The BIGGEST MISTAKES People Make When Trying To LOSE WEIGHT! | Dr. Jason Fung
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Dr. Jason Fung challenges the conventional wisdom of weight loss, asserting that counting calories and restricting energy intake simply does not work because it ignores the hormonal mechanisms governing metabolism. He explains that while thermodynamics suggests a calorie deficit leads to fat loss, this assumes a stable basal metabolic rate which is biologically incorrect; when caloric intake drops without addressing hormones, the body compensates by lowering its metabolic output rather than burning stored fat. The core issue lies in insulin, described as a nutrient sensor and storage hormone that signals the body to save energy for times of scarcity. When insulin levels are high due to eating processed carbohydrates or frequent meals, the body enters a "storage mode," effectively locking away fuel reserves and preventing access to existing body fat stores regardless of how few calories one consumes. Consequently, even significant caloric restriction fails if it is accompanied by chronic hyperinsulinemia, as seen in studies where diabetics on high insulin doses gained weight despite eating less than 700 calories a day. The discussion highlights that not all carbohydrates are equal and distinguishes between natural sources found in traditional diets versus highly processed refined sugars which lack satiety signals like ghrelin. While protein also stimulates insulin, it simultaneously triggers other hormones related to fullness and does not primarily serve as fuel for storage in the same way glucose or fat do; dietary fats bypass the liver's processing entirely and enter fat stores directly without requiring insulin. Fung emphasizes that weight gain is fundamentally a hormonal imbalance rather than a caloric one, noting that ice cream is far more fattening per calorie than salmon due to its impact on these regulatory systems. Furthermore, he points out that chronic damage drives obesity-related diseases like type 2 diabetes and kidney disease, making the reversal of insulin resistance critical for health longevity. Transitioning from metabolic health to oncology, Dr. Fung introduces "Cancer Paradigm 3.0," a shift away from viewing cancer solely as genetic mutations or uncontrolled cell growth (Paradigms 1.0 and 2.0). He argues that modern medicine has focused too much on correcting random genetic errors while ignoring the evolutionary nature of cancer cells, which revert to primitive, unicellular behaviors characterized by competition rather than cooperation. Using a vivid analogy of a wild bear wearing a tutu, he illustrates how these malignant cells are not necessarily new creations but ancient survivalist organisms that have stripped away their multicellular "civilization" layers due to chronic environmental stressors. This evolutionary perspective explains why cancer treatments often fail; they attempt to kill or genetically correct cells rather than addressing the underlying cause: an environment that selects for primitive, aggressive cell types. Fung elaborates on his "seed and soil" theory of carcinogenesis, explaining that while every human possesses the genetic seed for cancer in their unicellular ancestors, it requires a specific toxic environment—the wrong soil—to germinate. This chronic damage comes from persistent stressors like smoking, hepatitis B infection, or long-term exposure to low-dose radiation, rather than single acute events as seen with atomic bomb survivors who suffered minimal excess cancers because the damage was not continuous. The "soil" is created by a diet high in processed foods and sugars that induce chronic inflammation and hyperinsulinemia, both of which act as powerful growth factors for these primitive cells. By improving this environment through fasting, eliminating refined carbohydrates, reducing sugar intake, and managing weight to lower insulin levels, individuals can effectively starve the cancer seed before it grows, offering a proactive approach to prevention rather than relying solely on reactive chemotherapy or immunotherapy.
Read the full video transcript
Counting calories simply does not work
at all. And people will say, "Oh, but it
does, it does, it does." Well, if you
look at the scientific studies, it
doesn't.
[music]
Hey everybody, welcome to another
episode of Health Theory. I am here with
nephrologist and best-selling author Dr.
Jason Fung. Jason, thank you so much for
joining me.
Oh, thanks for having me. Great to be
here. Dude, I am really excited to um
talk to you about two things that I
think are really revolutionary um that I
don't see anybody talking about as well
as you or maybe even at all. And that is
you've really um
pushed for a paradigm shift in the way
that we think about both insulin and its
role in longevity, obesity, diabetes,
and on and on the list goes. And then
this whole idea of cancer paradigm 3.0,
which I find really really interesting.
Um I want to start with the role of
insulin um in weight loss, in
uh disease mitigation.
What is it that was sort of that key
insight for you that got you thinking
about this in a different way? And how
exactly is it that you think about it?
Well, it's interesting because the
question of weight loss is one that has
really become more and more important as
we've had more and more obesity. So, uh
over the years we've seen more people
with obesity, which has led to more
people with type 2 diabetes, which has
led them to get kidney disease, which is
where I kind of come in cuz I'm a kidney
[clears throat] specialist. So, it's
become a bigger and bigger part of the
practice. And it it uh sort of dawned on
me that eventually
got through my thick skull that uh
really weight loss is sort of really
critical to keeping people healthy
because it's uh sort of obvious. Like it
leads to type 2 diabetes, which is a
huge risk factor not only for kidney
disease, but for heart attacks and
strokes and cancer and it's a leading
cause of blindness and amputations and
diabetic infections and all kinds of bad
things. So, almost like
you know, 50% of what I do is related to
type 2 diabetes and the point was that
if you can reverse your type 2 diabetes,
then you're not going to get these
diabetic complications and in order to
do that you need to lose weight, which
is why I go became very interested about
8 years ago in the question of how to
lose weight. And I didn't know much
about it at the time, but people were
always, you know, what I had learned in
medical school was all about sort of
calories in, calories out sort of thing.
But the more I looked into it, one it's
a very, very
unsuccessful way to lose weight.
Counting calories simply does not work
at all and people will say, "Oh, but it
does, it does, it does." Well, if you
look at the scientific studies, it
doesn't.
Every single study that's looked at sort
of say, you know, trying to restrict
calories leads to at best a couple of
pounds of weight loss over like 8 years.
So, you acknowledge that if you if you
take calories out of somebody's diet
long enough, they are going to get lean
regardless of anything else. So, where
is where does that paradigm break down
in reality and is it just willpower that
people aren't sticking to it or is it
something else?
Well, it's something else and the whole
point is that it's not the number of
calories, it's what your body does with
those calories. Because if you take 100
calories, if you eat a cookie for
example, you take 100 calories,
[snorts]
your body has a decision to make. Do I
store that as body fat or do I burn it
for energy and say increase body heat
generation for example. And that's the
basal metabolic rate. That's the number
of calories that your body uses
in a day. So, which your body does with
that same 100 calories, you can either
become fatter or you can have a bit more
energy during the day. And which one
your body does really depends on the
hormones that are associated with the
foods that you're eating. And that's the
real key because if you simply cut
calories, and this is the way that, you
know, I was taught and everybody was
taught, you simply cut the fat, you eat
less fat because fat is very dense in
calories. You get less calories and
therefore your body is going to lose
body fat. But that's not necessarily
true. If you eat 500 calories less, your
body could simply decide to burn 500
calories less and you won't lose any
body fat. And it's not a matter of
thermodynamics because that's that whole
idea that it's just about thermodynamics
assumes that your basal metabolic rate
remains absolutely rock stable. That is
if you're using 2,000 calories a day
today,
you go on a diet, you'll still use 2,000
calories a day. But you won't. We know
we've known that for at least 100 years
of basic research that your body will
actually use less, fewer calories. So,
cutting 500 calories a day, which has
been the standard advice, is very
unsuccessful because if you don't change
the hormonal system in your body, the
the the and different foods contain
different hormonal instructions.
Your body could simply decide to burn
500 less and you will not lose body fat.
So, it's it's it's simply false to say
if you cut 500 calories a day down,
you'll lose a pound of body fat a week.
It's actually not true in any
way, [laughter] shape, or form. Um just
like if you say, well, if you make an
extra $100,
uh you know, this week, that you'll be
$100 richer. You may or may not be. If
you make $100 more and you spend $100 by
going out, you're not richer. Same thing
with your body. You You You You take 500
calories or less that day, but you burn
500 less because your metabolic rate
goes down, you're not losing body fat.
And that's the whole point. So, it's
It's not the total number of calories
that's important. It's what your body
does with those calories, and that
depends on hormones. And in fact,
everything in our body runs on hormones.
Those are the instructions that we give
to our body as to what to do. So,
everything your body does or doesn't do
depends on hormones. Those are the sort
of mediators. Do you have any sense of
why different foods have different
hormonal cues? Like, why is it that
carbohydrates
signal the body to secrete insulin, I
think, the most out of all the
macronutrients?
Given that that is the signal to the
body to store, like, why doesn't
protein, for instance, signal the body
to store? Why is it specifically
carbohydrates? Yeah, actually protein
does stimulate insulin as well. And
Equal amounts? Um some of some proteins
can actually stimulate quite a bit of
insulin. It doesn't So, if you eat
carbohydrates, your glucose goes up, and
then your insulin goes up. In protein,
your glucose doesn't go up, your insulin
does go up. And And it's really to do
with the way the body metabolizes. So,
insulin in a more general sense is a
nutrient sensor. So, that tells your
body that, "Hey, food is on the way in.
Therefore, let's switch over to storing
calories
as opposed to burning calories."
The reason dietary fat doesn't do that
is that it doesn't get metabolized
through the liver.
Dietary fat actually gets absorbed
through the intestines, goes into the
lymphatic system, and sort of goes
directly into your fat stores. So,
because it doesn't go through that whole
processing through the liver, it
actually never metabolizes
and therefore doesn't really need
insulin for that. But, one of the things
is that insulin you know, different
hormones, our body needs to know what's
coming in and what proportion. So,
insulin is a nutrient sensor, but so is
something called mTOR, which really is
very specific for proteins. It goes up
quite a lot, tells your body that
there's a lot of protein coming in. And
there's a lot of
associated things, but one of the things
that's important these nutrient sensors
are also linked to growth pathways. So,
therefore, your body really only wants
to grow when nutrients are available.
And therefore, when you do get take a
lot of
carbohydrates or even protein, your body
senses that there is food coming in and
therefore will turn on growth pathways
to grow muscles, to grow, you know,
stores of body fat, that kind of thing.
Is the key in this then, cuz the thing
that I found most interesting about what
you talk about is a focus on insulin, at
least that's been sort of my read on
what you talk about. Moving away from,
you know, for a long time you hear
people talk about glucose, blood
glucose, the body tightly regulates
that.
But, this idea, the analogy that you use
of the suitcase, right? And sort of
where this starts to become a problem is
what we call insulin resistance. It's
probably not the right way to think
about it.
We'll get to that in a second, but first
I want to talk about low-carb diets,
right? So, low-carb was wildly effective
for me in terms of reducing the body fat
that I had.
That's certainly something I've heard
you and other people say that reducing
your carbohydrate intake is, you know,
going to have a disproportionate
response in terms of body fat than
something like,
you know, dietary fat or protein.
Help me understand then the
relationship, if protein is spiking my
insulin and insulin is the thing that's
storing things into my fat cells,
why are carbohydrates more, quote
unquote, problematic when it comes to
storing fat.
I think it comes down to several things.
So, proteins is actually quite complex
because it's not primarily fuel. So,
carbohydrates and fat are primarily
fuel. We we burn it and we store it. So,
our body stores glucose, our body stores
fat, but our body doesn't really store
protein. So, it's primarily a structural
thing. So, your body isn't So, even
though insulin is stimulated, there's
it's actually quite complex because
glucagon is stimulated which keeps the
glucose normal. Um but then protein also
has very strong effects on satiety.
That is there are certain other hormones
that when you eat, for example, protein
are going to tell you, "Hey, you're
full. You you need to stop eating."
So, if you think about eating steak, for
example,
uh you can eat a certain amount of
steak. And then at some point, you can't
really just keep eating.
Uh you will actually just get nauseous.
As we've all done at the buffet when
we've eaten too much.
You can't just say, "Oh, that looks
good. I'm just going to have another
pork chop." It's really hard to do that
because those satiety hormones are very
powerful.
Uh the reason carbohydrates are very
problematic is that they tend to be
processed. So, processing removes a lot
of these satiety signals. So, even if
you've eaten a huge buffet and somebody
says, "Hey, do you want a few sips of uh
my soda?" You'd say, "Sure. No problem."
Because they don't activate your satiety
mechanisms. And same for like a cookie.
You could easily eat a cookie after
after you're full from dinner where you
would not eat another, you know, pound
of steak. So, it's it's a bit more
complex because there's multiple
interacting hormonal systems that
regulate how we respond.
Protein doesn't seem to be nearly as
bad. Even though it has a lot of insulin
effect, it has probably a lot of these
other hormonal effects that are just as
important and really stop us from
eating. Just like if you were to eat
steak and eggs in the morning, a lot of
fat, a lot of protein, it tends to keep
you more full than if you were to eat
white bread and jam. You eat that and
then at 10:30 you're looking for a
low-fat muffin, for example. And And
this is
one of the things which I always say is
like when you're thinking about weight
gain, weight loss, really have to think
about hormones because it's really a
hormonal imbalance, not a caloric
imbalance because the the calories in
all these foods
can actually be exactly the same. Um and
that's why I'm not and I you know, not
all carbohydrates are bad for you. Like
clearly there have been many, many um
societies that have lived primarily on
carbohydrates. Yet if you measure the
insulin um
response, they're actually quite good.
So, something like they they did a study
in Kitava, for example, which is a South
Pacific island and um
they measured their diet and it's about
70% carbohydrates, but natural
carbohydrates and they didn't weren't
eating all the time. Then when they
measured their insulin, their insulin
level was below the fifth percentile of
a reference sort of Swedish population.
So, that means that even though they're
eating a lot of carbohydrates, their
insulin levels are still very low. So,
there's lots of things, not only the
foods that you eat, but also the
frequency which with you eat them plays
a really important role and the amount
of processing that goes into it. And you
can see that effect in something like
the glycemic index where when you eat
white bread, things just spike way up,
but if you were to eat beans, which is
all carbohydrate, the glycemic index is
much, much, much lower. And most natural
foods are like that. You don't see that
huge spike that you get. So, the the
processing of the carbohydrates makes it
especially
problematic because it is a fuel source
for our body that our body is able to
use very easily.
And it's highly refined so that you
don't have any satiety and then you're
getting it sort of absorbed very quickly
because you've removed all the fiber,
you've removed all the fat. And that's,
you know, that's that's sort of what
goes into it. But focusing on the
hormones is really important because it
leads you away from focusing on
something like calories. The only
implication of focusing on the hormones
as opposed to calories is that some
foods are more fattening than other
foods. That's really the only
implication. It's like, boy, if you were
to ask your grandmother or
great-grandmother, she'd say, "Well,
duh. I hope you didn't have to go to
university to learn that. [laughter]
Of course some foods are more fattening
than other foods. Like cookies are
fattening. Like anybody could have told
you that. Anybody with an ounce of
common sense would have told you you
don't get fat eating broccoli. Like
these are just like
things that we take for granted that we
should know.
But you get so people get so so focused
on, "Oh, it's all calories. It's all
calories." that they say ice cream is as
fattening as salmon. It's like, no.
Obviously not. If you've ever lived, you
know,
in on this earth, you would know that
[laughter]
ice cream and salmon are not equally
fattening for the same amount of
calories. That's just common sense. So,
um this distinction between chronic
caloric restriction and fasting,
um
that I find really interesting. And let
us, for the sake of this discussion,
assume that we have a person who is
willing to endure an unlimited amount of
suffering.
Um and you even you've talked a lot
about the book Unbroken that you read
about World War II um people in Japanese
concentration camps, and they were
literally being starved.
And obviously all of them got lean. So,
what I want to understand is, okay,
fasting seems to have all these
tremendous benefits,
chronic caloric restriction has some,
but also has like this really damaging
psychological component. If there was no
damaging psychological component,
would they be equal, or is there still
some difference?
It all depends on how you do the caloric
restriction. So, because it's not just
about the calories, it's about the
hormones, right? So, you have to sort of
take it not to sort of this
two-compartment problem. You have to
take it to like a three-compartment
problem, right? There's what's coming
in, there's what's stored, and there's
what's being used, okay? So, most people
only think of sort of the two
compartments, and then the storage is
sort of left over. But, that's not the
way the body works.
If insulin is high, your body is going
to store calories. Remember, insulin is
a nutrient sensor. It tells your body
that, "Hey, energy is coming in. You're
eating. You need to store some of this."
Right? It's so it's so you eat
breakfast, lunch, dinner.
get somebody on a low-calorie diet, like
if you were on 700 calories a day, but I
gave you insulin, could I make you fat?
Yeah, absolutely.
Whoa.
Because think about it this way. If you
have insulin, your body
And so, if you think about it
physiologically,
if you have insulin, your body goes into
a storage mode, because it's a hormone,
insulin is a hormone. It tells your body
food is coming in, and even if you don't
give food, if you just give insulin,
you're going to switch your body into
this mode where it thinks that food is
coming in. So, it's going to store
energy. So, imagine that, for example,
you are a coal, you know, a coal plant,
right? A power plant. You get 2,000 tons
of coal coming in, and you burn 2,000
tons of coal. That's fine. You have a
storage compartment, too. So, if you're,
you know, if you do a thought
experiment, say say you have 2,000 tons
of coal coming in, but you divert the
whole thing over to
uh or 1,000 tons of coal into storage,
well you only have a thousand left. So,
you're going to feel tired and cold and
hungry.
And you're going to get fat at the same
time, right? That's what's going to
happen. But it's because of the way that
you've diverted off the energy. So,
think about it from a human body
standpoint.
[snorts]
Suppose you have 2,000 calories coming
in, 2,000 calories going out. Now you
artificially inject insulin.
Well, you shuttle a thousand calories
immediately into body fat and you have a
thousand calories left
to burn. Well, what's going to happen?
Your your your body heat generation is
going to go down, your heart rate is
going to slow, you're going to feel
tired, you're going to feel hungry
because you want to get more energy,
right? That's the signal for you to get
more energy so that you can get more you
can burn more.
Guess what? That's exactly what happens
when you go on a chronic calorie
restricted diet.
And the the point is that if you do it
correctly and you you correct that
insulin part of things
so that none of it's going into storage
and you can do that with chronic calorie
restriction, you certainly can. You have
to know that you have to do it properly
like cutting out
processed foods, cutting out refined
carbohydrates, that kind of thing. But
it all depends on that sort of that sort
of toggle in the middle that says how
much goes here, how much goes here.
Insulin
it what it does is it tells your body to
store fat, but it also turns off fat
burning. Remember, fat is purely a store
of energy. It's a store of calories. So,
you're immediately shuttling all your
energy into storage and you have nothing
left.
So, say you take 700 calories of it,
you're pumping people full of insulin.
So, that energy is going to go into into
storage. And 700 is probably the lower
limit of what you could really do, but
your body would then try to subsist on
say 5 600 calories of energy. You'd get
really hungry because you you you've got
no energy coming in. You probably
wouldn't be able to last very long, but
you could still gain weight. There's a
great experiment a few years ago where
they actually took the type 2 diabetics
and they gave them a lot of insulin. So,
they went from zero uh units a day to
100 units a day over a span of 6 months,
which is a lot. And they dropped the
number of calories that they ate by 300.
Okay, so they're taking insulin, but
they're eating less. 700 300 calories a
day less. So, over the span of 6 months,
on average, that group gained 20 lb.
20 lb by eating 300 [laughter] calories
a day less. Why? Because so, let's take
an example. You're eating 2,000
calories, you go down to 1,700,
but the insulin is shuttling 700 of that
immediately off to storage. So, you're
gaining body fat. Now, your body can
only burn 1,000 calories a day. So, you
feel like crap, you feel tired, you feel
hungry, and you're still gaining weight.
And guess what? If you do it wrong,
which is constantly snacking and eating
cutting out all the dietary fat and
eating all refined carbohydrates, which
remember is almost precisely what we
told people to do in the '80s and '90s.
Oh, I remember it well.
Yeah, actually
[laughter]
I had a tub of licorice because it was
fat-free, and I would just eat it and
eat it. I'm like, it's fat-free. What
What's happening? Why am I getting fat?
Yeah. [laughter]
That was a very confusing time.
It makes perfect sense from like because
but you have to think of that additional
step, that is what is the body actually
doing? It's this sort of flip this
switch. So, when you eat, you're storing
body fat. When you don't eat, when
insulin is going down, you're going to
burn body fat. You're going to actually
going to You can't burn body fat if
insulin is high. Let's ask then the
reverse question. So, I fully accept
that all food is a signaling molecule
that's triggering a some cascade of
hormones.
I know what to do if I want to store a
lot of fat. I'm going to eat a lot of
processed carbohydrates that are going
to remove all my society mechanisms and
it's going to spike my blood glucose
like crazy. My body's going to pump a
bunch of insulin to make sure that that
gets pulled out of the bloodstream. I'm
going to get fat. Okay.
Is there a diet that's optimized on the
exact opposite side where I'm taking in
very satiating amount of calories but
it's dropping my insulin or failing to
trigger my insulin is maybe the right
way to think of it
and therefore I'm eating maybe more than
your average bear but I'm actually
getting leaner.
Yeah, there's there's certainly lots of
them.
There and and the the principles are
much the same. One is you want to avoid
sugar cuz sugar, the way that we process
fructose is sort of particularly bad and
that's why sugar is particularly
fattening really and that's that's true
if you're a bear. You're eating a lot of
ripe berries and stuff because you're
trying to gain fat.
And it's also true as anybody knows if
you're eating a lot of cookies and
brownies, you're probably going to gain
weight. The
The other thing is you can't eat all the
time
because again, it's a cycle between
feeding and fasting. That's what we're
supposed to do. If you don't give your
body time to burn off all those calories
that it's taken in which means the
fasting period, you're going to overall
gain weight. It's like a one-way valve.
If you go in but don't come out,
eventually everything just gets bigger.
Same thing.
[snorts]
That energy cannot come out if your
insulin levels are high.
That's just the way it's designed and
it's it's sort of like, you know, if you
if you see a tanker, you know, those
tanker trucks on the side of the the
road. Sometimes they you think, "Oh,
they'll never run out of fuel because
they have all this fuel." But they do
run out of fuel, of course, because you
can't access that fuel that's in that
big container. Same thing with your body
fat, right? It's locked away. If you do
not lower your insulin levels, you will
never have access to those stores of
energy.
Once you lower it, hey, all that energy
just comes flowing in. And and for
people who are who are on long who have
done longer fast, and this is what's so
interesting about the whole process when
you actually do it is that the hunger
starts to go down significantly. The
psychological hunger goes up because
people are like, "Oh, I really want to
eat that." But, the physical hunger
actually tends to go down. Meaning
measured by things like ghrelin or
whatever.
Ghrelin. So, hunger hormones and so on.
And and people you talk to people and
you know, I've done it live. I know lots
of people have done it. And they they
all say the same thing. By day three,
day four, the hunger's almost completely
disappeared. And why is that? Well,
because you're fueling yourself from
your body fat stores. And therefore, you
actually have no no need to eat. It's
It's It's It's an interesting process
which people never think about, but it's
completely physiologic.
Yeah, so I've done my longest fast was 5
days.
Um I've done many fast that are 24 hours
to 72 hours. I find 72, while not
pleasant, I find it relatively easy. I
don't decline in performance. But, day
four and five, I do. And I'm super
curious to know um if I am doing
something wrong. Like, am I supposed to
be supplementing? And and I'm talking a
true water only fast.
Um
should I be eating salt? Should I be
taking magnesium? Like, what what is it?
Yeah, everybody's different. Certainly,
some people salt is probably the main
thing people get into trouble with
because we're on a relatively high salt
diet. And then to go to a
sort of zero which is water only zero
salt is a bit of a transition sometimes.
So some people find that their pressure
blood pressure goes low
and
that that makes them not feel so good.
So a lot of people have found better
from taking salt either salt and water
or just a salt
like a under the tongue even.
Magnesium is another one that that tend
to know and some people find it helpful
to supplement there as well. The other
things that people find useful is to
take some broth for example which is
going to give you it's not a true fast
none of these are. I was going to say
that sounds like cheating to me. Yeah
they're they're they're sort of like
I call them variants because they're not
water only fast is really a true fast.
But you can get a lot of the benefits by
taking some of these other things and it
makes it easier. So it's a sort of a
trade-off it's sort of like bulletproof
coffee which is of course not fasting
but it's a very very pure sort of fat
and therefore it's going to provide a
lot of satiety and then let you go
through the day maybe allows you to go
long and
overall you might wind up positive in
terms of weight loss and so on. So lots
of people certainly have found that
useful not everybody. But certainly it's
it's that but water only fast can be
more difficult because of the associated
electrolyte
problems. Your body is supposed to
handle it
but it doesn't always. Sure. So if we're
looking at longevity and we want to
prolong life as much as possible and
anti-cancer in fact this might be the
perfect transition into your
brilliant synthesis of what's going on
from cancer paradigm 1.0 to 2.0 to 3.0 I
found that absolutely fascinating in
your new book cancer code. It was subtle
and yet changes
everything. And if you can just like
give a a
sort of thesis on that 1 2 3 thing I
think that would really help people.
Yeah. Yeah, and and you know, I'm I'm
not the one who made it up. I just was
the one to sort of explain it sort of in
an accessible way. And honestly, it's
it's the most fascinating story in
medicine today, I think, is
cancer [clears throat] because it's
undergone this tremendous change in the
last sort of 10-20 years, and nobody
even talked about it. And what I talk
about is sort of the the these modern
paradigms of cancers, the way that we
look at cancer. And the reason they're
important is because they determine what
sort of treatments we use. So, the first
sort of modern paradigm of cancer is
sort of this cancer is a cell that grows
too much. So, you have breast cancer,
for example, you have a breast cell.
Now, something happens to that normal
breast cell, okay, so it starts off as a
normal cell, but somehow mutates into
this breast cancer cell or this lung
cancer cell. And this lung cancer cell
then grows and grows and grows, and then
it moves around, it spreads, or this is
called metastasis, then you die. So, the
first paradigm is, "Hey, this is a cell
that grows too much." So, therefore, our
treatments are actually ways to kill
cells. And that's the sort of core of
modern oncology is to cut it out, which
is surgery, you can burn it with
radiation, or you can poison it with
chemotherapy. Chemotherapy is really
nothing more than a selective toxin. It
kills some cells faster than it kills
another cell, so that's why you have
these horrific side effects. Their hair
falls out, they're nauseated, all this
stuff you think about with chemotherapy
is because the idea of chemotherapy is
to kill the cancer slightly faster than
you kill the patient. That's really it.
It's a selective toxin.
But that's the paradigm, and it makes
sense from that
you know, because if it's if it's
growing too much, then kill it. That's
basically it.
Now, that reached its limits probably by
the '60s. And by then we were talking
about genetics, so everybody started to
look at genetics, and then that's the
sort of next huge paradigm shift. Is
that we were trying to understand at a
deeper level
not we weren't saying that cancer cells
didn't grow. The question we're trying
to ask is why are they growing? And so
we said, "Well, the answer now is that
they have genetic mutations that lets
them grow too much." And sure enough
when we looked we found these oncogenes
and tumor suppressor genes, so genes
that control growth. And when the cell
gets a mutation in one of these critical
genes, then it would grow too much. And
that made perfect sense.
So, the point of
something like lung cancer and smoking,
cuz we know smoking for you know,
clearly causes lung cancer.
Smoking is not a targeted mutation
device.
It's very non-specific. You're just
creating damage all over the place. So,
what they said was that this is a random
genetic mutation. So, you're just
creating damage in the genome. And if
you're damaging a lot, you're getting a
lot of chances to hit this critical
growth gene area, and it's going to let
cells grow. So, this was the the genetic
paradigm, which really has dominated
cancer medicine for the last 50 years.
And so, instead of trying to kill cells,
this led to new treatments. And instead
of trying to kill cells, we're trying to
correct the genes that controlled it.
And the first few drugs of the sort of
genetic paradigm were just amazing. So,
by the 2000s, we were like, "We are
going to cure cancer." So, we did this
whole human genome project. We said,
"All we need to do is map out all the
genes, look at the cancers, map out
those genes, and see what's different.
We're going to find one or two genetic
mutations. We're going to find a drug to
cure that one or two genetic mutations,
boom, we're going to cure cancer. And
that was really what we thought at the
time. It was a time of incredible
promise.
But it didn't work. That was
like if you look at the number of
genetic treatments of cancer that really
made a difference, you're talking maybe
five. Right? In the last 40 years, five
really good drugs. That's not a lot. And
that's a long way from curing cancer.
And the problem is when we went back, so
they did the Human Genome Project, then
they did this Cancer Genome Atlas,
where they mapped out all these genes.
They took 30,000 cancers, mapped out the
genes, and said,
"What are the one or two critical
genetic mutations?" They didn't find one
or two. Each cancer had like 50 or 100
genetic mutations. And And it was crazy
because if you had a cancer clinic where
one patient had lung cancer, so patient
A had lung cancer, patient B had lung
cancer,
patient A's lung cancer had 50
mutations, patient B had 50 mutations,
completely different mutations.
So, how are you going to treat this? You
can't get 50 drugs for patient A and 50
completely new drugs for patient B. It's
just impossible. And that's why cancer
treatment just sort of slowed to an
absolute crawl. It was just uh you know,
a huge amount of disappointment.
Um and that sort of spelled the end. It
wasn't a random genetic mutation. So, it
wasn't that genes weren't mutated. It
was what is driving these mutations? And
that sort of spawned this whole next
paradigm shift to cancer paradigm three,
which so few people people talk about.
And I don't understand why, cuz I I I
find it endlessly fascinating. And what
we were trying to do, we weren't trying
to
uh invalidate that the these genetic
mutations, cuz clearly these genes had
mutations. What we're trying to
understand was, once again, try and get
to that one level deeper of why. Why are
these genes mutating? And the totally
fascinating answer that they came up
with is that it was an evolutionary
process,
not a forward-moving evolutionary
process. It was a backwards evolutionary
process towards a more primitive form of
our cell, which was there from
evolution. And what's fascinating is
that if you look at pathologists, like
the way that people who look under the
the microscope at cells,
that is exactly how they describe cancer
cells, primitive,
uh undifferentiated.
You've got to use You use a an analogy
or a metaphor in the book about a bear
in a tutu that I thought, "Oh my god."
Like it lets you conceptualize what this
is so perfectly. Will you walk people
through that?
Yeah, and the point is that the cancer
is actually a reversion to a more
primitive form of a cell, and it's a
sort of like if you have a wild bear,
you can raise it and teach it to dance
and wear a tutu, but it's still a wild
animal. So, if you provoke it, it'll
still kill you. Like it'll still wear a
tutu, but it'll still kill you. So, it
reverts to being that wild animal, and
our cells are very much like that. So,
we came from unicellular organisms. So,
all of us sort of evolved from small
bacterias and so on, fungi, and so on.
And under the right conditions, these
cells actually undergo an evolutionary
process back towards this more
survivalist sort of primitive cell, a
single-celled organism. Its primary
mandate is to compete with other cells,
as opposed to a multicellular organism
which its mandate is cooperation.
And they are fundamentally against each
other. As we move from cellular
competition to cellular cooperation,
we had to put on all these instructions
on top, these genetic instructions to
suppress all these competitive urges.
When you cause genetic damage and strip
away you damage all these sort of
controlling layers,
what shines through is that competitive
nature. And then the cells, the cancer
cells actually behave exactly like
unicellular organisms. And that's
fascinating again because our own immune
system has actually identified these
cells as foreign cells. Like there are,
you know, immune cells in our body that
identify sort of self, our own cells
versus other cells, so you avoid
friendly fire. And cancer cells are
actually identified intrinsically,
without being having seen them ever
before, your own body will identify
these as foreign cells and destroy them.
And that's really the reason why we
don't have cancer sort of
with 99% of the population cuz when you
suppress the immune system, of course,
you increase your risk significantly of
developing these cancers because it's
our immune system which is playing that
anti-cancer role. So what you're trying
to do is weed out so our body has these
very efficient anti-cancer mechanisms
where we go around and we're hunting
down these sort of, you know, anarchists
and stuff trying to these people who are
not going to follow the rules, who are
who are competitors, not cooperators. We
try and hunt those down and we kill them
so that we stay cancer-free. It's only
at the end of, you know, only with time
uh when stuff falls through or with
chronic damage such as with lung uh lung
cancer, for example, with smoking that
that you're you're damaging the genome
and those controlling organisms and
allowing to shine through, which is
called an activism, which explains a
huge amount. Like that this theory just
explains so much
about cancer because if if you think
about
say let's take lung cancer again. So you
have a 50 mutations
uh in patient A, 50 different mutations
in cancer in in patient B, but their
lung cancers look exactly the same under
the microscope.
How does that happen? Like if you have a
100 mutations, your cell should look
completely different than this other
guy's cell, yet they look precisely the
same under the microscope. It's because
it was the original sort of cell. You're
simply stripping stuff away. You're not
adding mutations on. You're actually
stripping those away. And what's
fascinating is that the genetic So all
this genetic stuff that we've done, when
you look at the mutations of cancer,
they're all concentrated
in this area, it which is the the the
the difference between unicellular and
multicellular organisms. So they did
these studies where they take all the
genes and they say, "Let's rank them by
evolutionary age." So these are the
ancient genes, these are the recent
genes, and they put them on and then
they say, "Where are the cancer
mutations?" And they're all clustered
right around the point between
unicellular and multicellular organisms.
And like that is
so interesting. So then of course the
reason it's important is because now you
have if this is an evolutionary problem,
if these are actually unicellular
organisms, well now we actually have
ways to fight these unicellular
organisms, and that's our immune system,
and that's led to this sort of explosion
in interest in immunotherapy because
we're not trying to kill cells with
immunotherapy. We're not trying to
We're not trying to fix genetic
mutations. What we're trying to do is
treat these cancers like a foreign
species, like an invasive foreign
species,
and be able to identify them and also
bolster our own immune system to attack
them. But now you're getting a totally
different paradigm because you're the
concept of what this disease is, it's an
evolutionary disease,
which requires immune system to fight it
cuz that's our own defenses. That's
fascinating. Like that's a totally
different paradigm and such an
interesting
way to look at it and it's going to lead
to all these new treatments. So in the
book I talk about immunotherapy, we talk
about the abscopal effect, which is how
radiation plus immunotherapy may
actually help unearth these things. We
talk about adaptive therapy where
perhaps you don't have to give maximally
tolerated doses of chemotherapy because
you may not need it. It may be more
effective to use smaller doses.
All stems from the understanding of the
evolutionary paradigm of cancer as
opposed to the genetic paradigm of
cancer where you would never be able to
understand why these treatments that are
coming up now are going to be effective.
Man, this this is really feels and you
talk about sort of the hope this brings
in the book and it really does feel
hopeful, you know, cuz if you've pursued
something to a dead end, it's like until
you have another path to go down, it's a
pretty ugly place to be.
One of the things that you outline in
the book that I thought was really
enlightening is what it is exactly. The
you you talk about the seed in the soil.
So what is it about our modern life that
creates this soil, that stresses the
cell just enough that it is like sort of
in scramble mode of whoa, I have to I'm
constantly looking for this new mutation
or stack of mutations that's going to
allow me some path through this
cigarette smoke, this dietary problem,
this whatever.
Um
if you can walk people through what
we've sort of done to the soil. And
please, if you can, mention the when you
talked about the bomb in in Hiroshima
and Nagasaki, how they were expecting a
certain cancer rate, but they didn't get
it. And why that is. I thought I thought
that so interesting. Yeah, I thought I
thought so, too.
[laughter]
Thanks.
Um this concept is that you need both
genetics as well as the environment.
Like both are important. I'm not saying
one is more important, but you have to
have a seed, which is obviously all the
genetic material that you need to become
a plant, for example.
[sighs and gasps]
But you have to plant it in the right
soil. So, you take a seed, you put it in
the desert, it doesn't grow. You put a
seed, put it in proper soil, and give it
water, it grows. So, cancer
the seed is there in every single one of
our cells.
And not just us, but every animal
practically that we know has that seed
of cancer, because cancer, of course, is
our sort of genetic ancestor. That was
the unicellular organism from way, way,
way back. So, that's
Be selfish.
Yeah, exactly. The selfish sort of the
unicellular organism. But that seed of
cancer is there. Luckily, if we prevent
it from growing by using proper soil, we
can actually prevent it. And you you
look at these things that cause
you know, cause cancer called
carcinogens.
Turns out our diet is one of the biggest
ones. So, other than tobacco smoke
diet is sort of way up there. And when
you look at carcinogens, there's a
specific sort of thing that have to be
chronic, and they have to be sort of
sub-lethally damaging, which is the
point about Hiroshima. That is radiation
we know causes cancer, for sure. So,
when they dropped the atomic bomb, they
thought, "Man, we're going to get a lot
of cancers coming down the pipes, but it
was a single large dose of radiation,
not a chronic low dose of radiation,
which does cause a lot of cancer. So,
they did these atomic they did they did
these studies where they followed people
for for years and years and there was a
little bit of extra cancer, but like on
on average, way less. So, when they
estimate how many months of you know,
months or years of life lost, it was
like two months, something like that.
So, people these people were living like
82 years and they estimate that that
that atomic radiation maybe cost them
like two months of of life. Way less,
cuz we are thinking that these people
were going to get
you know, cancers at age 20 sort of
thing and that didn't happen because it
wasn't this chronic thing. And that the
reason it has to be chronic is that
cancer is an evolutionary process. If
you do not have chronic selection
pressure, you don't get this change. If
you just have one and then another
the mutations and you need they're going
to be random and they need to occur over
time.
They have to occur continuously because
that's the way that selection pressure
works in an evolution in a in a
population of cells. That is, if you if
you select for certain cells and do it
once, that's not going to be that
effective.
If you keep selecting for those cells,
like you only take the the the the the
cells that are sort of survivalist,
which are the the sort of more primitive
cells, then you over time you're going
to select the population that's going to
have more of those sort of survivalist
cells. If you have a single event,
there's no further selection pressure.
That is, if you look at
you know, if you look at
evolution of species, it's the same
thing. You can't simply have one event.
It has to be a continuous selection
pressure that produces that change. And
that's why it has to be a chronic thing.
So, tobacco smoking for example, You
look at viruses. So, if you have a
single terrible virus, like hepatitis A,
which is causes fulminant hepatic
failure, it kills you, but it doesn't
give you cancer, as opposed to hepatitis
B, which is a chronic virus. It doesn't
kill you, but it certainly does give you
cancer. H. pylori in the stomach, for
example, a very low-grade chronic
infection is what gives you cancer, not
a single sort of fulminant episode of of
inflammation. That doesn't give you
cancer. So, um you know, all of these
these sort of things, UV light and so
on, they're all chronic damage, and
that's part of that soil, and diet plays
a huge role. And the promise, of course,
is that if you look at
traditional populations, like when they
looked at uh populations that lived very
simply, so very low sugar, very natural
foods, they weren't eating all the time,
very little obesity, so people in Africa
that they had studied, Dennis Burkitt in
the '50s and '60s, and then in the Inuit
people, which uh and live in the far
north, for example,
uh they used to send
these expeditions up to the Arctic
Circle to find why these these native
peoples, these Inuit, were immune to
cancer. Then, of course, they became
civilized, we we gave them uh you know,
sugar, we gave them white flour, because
they didn't go bad, then they got all
the same cancers. Turns out they weren't
immune at all.
It was their environment, it was the
soil that was so important. But, the
promise is that if you can fix that
soil, that means you could actually
overcome the genetics.
Not in all cases, but in many cases,
especially of these obesity-associated
cancers, the breast cancer, colorectal,
and so on. And that's the sort of really
important thing, and the sort of
take-home message for a lot of people is
that the diet actually plays a massive
role and by understanding it, perhaps
you can reduce your risk of cancer and
that's where fasting as a way to control
your weight, as a way to control type 2
diabetes, which is a risk factor, as a
those are going to lower the risk factor
for obesity, which is a big risk factor
for those obesity associated cancers,
but it's your lifestyle that's going to
play a big role, not necessarily some
drug that's or anything like that. So,
it's all in your own hands. It's
amazing.
That That is truly amazing. Now, as one
sort of final point on this,
is is the chronic stressor, is that
simply being tipped into growth mode or
is it inflammation coupled with the fact
that we're tipped into growth mode?
Like, what is it specifically about our
diet that's causing this perfect soil
for mutations over time um
that leads to cancer?
I think they're I think both are are
correct. So, if you have
uh chronic hyperinsulinemia, insulin is
a very powerful growth factor.
Uh inflammation as a cause of chronic
damage in itself will cause cancer. So,
you look at the disease such as
ulcerative colitis or Crohn's colitis,
these are called the the so-called
inflammatory bowel diseases.
There's this chronic inflammation in the
bowel and what you get is a super high
risk of cancer down the down the line.
So, uh both inflammation and uh
hyperinsulinemia and obesity, all of
them are risk factors and and this is
the important thing is that
there's a lot of different things that
can contribute to the risk of cancer.
It's not just that if one is right, then
the other is wrong. I mean, both are
correct. So, if you eat foods that are
highly inflammatory and a lot of people
feel that, for example, omega-6 seed
oils perhaps are in in these big doses
that we take, perhaps those are highly
inflammatory. That,
even if it doesn't cause obesity, could
be a factor because we know
inflammation, chronic inflammation, can
certainly do that. So, both can be very
important.
Whoo, man, I really hope people read
your book, The Cancer Code. It it was
very insightful. If people want to stay
connected with you, learn more, follow
your extraordinary clinical-based
thinking, where do they go?
Uh you can follow me on Twitter. Uh my
handle's @drjasonfung. That's
drjasonfung.
Um also, uh my website is
thefastingmethod.com.
And you can also find me on YouTube. Uh
my channel is Jason Fung and uh I have a
number of videos on fasting
um and and other things. Uh so,
check me out there and you know, I hope
uh you know, and then my books, of
course, The The Obesity Code, The
Diabetes Code, The Cancer Code.
Love it. Awesome. Jason, thank you so
much for joining me today. I really,
really enjoyed our time together and I
really enjoyed researching you as well.
Um so super grateful. And speaking of
things you'll be grateful for, if you
haven't already, be sure to subscribe.
And until next time, my friends, be
legendary. Take care.
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