bit on what your perspective is.
So, if you’re talking about elite athletes,
then it’s something totally different than
what I’m talking about for the most part
which is sort of middle aged
and elderly people who are mostly obese.
So, there’s a lot
of excess proteins sitting there,
so if you look at, again we’re not talking
about elite athletes,
but if you’re measuring it, there have been
studies and they say
that obese people generally have 20%
to 50% more protein, than a normal person
and that’s all skin, that’s all connective
tissue, there’s a lot of skin.
If you look at those programs
where they have skin surgery,
they’re taking, you know like 40 pounds
of skin, that’s not fat, that’s protein.
So, there is excess protein,
when you’re talking in that specific
sort of obesity type 2 diabetes situation,
and you have to think that the body
is going to maybe use some of that
because that’s all protein
that needs to go.
And again if you look at studies that have
compared intermittent energy restrictions
or IER versus CR which is chronic restriction
and there has been a few,
most of them generally show that there is
less loss of lean mass as a percentage.
So one study from 2016 that was published
in obesity for example,
showed that you know you get about
0.5 increase in percentage of lean mass,
because people are losing weight
with chronic caloric restriction
but it goes up by 2.2% in intermittent
energy restriction or fasting.
So you’re preserving lean mass much better
if you’re using the fasting strategy,
but this is sort of short term,
24 hours or less strategies.
So, again if you think about it,
it’s like okay,
if you think that the body is–
when it has no food,
it’s going to bypass
your excess protein skin connected tissue
and go right for your heart muscles,
it’s like you must think that the body
is really, really stupid.
I mean, like honestly,
you don’t eat for 24 hours
and oh you’re going to start breaking down
your diaphragm.
Like why would the body do that?
#1A muscle is a muscle, basically.
So how does it know to target
certain muscles and not others?
#2Exactly, it wouldn’t.
It’s going to go for the stuff
that’s not needed
and how would we have survived
if our bodies were so incredibly stupid,
that every time you don’t eat,
it starts breaking down your muscle,
like let’s think about this for a second.
Like I do fairly regular fasting,
so if I’m losing like quarter of a pound
of muscle every time I fast for 24 hours,
it’s like yeah,
I should have zero muscle right now.
I should be this giant glob of fat.
Instead, I’m pretty much the same,
you know, composition
as I was a couple of years ago when I didn’t
fast, it just didn’t make any difference.
#1Do you recommend resistance training
to try and stimulate muscle growth
or maintain muscle during the fast,
or do you think that’s not necessary?
#2I think it’s always good to do it,
no doubt,
but the thing about it is that the body is–
honestly the body is incredibly smart.
So, if you put a strain on the system,
it will respond by getting stronger,
so muscles work like that.
So you put a little bit of damage on your
muscles and it rebuilds it to get stronger.
You put weight on the bones
and they respond by getting stronger.
So if you look at astronauts,
you take away gravity
and all of a sudden
their bones deteriorate like crazy,
their muscles deteriorate like crazy.
You put a man, hospitalize him
and put him in bed rest only,
which was the remember the–
five days of bed rest.
What you do is you take
the strain off the muscles,
so you take the stress off and
you immediately start losing muscle,
so if you want to lose muscle, that is
the way to lose muscle, sit in bed all day.
Like why would the eating
have anything to do with it?
Eating doesn’t make you gain muscle,
otherwise we would all be a nation of like
you know Arnold Schwarzenegger’s, right?
It doesn’t happen,
they are two totally separate things.
You build muscle
because you are working it,
then you lose muscle
because you aren’t working it.
If you’re working it and not eating,
your body is going to come up
with a way to build that muscle,
just the way it is, otherwise, again
if you look at these Native Americans
and all these people that used to go
through these feast and famine cycles,
and it was not like they were little globs
of fat running around the prairies
when the pioneers came.
They were lean
and muscular and, you know, strong
because your body responds to that,
and I think it’s really silly to think
that our body is just so maladapted to life.
#1Interesting perspective,
that the body knows,
and we just have to listen
and help it on its way.
And then there are obviously
a number of other issues
about making sure that you’re well hydrated
and have adequate sodium intake
and reduce medications if necessary
and I think that’s a big issue
of doing this on your own
versus doing it with professional guidance.
So tell us your perspective on that
and what you’re doing to help with that.
#2So, yeah that’s our IDM program
and it’s basically to provide the education
people need because it’s not easy.
It works but it’s not easy,
it’s not fun, right?
I would rather be eating donuts myself,
but it’s healthy and that’s the thing,
it is something that will improve
your health,
so you need to get educated
as to what to expect.
So, if you know for example
that headaches are very common
but they’ll go away, you can deal with it.
If you know
that you’re going to get hungry
and there are tips that might help you deal
with that hunger,
then that’s going to help you
in terms of the fasting.
So, it’s about getting
the proper education
and that’s what we provide
with our IDM program
and also providing
a support of community
and that’s is what is really the secret
behind a lot of things,
not just for weight loss,
like Weight Watchers for example…
they started out not with a diet
but with those meetings,
those Weight Watchers meetings
and that’s the secret sauce right?
Same for Alcoholics Anonymous.
It’s not like they didn’t know to–
hey stop drinking.
It was that you had a supportive group,
a sponsor and that sort of thing.
So doing it with a community
is just way easier
and that’s the secret of how all
these communities use to fast,
they do Ramadan, hey everybody’s fasting,
hey it’s lent, everybody’s fasting,
hey it’s Yom Kippur, everybody’s fasting,
so it’s not fun
but it’s as hard as it would otherwise be.
Because if you’re trying to fast and
everybody is telling you you’re stupid
and eating, like you know in front of you,
that’s not like the easiest thing to do,
so don’t you know you’ve got to set
yourself up for success
and that’s what we hope to do for
with the IDM program.
#1That’s a great point and there’s a lot
of communities built around fasting
that are sort of popping up
so people can support themselves,
and I think that’s valuable.
Now with fasting you can look at it
from two perspectives,
in terms of what you are treating.
One is treating diabetes and obesity
and insulin resistance
and another is just promoting longevity
and that’s a whole other field of research.
Now, with your book,
The Longevity Solution,
it looks like you’ve sort of delved more
into longevity,
so tell us a little bit on how the mindset
changes when you’re focusing on longevity
rather than just treating
and reversing a medical condition.
#2Yeah, that’s a great question,
I think it’s really a matter of how
to sort of maintain health throughout life
and so then we looked in this book
at a lot of sort of ancient wellness practices
because I’m not about selling
the latest supplement
that’s going to make you
live forever, right?
I don’t think that exists,
but there are certain practices that
have sort of withstood the test of time,
that is they were considered to be
wellness practices 2000 years ago
and I think that has merit
because those practices
have withstood the crucible of time,
like if something is really bad for you
and people do it, they’ll like die out.
So, the fact that these practices or these
foods or whatever have survived
means that there probably is something
and what’s interesting is a thing
that science is starting to catch up
and fasting is one of these things
and if you look at the science of longevity,
the one thing that really stands out huge
is calorie restrictions.
That is probably the single
most well studied mechanism
for longevity in animal studies mostly.
But intermittent fasting
is sort of a play on that
and it is a way to restrict overall calories
and maybe there’s a better way to do it,
but at least it’s been used for a long time
as opposed to sort of protein restrictions
and or carbohydrate restrictions,
those have not been used for as long.
Intermittent fasting is a way to do that,
and the physiology is…
you know, a lot of these growth factors
are also nutrient sensors
and I think that this
is a really interesting thing
if you look at the theories of aging
and why we age,
or there’s sort of, there’s trade-off
between growth and longevity.
Okay so if you look at a car for example,
if you rev its engine,
you can get high performance out of it,
it’s not going to last very long
because it’s just going to burn out.
It’s the same thing, if your body is growing,
growing, growing like crazy,
it probably does the same thing;
it burns out quicker.
So the growth program is probably at odds
with the longevity program,
because it’s probably the same program.
#1And is part of that when you’re triggering
growth or stimulating growth,
you’re going to grow the healthy cells
but you’re also not going to be able
to just limit it to the healthy cells,
so potential cancer cell growth or abnormal
cell growth will lead to chronic disease
so we can’t necessarily differentiate it.
#2Exactly because they’re part and parcel
of the same thing.
When you look
at the growth pathways for example,
you have something like GF1,
which is insulin growth factor one
and so insulin, both insulin
and like growth factor one are very similar
and they’re growth hormones.
So you can look at a population
of Ecuadorian dwarves for example,
called the Laron dwarves,
and what was super fascinating
is that this group of dwarves
which– they were persecuted in Spain,
the inquisition forced them into Ecuador
and of course there’s
this founder effect where–
because there’s only a few of these dwarves
and they all married each other,
the small population, there’s a lot of these–
this dwarfism occurred,
and a few years ago it was– when they
were following these dwarves
they realized hey these guys actually
don’t get cancer or diabetes either
and then they’re like, what’s the difference
between this dwarf and the other one.
It’s like they have no IGF1, it’s like wow.
So, here’s a you know– the thing is if you
slow down the growth program,
then you might be able to age better,
it all depends also on what stage of life;
so if you’re a child, an adolescent,
you want that growth program running.
#1Right.
Growth isn’t by its definition bad.
We need to grow, we need to build muscle
which is part of health as well,
but it’s finding the balance,
which can be tricky.
#2Yeah, but now
if you’re going for longevity,
so if you’re an average age of like you know,
if you’re in the middle ages,
your average age is 30,
then yeah it doesn’t matter, you know,
run that as hard as you want,
it doesn’t matter because you’re going
to die of the black death or something, right?
So it’s like it doesn’t matter
but now if you’re trying to get out
to like 80 or 90 years old,
you have to be a bit smart,
so just like that engine,
you can’t run at full speed, you’ve got
to cut back at some point though
if you look at what stimulates growth
the most, it’s things like insulin,
like growth factor mTOR and AMPK,
which are all nutrient sensors
and this is what’s really interesting
is that the nutrient sensing pathways
are actually the same growth pathways
because the body has to know
when the nutrients are available.
#1So, nutrient sensors mean
they’re turned on or inhibited
just by having nutrients in your body.
#2Exactly.
So, if you like have an ovary for example,
that’s way on the inside,
how is it supposed to now
if there’s food coming in?
Well, it knows it because you eat,
insulin goes up,
protein, mTOR goes up, for example and
if you eat fat AMPK is also, it goes down
so those are nutrient sensors
because it’s the body’s way of sensing
if nutrients are available,
and they are actually
the exact same ones as growth.
So, now if you want to say, okay well this
growth pathway after, you know age 30–
I don’t really want to go full boar on growth
because I want to live until 80.
If you want now longevity, you actually
have to cut down your growth pathway,
which means reducing those nutrient
sensing pathways, which is insulin,
which is mTOR and AMPK,
which is something that fasting does.
#1So, the question always is,
where is the threshold for this, right,
because again chronic caloric restriction
can sort of lower the stimulation of it,
you know the old saying,
it may not make you live longer
but it sure makes life feel longer.
It’s not as enjoyable to do.
Yeah, so with the intermittent calorie
restriction or intermittent fasting,
where is that threshold
and how do we know?
Because we can’t necessarily measure
mTOR and AMP kinase.
It’s harder to measure so we have to use
surrogate markers,
so what do you use as your guidelines
to say here is where you’re getting
the biggest bang for your buck
to do this level of fasting
to help promote your longevity?
#2Yeah, that’s a really good question
and it really comes down to maintaining
a sort of stable body weight
and making sure
you don’t have the visceral obesity.
Because the one thing we know of course,
is that the metabolic syndrome
is going to shorten your life, right.
It’s going to give you heart attacks,
it’s going to give you all kinds of stuff,
cancer and so on.
And that’s dependent on not body weight
but waist circumference,
type 2 diabetes and hypertriglyceridemia
and all that sort of thing,
so we know that those
are all very important
and those are obviously highly linked in
to hyperinsulinemia and so on.
So you’re looking for a surrogate marker
that’s been clearly correlated to disease
and that’s going to affect longevity
and all those things.
So if you are fasting and your weight
is just way, way down,
then yeah, you probably
don’t need to be doing that.
But on the other hand, doing it so often
might be something that is very beneficial
and again if you look at it, it’s like there’s
that sort of ancient wellness practice
that people have done
for thousands of years.
Once a year, do a longer fast,
just to sort of clean everything out,
reset everything and then go from there,
do you need to do it for longer? Maybe not.
But if you’re 300 pounds
and have type 2 diabetes,
you probably need to be doing more,
because you know that those insulin growth
pathways are way, way too high.
It’s harder for mTOR right
and that’s really the tough part
and we spend a lot of time talking
about sort of optimal protein and stuff
but that’s really, really hard to measure
because it’s not as easy to see.
#1Yeah for something
that’s so hard to measure,
mTOR sure gets a lot of airtime
and a lot of discussion.
And it’s pretty controversial
because we need it to grow,
we need it for immune function
and yet we can’t have it,
we shouldn’t have it turned on all the time
and part of that concern is cancer.
So this is another field
you’ve been fairly vocal about,
about fasting and insulin as it relates
to cancer and that can be controversial as well
because cancer, there’s the one theory
that it’s sort of all of a genetic mutation
and you know the drugs we’re developing
is high powered weapons so to speak
to target specific
genetic variations of cancer,
and then there’s the sort of the opposite
side of a metabolic disease
or maybe it’s a combination of them both.
So, how do you incorporate that
into your thinking and fasting
in terms of cancer prevention
or treatment?
#2Yeah, and I think that the cancer
is a fascinating story.
You know since I was in medical school
we all talked about genetics,
it was all a genetic disease right,
it was just genetics, genetics, genetics
and it’s a mutation, it’s genetic mutations,
so if we can find the mutation,
then we can block it, we’re going to cure
cancer of course, but that didn’t happen.
So, we got the human genome project
because it was going to cure cancer
and then you had the cancer genome atlas
which was an even more ambitious attempt
to find out the mutations of cancer because
we thought there was one or two mutations.
It turns out there were
like hundreds of mutations
and not only mutations
like between people,
so one breast cancer cell
to the next person’s breast cancer
might have like a hundred mutations
and 100 complete different mutations
on the other guy,
even within the same tumor
there are different mutations.
So there’s mutations everywhere
and clearly you’re not going to develop
100 medications to block every single–
100 different medications
to block every single mutation,
so that was sort of a dead end theory.
And the other thing is,
it’s not about genetics,
it’s about the interaction of genetics
and the environment,
that we sort of forgot
that it depends on the environment.
So looking at obesity for example,
the World Health Organization lists
13 cancers as obesity related,
and including breast cancer
and colon rectal cancer,
sort of the number two
and number three cancers after lung.
#1Which doesn’t mean
obesity causes these cancers.
#2No, it plays a role.
#1Plays a role and makes it more likely–
so sort of if you have a genetic mutation
and you’re obese,
now the deck is really stacked against you.
#2Exactly, but now there’s something
you can do about it,
because if you have a genetic mutation,
there’s nothing you can do about it,
you have it, like I’m not going to change it,
if you have it, you have it
and I can’t do anything about it.
But I can change the environment
in which that cancer cell lies
because we know it’s vitally important.
You take a Japanese woman in Japan and
you move her to Hawaii and San Francisco,
the rate of breast cancer like triples, even
though the genetics are exactly the same.
So what’s the difference?
The difference is clearly the diet
and the environment in which
that breast cancer cell is living,
so again what is going to stimulate
breast cancer cells to grow–
And in the lab the answer is very clear,
insulin is what breast cancer cells need.
You can’t barely grow breast cancer cells
in a dish without insulin.
If you take away the insulin,
they all like die.
And if you give them lots of insulin,
they grow,
because the nutrient sensing pathways
are the same as the growth pathway.
So you take this breast cancer cell,
and remember the obesity
didn’t cause the cancer,
but after that cancer cell is there,
you’re going to stimulate it to grow
if you have a lot of insulin,
so type 2 diabetes, a disease
of hyperinsulinemia, higher risk of cancer,
obesity, disease of hyperinsulinemia,
higher risk of cancer,
and then you say
what about the other ones?
What about AMPK for example…
what blocks the AMPK or what affects
the AMPK? Metformin.
It’s like, oh well you know that
metformin in a lot of studies
has been associated with a
significantly decreased rate of breast cancer
and is it like the effect on AMPK, it’s a very
interesting hypothesis, what about mTOR?
It’s like because they are
the three nutrient sensing pathways.
Well, mTOR,
you can block mTOR with rapamycin,
which is an anti-cancer medication, right.
Why?
Because you’re blocking the pathways.
So rapamycin is super super interesting
because it blocks mTOR right.
So, it’s developed
as an immune suppressing drug
and the thing about immune suppressants,
is that they generally increase
the rate of cancer
and the immune system
sort of destroys cancer on site.
So, if you give a drug
that suppresses the immune system,
like you give these transplant patients tons
of drugs to suppress the immune system,
cancer goes crazy and that’s why–
#1Infections.
#2Infections, absolutely, but sort of unique
amongst these immune suppressants,
cancers went down, it’s like wow.
#1The specific one – rapamycin.
#2With rapamycin, yeah it’s like fascinating
because you’re blocking mTOR,
so because you’re blocking growth
pathways, you don’t have the–
that’s why it blocks your immune system
but it also blocks cancer,
it very specifically targets this nutrient
sensing growth pathway,
which is the same thing,
which is now a man humble pie.
The diet… it’s like… wow!
#1So, it’s a fascinating field and one
of the things that’s important though
is to talk about the level
of evidence of support.
So what you’ve been talking about
is a mechanistic level of evidence of support
and with the Japanese women
moving to the United States,
sort of the epidemiological
or observational,
so we don’t know it was the diet,
we know it was an environmental change
in the diet, which is a big part of that
and the mechanisms you’re describing
certainly make sense.
So it all seems to fit, but yet we
don’t quite have those human trials,
to say yes it works which can make it
a little bit uncomfortable for you
to recommend fasting for that.
#2For sure, because you don’t know
what the effect is,
but you know that for example
if you use fasting to reduce obesity,
you’re a likely going to have
a beneficial effect
but you can’t say that for sure.
And the other thing is that we’re,
this is prevention right,
so this is you talking, you don’t know
if you’re going to prevent it
because you don’t know
if someone’s going to get it or not.
You’re not doing those big trials
that are going to say we fasted sort of
a million women and this is what happened.
Those trials don’t exist so now
we’re talking about going into treatment
and that’s a totally different thing.
One I don’t think
there’s much data whatsoever
but there is some super interesting data
about sort of combination therapy, right.
So, you say okay well diet is not going
to cut it for a treatment,
like you can’t have breast cancer
and think you’re just going to fast
and yes there’s a few case reports
and so forth
but for the most part
that is not going to work for most people.
But can you combine it with say
chemotherapy to make it better?
And that’s something
that’s really, really fascinating
because for example fasting reduces
the side effects of chemotherapy.
We know that because chemotherapy,
and there’s been a couple of papers on that,
the chemotherapy affects
the most rapidly dividing cells
so in the human body the normal body,
the cancer cells are growing faster,
that’s why you are targeting
rapidly growing cells,
the hair follicles grow quickly,
the epithelial cells in the intestinal system
for example are very rapidly growing
so therefore you get nausea
and vomiting and hair loss.
So, if you put these,
if you now fast for 48 hours for example,
and you get these cells
to ramp down their growth,
they will enter
a sort of a more quiescent state,
now you whack them
with big doses of chemotherapy,
you’re going to get less side effects,
so if you get less side effects,
one you’re going to be able to get
a lot of treatments have to be ramped back,
because there’s too many side effects,
so you would get the full treatment.
Or maybe you can get
a higher dose treatment
because you’re looking
for this maximal tolerated dose,
and then there’s some interesting data
to suggest that maybe that–
So the worry there of course
is that the cancer cells will also go
into this protective state,
but apparently some preliminary data
suggests that this doesn’t happen
because they are stuck in this sort
of on mode,
that’s the whole point of cancer
that they are in this sort of growth mode.
#1They don’t have the normal feedback
loops so–
#2Exactly.
For prevention you might be able
to do something about it
but for treatment,
maybe you can combine it.
And they talk about combining
a ketogenic diet with drugs for example
are going
to be beneficial
so they do these things so the PI3K pathway
is actually the growth pathway,
and they have drugs that can block it.
And they say what if you down regulate
insulin by eating a ketogenic diet
and then by giving the drug, like can you do
better than doing either one alone.
Those studies are very interesting,
there’s not a lot of data,
so cancer is more of an evolving story
that I think you know would be.
You know, it’s super interesting but …
#1It’s safe to say it’s in its infancy
but shows promise
and so maybe in the next five to 10 years,
we’ll have a completely different discussion
and say yes here’s what the evidence shows,
one way or the other.
#2The one thing you know for sure is that in
the prevention you can prevent the obesity
and you can prevent the type 2 diabetes
and there is a good chance you’re going
to prevent some of these diseases.
So remember color rectal
and breast cancer are the big ones
in terms of obesity related cancers,
because they have already been declared
obesity related cancers,
so with the idea that hey reducing obesity is
going to reduce the breast cancer for example.
#1Yeah, that certainly makes sense.
So, now transitioning from longevity
and cancer to procreation
and so you gave a talk today about PCOS,
polycystic ovarian syndrome
and you know you’re a nephrologist,
so you did mention,
so what is a kidney doctor
doing talking about the ovaries?
So draw the line
and connect the dots for us.
#2Yeah and I was saying that, I wasn’t
very interested in the whole disease
until a few years ago when we started
really treating people
and Nadia who work with us
at the IDM program.
She was one of the educators
and all these women are getting pregnant,
like 15, 20 women have gotten pregnant,
and I’m like whoa, that is really interesting
and we’ve always known that PCOS,
polycystic ovarian syndrome
is related to obesity and the insulin
resistance and type 2 diabetes.
So it was sort of part
of that whole metabolic syndrome spectrum
that I had been talking about,
but I hadn’t really looked closely into it
and you know as I got interested
I said okay let’s look
at what happens with it,
let’s look at the path of physiology,
why are people getting PCOS.
And it’s been well worked out
and I showed a New England Journal
of Medicine review article
that sort of spells it all out so
under the influence of too much insulin,
your ovaries start to actually produce
a lot of testosterone.
And when you have a lot of insulin, the liver
decreases sex hormone binding globulin,
so the effect of the testosterone
is increased
because there’s not
a lot of globulin to bind it
so the free testosterone is more active.
So, therefore you get all the symptoms
and the hair growth and the acne,
clitoral enlargement,
things that are sort of typical.
#1And the infertility.
#2Yeah, the infertility comes
from the unovulatory cycles.
So, you know, if you look at the insulin,
what it does is it causes something
called follicular arrest.
So during the normal menstrual cycle,
you have a developing follicle
and then the sort of
like the egg pops out
and then it becomes a corpus luteum
that involutes,
that’s a normal menstrual cycle.
If it doesn’t get pregnant,
then you get the bleeding and the period.
So, if you have too much insulin,
then you get follicular arrest
and that means that the follicle stops
developing at a certain point,
so it never ovulates, it never reaches
the size that it’s going to ovulate
and if it doesn’t ovulate then there’s no egg
and you can’t get pregnant.
so that’s another– that’s the infertility.
And the thing is if it doesn’t ovulate,
it doesn’t become
the luteal body which then involutes,
which means that it just
sort of gets reabsorbed into the body.
So, you’ve stopped the follicular development
at a stage where it doesn’t ever go away,
so you’ve got these cysts
that develop over time.
So, okay so those are the three
sort of criteria of PCOS.
You’ve got too much insulin which causes
the follicular arrests which causes the cysts,
you’ve got too much insulin
which causes the follicular arrests
which causes the unovulatory cycles
and then you’ve got too much insulin
which causes the hyperandrogynism.
So the whole disease is a disease
of too much insulin
and it’s been well worked out
and it’s been in this review article…
So it was like are okay…
well like if it’s too much insulin,
then bring down the insulin,
that’s how you’re going
to make the disease better.
That’s the root cause treated.
Instead, that’s not how we treat it,
we give drugs.
#1-We give drugs.
#2-It’s like, oh, my God.
This is a total replay
of like type 2 diabetes.
So, here you know the cause
and you know the answer.
The answer is if insulin is too high
you got to drop it.
How are you going to do that?
Low carbohydrate diets, ketogenic diets,
intermittent fasting.
Instead we give birth control pills,
we use Clomid, which is a–
you know, causes the ovaries
to start hyper secreting
and that’s like,
okay it’s not the answer, right?
#1So getting mechanistically makes
complete sense
and now the level of evidence
to my understanding
is low-carb diets that can reverse a lot
of the hirsutism, the hair growth,
but I don’t know if we have any evidence
saying it improves fertility
but yet there’s lots of anecdotal evidence
of that happening.
Do you think we’re going to bridge
that gap
so that this will become
a more common treatment?
#2It depends if anybody is interested
in actually looking at it,
that’s for sure, that’s right.
You know and this is one of the reasons
they use metformin
because they use it as a sort of,
you know, insulin sensitizer,
which makes a little bit of sense so I–
at least that makes a little bit of sense.
But you know the question is
who’s looking at it,
like these low carbohydrate diets
haven’t been used for a long time
because we worry about the dietary fats.
And intermittent fasting hasn’t been used.
When I started talking about it
like six years ago,
like I was really just a lonely voice
in the wilderness.
Nobody, but nobody was studying this.
So, are the studies going to come?
I hope so.
I don’t know that there’s a lot of people
interested in it, but here’s the thing
and this is sort of the art of medicine
as opposed to the science of medicine.
Everything in medicine
comes down to risk versus reward,
so if you give a drug like a beta block
or you do a stent or something,
what’s the risk of doing a stent?
Because there’s risk,
because everything has risk,
and what’s the reward?
If the risk is more than the reward,
then you don’t do it.
If the reward is more than the risk,
you go ahead and plop in a stent,
or you give aspirin
or you give beta blockers or whatever it is.
So, what’s the risk if you don’t eat,
you know for 16 hours of the day.
What’s the cost like… zero?
What’s the risk?
If you are overweight,
there’s practically no risk,
so then you say well okay there’s no risk
so any reward you can get is a plus
and here’s the thing,
you don’t have to prove.
If you’re a patient with PCOS,
if you’re somebody with PCOS,
you don’t have to prove
that it works in everybody,
you only have to prove
that it works in yourself.
So, if you have type 2 diabetes, if you have
PCOS or any of these diseases,
you can simply say, I’m going to try it.
I’m going to try it for two months
because it’s not going to cost me anything,
I’m going to do low carbohydrate diets,
I’m going to do intermittent fasting
and see what happens.
If nothing happens and your disease
is just as bad as before
then you haven’t lost anything,
you can go ahead and just do it,
but what if your disease
completely goes away?
Right, now you’ve done something that all
the drugs haven’t been able to do for you
and the thing is that it’s big money here.
So IVF is big money,
it’s like four plus billion dollars a year,
so these people who are doing fertility
treatments and all the sort of stuff–
like if you ever go into one of those clinics
they are really nice, they look like a spa.
#1Right and it’s also miserable
for the women,
I mean it is so uncomfortable
and difficult to do
and it can all be changed
potentially with nutrition, yeah.
#2Potentially, yeah, and it’s not just
the discomfort of the IVF,
it’s like if you want a baby, it’s like you
want a baby, it’s like very totally like–
#1It’s an emotional cost.
#2It’s a huge emotional cost
and the time is ticking
because people are getting married later,
we know that,
people are having their babies’ later.
It’s funny you know because, you know,
my sister got married at like 22
and had her kids at like 24,
she was like the latest of her friends.
#1Wow, right.
#2It’s like nowadays people
are getting married at like 35
and having their baby at like 38
or something like that right.
So if you’re having your baby at like 35+,
I mean that used to be considered
as low fertility time.
#1Right, that’s advanced maternal age.
#2Exactly, because fertility
sort of peaks around 20 right,
like you can’t stop getting pregnant
at 18 or 20, right,
but at 35 it’s not as easy as it was,
so if you’re wasting time because you’re
like saying I got to wait for the evidence
and you know I’m going to do cycles of IVF,
it’s well like why not, like you can do that.
But why can’t you add it
to or just use it instead?
It just makes no sense and that’s what
I mean, it’s sort of the art of medicine,
because it’s not like do I not have evidence
that works, no, but…
#1Yeah, it’s a good perspective.
We talk a lot about
evidence based medicine
and that is important to understand
the quality of the evidence,
especially when there is a risk
to the treatment, like you’re saying.
So, I think that was a good perspective
for you to talk about weighing the risks
and the benefits
is what we do for everything.
If the risk is very low then the need
for evidence is also a little bit lower
if there’s a potential upside,
it seems like one of those circumstances.
Yeah it was sort of a whirlwind tour
through the fasting, through longevity,
through cancer, through fertility and it all
tends to have a common theme, doesn’t it.
#2Yeah, this is the thing, the thing is that
we look at the–
and I went over this
and the diabetes code is that–
if you look at the five sort of things
that deal with metabolic syndrome,
so the waist circumference, type 2 diabetes,
high triglycerides, low HDL and hypertension,
they’re actually all linked
to hyperinsulinemia,
but there’s actually
so much more to it
because it’s like
after the metabolic syndrome
it’s like obesity linked I think
mechanistically really to hyperinsulinemia,
type 2 diabetes,
linked to hyperinsulinemia,
PCOS linked to hyperinsulinemia,
but also things like cancer where it may play
not a sort of causative role
but sort of facilitative role.
I mean you’re talking about
the biggest killers in America,
so heart disease, stroke, diabetes, cancer
are sort of like at least four of the top five
and all of them are impacted
by hyperinsulinemia.
I think that’s a better term
than insulin resistance
as it immediately tells you
what you need to do.
So, insulin resistance
doesn’t tell you what you need to do.
#1Good point.
#2So, if you say, I have insulin resistance,
people will say what caused it,
and then there’s all this debate, oh maybe
it’s a high fat cause in insulin resistance,
I don’t think so, but if you say now,
that the problem is hyperinsulinemia,
then you say okay well
I have too much insulin, bring it down.
It’s like well it seems pretty obvious
how you can bring it down.
Cut the carbs and don’t eat,
so it’s much more powerful.
So just changing that word, makes it so
much more powerfully clear to people,
what you’re supposed to do because
there’s been a shift in medicine, right.
If you look at the causes of death,
there’s a complete shift from sort of
100 years ago and you’re talking–
#1Trauma, infection.
#2Exactly, right, the infections and diarrhea,
you now, that sort of thing
to what are now,
you know well the top two, sort of,
if you’re looking at the cause of death too
and then there’s everything else.
Heart disease and cancer are off the scale
in terms of the amount of people they kill
and then everything else
is actually quite a bit lower than that.
So, and those are diseases
which are going to be impacted by metabolic
syndrome
and also we know cancer,
like for so many years
was thought about as a genetic disease,
it’s like what about the genetics when
you put it in a high growth environment,
which is a high nutrient environment,
and it’s like okay,
well you know that cancer,
you go back to sort of those traditional
African societies and stuff.
They had cancer right, a lot of them
were viral cancers, lymphoma and so on,
but those cancers like breast cancer,
they practically didn’t exist.
The Eskimo, or the Inuit that we call them
now, in the far north of Canada,
they actually studied them, very intensively
to see why they were immune to cancer.
#1Immune?
#2They’re immune to cancer, except for EBV
they got nasopharyngeal carcinoma and stuff,
but they didn’t get breast cancer
and they didn’t get colon rectal cancer.
And then of course, we took them away
from their traditional lifestyle
of hunting and gathering
and gave them white bread
and you know seed oils and sugar
and all of a sudden
cancer just goes way, way, way up.
So, we pretend that cancer is this disease
of all genetics, genetics, genetics
but it’s not because two of the sort of–
okay if you talk about the big three cancers,
lung cancer, obviously it’s just smoking,
right? Let’s forget that.
So the next two are breast cancer
and colon rectal cancer,
prostate cancer is number four
and is actually very common,
but doesn’t kill as many people
because it’s slow growing
and it doesn’t sort of effect
the younger groups as much.
So, breast cancer and colon rectal cancer,
which we’ve already declared
are obesity related cancer,
so it’s like let’s face the fact
that these are actually diseases
that may have something
to do with insulin
and reducing a state of hyperinsulinemia
might be highly beneficial for them,
and again what’s the downside?
#1-What’s the risk, yeah.
#2-Exactly.
#1So, when done safely, that’s the key.
When done safely when fasting,
with low-carb nutrition,
when done safely can make
a big impact with very little downside.
#2Yeah, absolutely.
#1Well, it was a great summary
and a great discussion of all that,
so thank you very much for taking the time.
Give us a little hint, what’s next for you
and where can people learn more about you?
#2Yeah, so they can go to our website
which is idmprogram.com,
which stands for intensive
dietary management
and there’s lots of resources, free resources
and paid resources if you want more.
You can go on Twitter,
I’m usually fairly active there.
I’ve got the books, you know.
Next up, you know
I’m writing a book about PCOS
which is sort of you know
about what we talked about
and also, I’m doing that with Nadia
and then also a cancer book as well.
Just talking about sort of,
it’s not like a how to cure cancer,
because that’s not going to happen,
but it’s sort of this, you know I’m really,
really fascinated
because the whole story of cancer
has changed
so completely from what
we thought it was.
We thought it was just a bunch of randomly
accumulated genetic mutations
and sort of from 1990-ish, you know
when I went into medical school in 92
sort of to 2010 probably,
it was all considered genetic mutations.
But now the whole theory of what cancer is
has completely changed
and now we’re talking about evolution,
using evolutionary biology
and trying to understand
how cancers develop
and we’re trying, talking about, you know–
One of the really fascinating things
about cancer
is why it occurs in every single cell
in the body,
like almost every single cell in the body
can become cancerous,
and that’s really weird,
and it’s not just that.
Almost every multi cellular animal
in existence can develop cancer,
even a hydra which is one of the most
primitive multi cellular organisms
can develop cancer.
So cancer is not a disease of just humans,
it actually predates humanity by a lot.
It’s a much, much more ancient than
we knew,
and it actually probably dates back
to the transition between uni-cellularity
and multi-cellularity,
which is, you know what is,
and that’s really what the fascinating story
of cancer really is, and that’s …
#1That almost speaks against insulin
resistance, as being a contributor,
so I think it’s more complicated than–
#2It’s definitely more complicated.
But insulin resistance or hyperinsulinemia
is going to play a sort of facilitative role,
it’s going to make–
it’s not going to cause cancer.
#1I think that’s an important
differentiation.
#2If the cancer is there,
it’s going to make it grow faster.
That’s the difference, you take a Japanese
woman from Japan
and she may get breast cancer
but if you put her
in a high nutrient environment,
which is a high growth environment,
that is give her lots of you know, bread and
insulin goes way up and MTOR goes way up,
well you know all of a sudden that breast
cancer, which wasn’t a problem, back then–
You take a look at the Inuit for example,
they clearly have the potential
to develop cancer,
but they’re keeping insulin
so low for example
that those cells never get
the growth–
#!Environment matters.
#2It’s the environment that matters
but then you put them in–
you give them you know fried bread,
which is basically like white bread
fried in oil, that’s what they eat.
Now you give them
a high growth environment
and now those cells that would not
have grown, do grow
and that’s when you start to see cancer.
So we go from a time where we consider
the Inuit to be completely immune to cancer,
these people don’t get cancer ever,
to hey they get a lot of cancer over here,
and it’s because of the environment,
not because of the genetics.
So, that is the sort of story of cancer,
so it’s
not really just about fasting and so on,
actually you know, I’m more interested
in the deeper story which is changing
and I don’t think it’s the end of–
I don’t think it’s the final answer,
there’s just so much more
to be learned about it.
But it’s just very interesting
as we move from that transition,
from a paradigm of pure genetics
to a paradigm of evolutionary biology,
which to me is a much more fascinating.
#1Interesting structure change, for sure.
Well, thank you for all your information
and all you’re doing online
and all you’re doing to help people and
promote the idea that insulin matters
and environment matters,
thank you very much.
#2Thank you.